Digital reminiscence systems could improve quality of life for people with mild dementia.
Dementia is on the increase, but for the sake of the quality of life of sufferers and their family and friends finding ways to allow the patient to remain in their own home and to live independently is an issue that must be addressed. At the same time, enabling independent living could also reduce the economic burden.
Sufferers of mild dementia often have difficulties with their daily lives, they cannot remember names, faces, details of their day, and how to navigate home or to other places. They might also be unable to do even mundane tasks such as preparing a meal, because they cannot remember the steps involved, and if they succeed they may forget to serve it. Their ability to maintain an independent living is thus reduced and they risk losing social contacts while becoming increasingly frustrated, affecting not only themselves but also the people around them. One approach to addressing this problem is to use memory aids, such as notebooks, calendars, diaries, alarms, whiteboards and other such equipment. Some people with mild dementia also rely heavily on their carers to cope with their memory problems, which can lead to depression in the carer.
A digital memory aid based on capturing images of the patient's surroundings automatically has been tested using Microsoft's SenseCam, known as ViconRevue, and other devices. However, such devices require substantial computer processing, and although tests have been positive to some degree, digital memory aids of this time have not been adopted widely yet.
Basel Kikhia and colleagues at Lule?? University of Technology and Johan E. Bengtsson of InterNIT, Lule??, Sweden, suggest that a more holistic approach to memory aid, known as life-logging, might be more effective and easier to implement. "Life-logging is recording activities that a person experiences for later retrieval, while context-awareness is reacting on changes in contexts," the team explains. "For example, logging a picture when a person changes location. The aim is to create a semi-automated system which helps persons with mild dementia in supporting and maintaining their life story." An entirely portable, lightweight and simple to use device that could be worn at all times would be ideal and the time has devised just such a system. The device will focus on support for reminiscence and having access to information about previous activities to support memory recollection as well as allowing the patient to annotate images, diary entries, and notes, either alone or with their carer.
"A digital reminiscence system will provide a visualization of life experiences and allow a person with mild dementia to reminisce on their life story based on persons, places, and images," Kikhia says.
Sources: Inderscience, AlphaGalileo Foundation.
вторник, 28 июня 2011 г.
суббота, 25 июня 2011 г.
Memory Loss Linked With Defects In Crucial Brain Protein
The ability to recognize familiar objects and companions is lost when levels of a protein crucial for recycling a chemical messenger in the brain are reduced, mimicking some of the symptoms of Alzheimer's disease, an international team led by Duke University Medical Center scientists has discovered.
Mice genetically engineered to have modest defects in this recycling protein display symptoms that resemble those in Alzheimer's, such as the inability to remember familiar faces, according to the researchers. The crucial protein recycles a chemical called acetylcholine that carries messages between nerves cells, the scientists said.
"By using these genetically engineered mice as models of Alzheimer's, we can learn more about the neuronal circuitry of the brain, and perhaps even discover new ways to alleviate the symptoms of this devastating disease," said senior study investigator Marc G. Caron, Ph.D., James B. Duke professor of cell biology.
The team reports its findings in the Sept. 7, 2006, issue of the journal Neuron. The research was supported by the National Institutes of Health and American Health Assistance Foundation.
Acetylcholine is a neurotransmitter that carries a number of vital signals from one nerve cell, or neuron, to another. Normally, when a signal needs to travel through the brain, neurons release acetylcholine to transport the signal across the gap, or synapse, between neurons. Acetylcholine is stored in tiny hollow spheres, called vesicles, that bud off of the end of the neurons. A kind of protein pump, called a transporter, located in each neuron controls the storage and release of acetylcholine from these vesicles, recycling the neurotransmitter back to the nerve cell vesicles in preparation for the next burst of signal.
It is this acetylcholine transporter protein that the researchers targeted by disrupting the gene that controls its production.
"Acetylcholine is important for every function in the body -- breathing, eating, walking, practically everything," Duke's Caron said. "If we knocked out the function of the protein completely, then the mice would die. So instead, we just knocked its function down to a low level."
In the study, the researchers took advantage of a built-in trait of their animal models -- that is, the fact that mice are innately curious and tend to explore new objects and companions extensively by sniffing and touching. The scientists ran mutant mice, in which the acetylcholine transporter gene was defective, through a series of tests to evaluate their performance in behavioral tasks. They ran normal mice through the same tests to serve as a control group.
The first test assessed the mice's ability to discriminate unfamiliar objects. The researchers gave the mutant and normal mice two objects to explore, and then took the objects away. A short time later, the scientists gave the mice back one of the objects, along with a nonfamiliar object. Both the normal and mutant mice initially explored the two objects to the same degree, but after the break the mutants had trouble remembering the familiar object, said lead study investigator Vania F. Prado, Ph.D., an associate professor of biochemistry at Universidade Federal de Minas Gerais, in Belo Horizonte, Brazil.
The second test of memory was similar to the first, but instead of giving the mice objects to explore, the scientists introduced a new mouse into the cage of their test subjects. The normal mice extensively explored the "intruder" mouse, but over time they showed less and less interest, the researchers said. This behavior, they said, demonstrated that the normal mice had become familiar with the intruder. In contrast, the mutant mice failed to recognize the intruder even after several meetings, thus displaying a defect in what the researchers called "social memory."
These findings suggested that the decreased levels of acetylcholine in the mutant mice resulted in their trouble with social memory, the scientists said.
To determine if this theory was true, the researchers set out to correct the behavioral defect by treating the mice with drugs that increase levels of acetylcholine in the brain. Called cholinesterase inhibitors, the drugs block a brain enzyme that typically breaks down acetylcholine, thus leaving more of the neurotransmitter available for sending the signals involved in learning and memory. Physicians give cholinesterase inhibitors to people with Alzheimer's to slow their memory loss and enable them to perform daily tasks, lessening the symptoms of the disease.
Mutant mice treated with the drugs, when run through the same tests, recognized intruder mice after several meetings, the researchers said, adding that this observed improvement in the performance of social recognition confirmed that the defects stemmed from the reduced amounts of acetylcholine.
"Now we can use our animal model to screen for similar drugs that can improve the function of acetylcholine in the brain," said Marco A. M. Prado, Ph.D., an associate professor of pharmacology at Universidade Federal de Minas Gerais and senior investigator of the study. "This is of importance because decreases in acetylcholine are thought to be relevant for the diminishing cognitive function found in aging and also are believed to be associated with some of the behavioral and cognitive symptoms in Alzheimer's disease."
Approximately 4 million Americans have Alzheimer's disease, and 100,000 people die from the disease each year.
Other researchers participating in the study included Amy J. Ramsey, Tatyana D. Sotnikova, Hyung-Gun Kim, Hui Quan, William C. Wetsel, and Raul R. Gainetdinov of Duke University Medical Center; Cristina Martins-Silva, Braulio M. de Castro, Ricardo F. Lima, Vinicius R. Cota, Marcio F. D. Moraes, Marcus V. Gomez, Christopher Kushmerick, Grace S. Pereira, Ernani Amarai, Janaina Koenen and Cristina Guatimosim of Universidade Federal de Minas Gerais; and Daniela M. Barros, Maria R. Ramirez, Janine L. Rossato, and Ivan Izquierdo of Pontificia Universidade Catolica de Rio Grande do Sul, in Porto Alegre, Brazil.
Contact: Marla Vacek Broadfoot
Duke University Medical Center
Mice genetically engineered to have modest defects in this recycling protein display symptoms that resemble those in Alzheimer's, such as the inability to remember familiar faces, according to the researchers. The crucial protein recycles a chemical called acetylcholine that carries messages between nerves cells, the scientists said.
"By using these genetically engineered mice as models of Alzheimer's, we can learn more about the neuronal circuitry of the brain, and perhaps even discover new ways to alleviate the symptoms of this devastating disease," said senior study investigator Marc G. Caron, Ph.D., James B. Duke professor of cell biology.
The team reports its findings in the Sept. 7, 2006, issue of the journal Neuron. The research was supported by the National Institutes of Health and American Health Assistance Foundation.
Acetylcholine is a neurotransmitter that carries a number of vital signals from one nerve cell, or neuron, to another. Normally, when a signal needs to travel through the brain, neurons release acetylcholine to transport the signal across the gap, or synapse, between neurons. Acetylcholine is stored in tiny hollow spheres, called vesicles, that bud off of the end of the neurons. A kind of protein pump, called a transporter, located in each neuron controls the storage and release of acetylcholine from these vesicles, recycling the neurotransmitter back to the nerve cell vesicles in preparation for the next burst of signal.
It is this acetylcholine transporter protein that the researchers targeted by disrupting the gene that controls its production.
"Acetylcholine is important for every function in the body -- breathing, eating, walking, practically everything," Duke's Caron said. "If we knocked out the function of the protein completely, then the mice would die. So instead, we just knocked its function down to a low level."
In the study, the researchers took advantage of a built-in trait of their animal models -- that is, the fact that mice are innately curious and tend to explore new objects and companions extensively by sniffing and touching. The scientists ran mutant mice, in which the acetylcholine transporter gene was defective, through a series of tests to evaluate their performance in behavioral tasks. They ran normal mice through the same tests to serve as a control group.
The first test assessed the mice's ability to discriminate unfamiliar objects. The researchers gave the mutant and normal mice two objects to explore, and then took the objects away. A short time later, the scientists gave the mice back one of the objects, along with a nonfamiliar object. Both the normal and mutant mice initially explored the two objects to the same degree, but after the break the mutants had trouble remembering the familiar object, said lead study investigator Vania F. Prado, Ph.D., an associate professor of biochemistry at Universidade Federal de Minas Gerais, in Belo Horizonte, Brazil.
The second test of memory was similar to the first, but instead of giving the mice objects to explore, the scientists introduced a new mouse into the cage of their test subjects. The normal mice extensively explored the "intruder" mouse, but over time they showed less and less interest, the researchers said. This behavior, they said, demonstrated that the normal mice had become familiar with the intruder. In contrast, the mutant mice failed to recognize the intruder even after several meetings, thus displaying a defect in what the researchers called "social memory."
These findings suggested that the decreased levels of acetylcholine in the mutant mice resulted in their trouble with social memory, the scientists said.
To determine if this theory was true, the researchers set out to correct the behavioral defect by treating the mice with drugs that increase levels of acetylcholine in the brain. Called cholinesterase inhibitors, the drugs block a brain enzyme that typically breaks down acetylcholine, thus leaving more of the neurotransmitter available for sending the signals involved in learning and memory. Physicians give cholinesterase inhibitors to people with Alzheimer's to slow their memory loss and enable them to perform daily tasks, lessening the symptoms of the disease.
Mutant mice treated with the drugs, when run through the same tests, recognized intruder mice after several meetings, the researchers said, adding that this observed improvement in the performance of social recognition confirmed that the defects stemmed from the reduced amounts of acetylcholine.
"Now we can use our animal model to screen for similar drugs that can improve the function of acetylcholine in the brain," said Marco A. M. Prado, Ph.D., an associate professor of pharmacology at Universidade Federal de Minas Gerais and senior investigator of the study. "This is of importance because decreases in acetylcholine are thought to be relevant for the diminishing cognitive function found in aging and also are believed to be associated with some of the behavioral and cognitive symptoms in Alzheimer's disease."
Approximately 4 million Americans have Alzheimer's disease, and 100,000 people die from the disease each year.
Other researchers participating in the study included Amy J. Ramsey, Tatyana D. Sotnikova, Hyung-Gun Kim, Hui Quan, William C. Wetsel, and Raul R. Gainetdinov of Duke University Medical Center; Cristina Martins-Silva, Braulio M. de Castro, Ricardo F. Lima, Vinicius R. Cota, Marcio F. D. Moraes, Marcus V. Gomez, Christopher Kushmerick, Grace S. Pereira, Ernani Amarai, Janaina Koenen and Cristina Guatimosim of Universidade Federal de Minas Gerais; and Daniela M. Barros, Maria R. Ramirez, Janine L. Rossato, and Ivan Izquierdo of Pontificia Universidade Catolica de Rio Grande do Sul, in Porto Alegre, Brazil.
Contact: Marla Vacek Broadfoot
Duke University Medical Center
среда, 22 июня 2011 г.
People With Alzheimer's Disease Speak Out In First Ever Global Survey
Today, Alzheimer's Disease International (ADI) announced the results of a global survey investigating the unmet needs, challenges and communication gaps faced by patients with mild-to-moderate Alzheimer's disease (AD) and caregivers in six countries on three continents: the United States, Canada, France, Germany, Spain and Brazil.
This is a landmark survey as it is the first time a survey has included responses of people with Alzheimer's disease as well as caregivers. The results coincide with World Alzheimer's Day 2007, a day of global solidarity between individuals and organisations fighting against the threat of Alzheimer's disease and other forms of dementia.
"Our theme for the 2007 World Alzheimer's Day Campaign is 'People with Dementia Speak Out!'. 24 million people around the world and millions more families have to live with the daily challenges and persistent stigma of dementia. It is time for them to have their voice heard on a global stage. This survey is an important step in this journey," said Orien Reid, Chairman of ADI.
"I think it is long overdue that we hear from Alzheimer's patients", said Alexander Kurz, MD, Professor of Psychiatry and Head of the Centre for Cognitive Disorders at the Department of Psychiatry and Psychotherapy of Technische Universit?¤t M??nchen, Munich, Germany. "This landmark survey gives us good insight into how the patient and caregiver see and respond to this disease from their perspective."
Survey Results:
1. Quality of Life
The results showed that most of the Alzheimer's patients surveyed still have the ability to enjoy life, have a warm relationship with their carer and feel safe and supported at home. This is testament to the hard work and devotion of caregivers, nearly all of whom surveyed said providing the best quality of life to the person in their care was important to them.
Well over 80% of the AD patients felt that they continued to "keep a social life with their family and friends" and still feel "well-respected by family members."
While the majority of caregivers said "caring for someone with AD is burdensome," over 70% reported that caring for an AD patient also helps them "appreciate what's really important" in life. Three-fourths of the caregivers replied that being a caregiver is "one way I can repay some of the love and care I received in the past" and more than half said it is "rewarding."
2. Access to Information & Support Services
In all participating countries, the primary source of AD information is the patient's physician for both patients and caregivers. Overall, caregivers look to family and friends as a secondary source of information; for patients, magazines and newspaper articles rank second. After the physician, caregivers in the United States and Canada search the Internet as a secondary source for AD information.
Alzheimer associations are the tertiary source of information. According to the survey, Alzheimer association support services are utilized about a third more by caregivers and patients in the participating European countries as compared to those from North America. Generally Alzheimer associations are looked to for listings of local peer support groups and physicians, information on new treatments and information on social events for those living with Alzheimer's disease.
In general, patients and caregivers from participating European countries reported a much higher rate of utilization of support services (to include professional home care, away-from-home day programs, and organized peer support groups) than those from the U.S.
Mr Marc Wortmann, the Executive Director of Alzheimer's Disease International, which helped conduct the survey, said, "people with Alzheimer's disease and their caregivers do not fully take advantage of the all the support services available to them through their local Alzheimer association. The work of these organizations is often underestimated, but this survey shows they have an important role. We hope that we can continue to raise awareness not only of Alzheimer's, but also of the many resources available to those living with it."
3. Views on Alzheimer's Disease Treatment
For those patients on Alzheimer's medication, more than 70% are either "satisfied" or "somewhat satisfied" with the treatment and feel that the medicine is helping control symptoms. Caregivers, more so than patients, expressed their desire that AD medications "come in a form that was easier to take" and with a "dosing regimen that was easier to comply with." This may be a reflection of the fact that in many cases it is the caregiver who manages the medication and caregivers put more importance on "knowing that the medications are being taken properly" than patients.
About the Study
The study was commissioned by ADI and conducted by Harris Interactive between June 14th and August 20th, 2007 among patients and caregivers of patients with early-stage Alzheimer's disease in the US, Canada, France, Germany, Spain and Brazil.
100 to 102 patients were interviewed in each of France, Germany, Spain, Brazil and the US (There was insufficient patient participation in Canada to be included in the study). 100 to 114 caregivers were interviewed in each of the same countries and in Canada. Patients and caregivers were invited to complete the 10 minute survey over the phone. Study participants were recruited through Harris' network of physicians, through nursing homes, Harris General and/or Chronic Illness Panels, referrals from AD organizations via advertisements, and vendor-supplied lists of AD sufferers and household members.
This survey was supported by an unrestricted grant from Novartis
alz/
This is a landmark survey as it is the first time a survey has included responses of people with Alzheimer's disease as well as caregivers. The results coincide with World Alzheimer's Day 2007, a day of global solidarity between individuals and organisations fighting against the threat of Alzheimer's disease and other forms of dementia.
"Our theme for the 2007 World Alzheimer's Day Campaign is 'People with Dementia Speak Out!'. 24 million people around the world and millions more families have to live with the daily challenges and persistent stigma of dementia. It is time for them to have their voice heard on a global stage. This survey is an important step in this journey," said Orien Reid, Chairman of ADI.
"I think it is long overdue that we hear from Alzheimer's patients", said Alexander Kurz, MD, Professor of Psychiatry and Head of the Centre for Cognitive Disorders at the Department of Psychiatry and Psychotherapy of Technische Universit?¤t M??nchen, Munich, Germany. "This landmark survey gives us good insight into how the patient and caregiver see and respond to this disease from their perspective."
Survey Results:
1. Quality of Life
The results showed that most of the Alzheimer's patients surveyed still have the ability to enjoy life, have a warm relationship with their carer and feel safe and supported at home. This is testament to the hard work and devotion of caregivers, nearly all of whom surveyed said providing the best quality of life to the person in their care was important to them.
Well over 80% of the AD patients felt that they continued to "keep a social life with their family and friends" and still feel "well-respected by family members."
While the majority of caregivers said "caring for someone with AD is burdensome," over 70% reported that caring for an AD patient also helps them "appreciate what's really important" in life. Three-fourths of the caregivers replied that being a caregiver is "one way I can repay some of the love and care I received in the past" and more than half said it is "rewarding."
2. Access to Information & Support Services
In all participating countries, the primary source of AD information is the patient's physician for both patients and caregivers. Overall, caregivers look to family and friends as a secondary source of information; for patients, magazines and newspaper articles rank second. After the physician, caregivers in the United States and Canada search the Internet as a secondary source for AD information.
Alzheimer associations are the tertiary source of information. According to the survey, Alzheimer association support services are utilized about a third more by caregivers and patients in the participating European countries as compared to those from North America. Generally Alzheimer associations are looked to for listings of local peer support groups and physicians, information on new treatments and information on social events for those living with Alzheimer's disease.
In general, patients and caregivers from participating European countries reported a much higher rate of utilization of support services (to include professional home care, away-from-home day programs, and organized peer support groups) than those from the U.S.
Mr Marc Wortmann, the Executive Director of Alzheimer's Disease International, which helped conduct the survey, said, "people with Alzheimer's disease and their caregivers do not fully take advantage of the all the support services available to them through their local Alzheimer association. The work of these organizations is often underestimated, but this survey shows they have an important role. We hope that we can continue to raise awareness not only of Alzheimer's, but also of the many resources available to those living with it."
3. Views on Alzheimer's Disease Treatment
For those patients on Alzheimer's medication, more than 70% are either "satisfied" or "somewhat satisfied" with the treatment and feel that the medicine is helping control symptoms. Caregivers, more so than patients, expressed their desire that AD medications "come in a form that was easier to take" and with a "dosing regimen that was easier to comply with." This may be a reflection of the fact that in many cases it is the caregiver who manages the medication and caregivers put more importance on "knowing that the medications are being taken properly" than patients.
About the Study
The study was commissioned by ADI and conducted by Harris Interactive between June 14th and August 20th, 2007 among patients and caregivers of patients with early-stage Alzheimer's disease in the US, Canada, France, Germany, Spain and Brazil.
100 to 102 patients were interviewed in each of France, Germany, Spain, Brazil and the US (There was insufficient patient participation in Canada to be included in the study). 100 to 114 caregivers were interviewed in each of the same countries and in Canada. Patients and caregivers were invited to complete the 10 minute survey over the phone. Study participants were recruited through Harris' network of physicians, through nursing homes, Harris General and/or Chronic Illness Panels, referrals from AD organizations via advertisements, and vendor-supplied lists of AD sufferers and household members.
This survey was supported by an unrestricted grant from Novartis
alz/
воскресенье, 19 июня 2011 г.
British Blackcurrants Could Prevent Alzheimer's Disease
Research news in the Journal of the Science of Food and Agriculture Compounds in blackcurrants could prevent Alzheimer's disease and the characteristics of British berries suggest they do it best, writes Jennifer Rohn in Chemistry & Industry magazine.
New research led by Dilip Ghosh of the Horticulture and Food Research Institute in New Zealand, shows that compounds in blackcurrants have a potent protective effect in cultured neuronal cells against the types of stress caused by dopamine and amyloid-b, a peptide associated with Alzheimer's disease.
'These compounds also work in hippocampal cells taken straight from the brain,' researcher James Joseph of Tufts University told Chemistry & Industry. Joseph says that the effect will likely be reproduced in the human body and that blackcurrants could help prevent or significantly delay the onset of Alzheimer's.
Blackcurrants and boysenberries, more common in the US, both contain anthocyanins and polyphenolics. British blackcurrants are bred to be darker, which means they have more anthocyanins and are likely to be more potent.
Compounds from these berries are already known to act as antioxidants, but a role in neuroprotection has not been demonstrated previously, according to the researchers.
The mechanism of action is unclear. But James said: 'We have evidence that the compounds protect against Alzheimer's by influencing the early gene expression in learning and memory, which influences cell signaling pathways that help neuronal cells communicate with each other.'
Dilip's team recently demonstrated the potent protective effect of blackcurrant compounds on cultured human promyeloyte and neuroblastoma cells assaulted by hydrogen peroxide (JSFA doi: 10.1002/jsfa.0247).
Article: "Effects of anthocyanins and other phenolics of boysenberry and blackcurrant as inhibitors of oxidative stress and damage to cellular DNA in SY-SY5Y and HY-60 cells" by D. Ghosh et. al JSFA, 10.1002/jsfa.2409.
About The Journal of the Science of Food and Agriculture
The Journal of the Science of Food and Agriculture (JSFA) publishes peer-reviewed original research and critical reviews in these areas, with particular emphasis on interdisciplinary studies at the agriculture/food interface. This international journal covers fundamental and applied research.
JSFA is an SCI journal, published by John Wiley & Sons, on behalf of the Society of Chemical Industry, and is available in print (ISSN: 0022-5142) and online (ISSN: 1097-0010) via Wiley InterScience interscience.wiley
For further information about the journal go to interscience.wiley/jsfa
About SCI
SCI is a unique international forum where science meets business on independent, impartial ground. Anyone can join, and the Society offers a chance to share information between sectors as diverse as food and agriculture, pharmaceuticals, biotechnology, environmental science and safety. As well as publishing new research and running events, SCI has a growing database of member specialists who can give background information on a wide range of scientific issues. Originally established in 1881, SCI is a registered charity with members in over 70 countries.
John Wiley & Sons, Inc.
interscience.wiley
New research led by Dilip Ghosh of the Horticulture and Food Research Institute in New Zealand, shows that compounds in blackcurrants have a potent protective effect in cultured neuronal cells against the types of stress caused by dopamine and amyloid-b, a peptide associated with Alzheimer's disease.
'These compounds also work in hippocampal cells taken straight from the brain,' researcher James Joseph of Tufts University told Chemistry & Industry. Joseph says that the effect will likely be reproduced in the human body and that blackcurrants could help prevent or significantly delay the onset of Alzheimer's.
Blackcurrants and boysenberries, more common in the US, both contain anthocyanins and polyphenolics. British blackcurrants are bred to be darker, which means they have more anthocyanins and are likely to be more potent.
Compounds from these berries are already known to act as antioxidants, but a role in neuroprotection has not been demonstrated previously, according to the researchers.
The mechanism of action is unclear. But James said: 'We have evidence that the compounds protect against Alzheimer's by influencing the early gene expression in learning and memory, which influences cell signaling pathways that help neuronal cells communicate with each other.'
Dilip's team recently demonstrated the potent protective effect of blackcurrant compounds on cultured human promyeloyte and neuroblastoma cells assaulted by hydrogen peroxide (JSFA doi: 10.1002/jsfa.0247).
Article: "Effects of anthocyanins and other phenolics of boysenberry and blackcurrant as inhibitors of oxidative stress and damage to cellular DNA in SY-SY5Y and HY-60 cells" by D. Ghosh et. al JSFA, 10.1002/jsfa.2409.
About The Journal of the Science of Food and Agriculture
The Journal of the Science of Food and Agriculture (JSFA) publishes peer-reviewed original research and critical reviews in these areas, with particular emphasis on interdisciplinary studies at the agriculture/food interface. This international journal covers fundamental and applied research.
JSFA is an SCI journal, published by John Wiley & Sons, on behalf of the Society of Chemical Industry, and is available in print (ISSN: 0022-5142) and online (ISSN: 1097-0010) via Wiley InterScience interscience.wiley
For further information about the journal go to interscience.wiley/jsfa
About SCI
SCI is a unique international forum where science meets business on independent, impartial ground. Anyone can join, and the Society offers a chance to share information between sectors as diverse as food and agriculture, pharmaceuticals, biotechnology, environmental science and safety. As well as publishing new research and running events, SCI has a growing database of member specialists who can give background information on a wide range of scientific issues. Originally established in 1881, SCI is a registered charity with members in over 70 countries.
John Wiley & Sons, Inc.
interscience.wiley
APP -- Good, Bad Or Both?
New data about amyloid precursor protein, or APP, a protein implicated in development of Alzheimer's disease, suggests it also may have a positive role -- directly affecting learning and memory during brain development. So is APP good or bad? Researchers at Georgetown University Medical Center say both, and that a balance of APP is critical.
Alzheimer's disease, the fourth leading cause of death in the United States, is characterized by neuronal cell death and a progressive loss of functioning in the brain. Symptoms of Alzheimer's (AD) include memory loss and impaired judgment. Abeta is one of many proteins found to be associated with the disease. It is released when APP, a larger protein, is cut by several enzymes. Research suggests this occurs when APP is abnormally processed, possibly due to trauma, cholesterol levels or oxidative stress. When Abeta is released, it can form plaque, a contributing factor in AD. Thus, Abeta and APP are involved in the early process of AD development.
APP is also known to be present at the synapses between neurons though its molecular action is not understood. Synapse loss is thought to be one of the main contributors to the cognitive decline seen in AD.
In a presentation at the 39th annual meeting of the Society for Neuroscience, Georgetown University Medical Center researchers say that while APP is negatively associated with AD, it appears to play a critical role in brain development.
Many studies have elucidated the importance of synapses and dendritic spines, the protrusions that allow communication between brain neurons, in learning and memory. In this new research, the GUMC scientists found decreased spine density in mice that have been genetically modified to not produce APP. The scientists then looked at four-week-old mice that over produced APP and found a significant increase in spine density. At one year old, however, these mice have Abeta plaques, as well as a decrease in spine density due to the effect of Abeta, which is known to be neurotoxic.
"Our work suggests that APP balance is critical for normal neuronal development, connection of synapses, and dendritic spine development, all of which have implications for the extensive synapse loss and cognitive decline seen in Alzheimer's disease," explains the study's author, Hyang-Sook Hoe, PhD, a research scientist in the department of neuroscience. "One strategy to counteract development of Alzheimer's disease is to maintain balance in APP protein expression in order to prevent production of Abeta."
This research was funded by grants from the National Institutes of Health. The authors report no related financial interests.
Source:
Karen Mallet
Georgetown University Medical Center
Alzheimer's disease, the fourth leading cause of death in the United States, is characterized by neuronal cell death and a progressive loss of functioning in the brain. Symptoms of Alzheimer's (AD) include memory loss and impaired judgment. Abeta is one of many proteins found to be associated with the disease. It is released when APP, a larger protein, is cut by several enzymes. Research suggests this occurs when APP is abnormally processed, possibly due to trauma, cholesterol levels or oxidative stress. When Abeta is released, it can form plaque, a contributing factor in AD. Thus, Abeta and APP are involved in the early process of AD development.
APP is also known to be present at the synapses between neurons though its molecular action is not understood. Synapse loss is thought to be one of the main contributors to the cognitive decline seen in AD.
In a presentation at the 39th annual meeting of the Society for Neuroscience, Georgetown University Medical Center researchers say that while APP is negatively associated with AD, it appears to play a critical role in brain development.
Many studies have elucidated the importance of synapses and dendritic spines, the protrusions that allow communication between brain neurons, in learning and memory. In this new research, the GUMC scientists found decreased spine density in mice that have been genetically modified to not produce APP. The scientists then looked at four-week-old mice that over produced APP and found a significant increase in spine density. At one year old, however, these mice have Abeta plaques, as well as a decrease in spine density due to the effect of Abeta, which is known to be neurotoxic.
"Our work suggests that APP balance is critical for normal neuronal development, connection of synapses, and dendritic spine development, all of which have implications for the extensive synapse loss and cognitive decline seen in Alzheimer's disease," explains the study's author, Hyang-Sook Hoe, PhD, a research scientist in the department of neuroscience. "One strategy to counteract development of Alzheimer's disease is to maintain balance in APP protein expression in order to prevent production of Abeta."
This research was funded by grants from the National Institutes of Health. The authors report no related financial interests.
Source:
Karen Mallet
Georgetown University Medical Center
суббота, 18 июня 2011 г.
Alzheimer's Society Calls For An End To Complex Care Charging System
A fifth of carers face difficulties in applying for benefits under the current 'complex and confusing' system according to The Public Accounts Committee.
The group of MPs has published a report examining the steps the Department for Work and Pensions has taken to improve the delivery of benefits to carers and the support it provides to help them find employment.
'People with dementia and their carers are among those who are the hardest hit by the financial costs of disability. The support carers provide saves the government over ??6 billion a year alone. Carers are doing a hard enough job as it is without having to jump through hoops to apply for necessary benefits and allowances.
'This report by the PAC adds further weight to the call for the government's forthcoming green paper to radically overhaul the current charging system and deliver a transparent and fair deal for carers.'
Neil Hunt
Chief Executive
Source
Alzheimer's Society
The group of MPs has published a report examining the steps the Department for Work and Pensions has taken to improve the delivery of benefits to carers and the support it provides to help them find employment.
'People with dementia and their carers are among those who are the hardest hit by the financial costs of disability. The support carers provide saves the government over ??6 billion a year alone. Carers are doing a hard enough job as it is without having to jump through hoops to apply for necessary benefits and allowances.
'This report by the PAC adds further weight to the call for the government's forthcoming green paper to radically overhaul the current charging system and deliver a transparent and fair deal for carers.'
Neil Hunt
Chief Executive
Source
Alzheimer's Society
пятница, 17 июня 2011 г.
Test Quickly Assesses Whether Alzheimer's Drugs Are Hitting Their Target
A test developed by physician-scientists at Washington University School of Medicine in St. Louis may help assess more quickly the ability of Alzheimer's drugs to affect one of the possible underlying causes of Alzheimer's disease in humans, accelerating the development of new treatments.
Scientists used the test to show that an Alzheimer's drug given to healthy volunteers reduced production of a substance known as amyloid beta (A-beta), a normal byproduct of human metabolism that builds to unhealthy levels forming brain plaques in Alzheimer's patients. The drug candidate, LY450139, which is also known as semagacestat, is being studied in clinical trials by Eli Lilly and Company.
Ongoing clinical trials are studying the effect that semagacestat may have on cognitive function and biochemical and brain imaging biomarkers in patients with Alzheimer's disease. Washington University researchers wanted to see whether the new measurement technique, stable isotope-linked kinetics (SILK), could detect the study drug's impact on A-beta synthesis in healthy volunteers.
"Bringing an Alzheimer's disease drug into clinical trials from tests in animal models has always been challenging," says study director Randall Bateman, M.D., a Washington University neurologist who treats patients at Barnes-Jewish Hospital. "We haven't had a way to quickly and accurately assess a drug's effects, and that meant there always had to be some degree of educated guesswork when it came to setting the optimal dosage for humans. SILK may help to eliminate much of that guesswork."
The results appear online in Annals of Neurology on April 10.
Scientists are unsure whether increased A-beta production, reduced clearance or a combination of the two lead to the A-beta buildup in the brain, a process that many believe triggers Alzheimer's disease. Bateman and his colleagues are currently using SILK to try to answer this question.
Until SILK, there has not been a way to directly measure the production or clearance of A-beta. The efficacy of potential new Alzheimer's drug candidates has been assessed by monitoring the cognitive functions of patients with the disease for extended periods of time, which require large, lengthy and expensive studies.
In their double-blind study, scientists gave 20 healthy volunteers varying doses of either a study drug or a placebo. At the start of the SILK test, volunteers were connected to an intravenous drip that gave them a slightly altered form of the amino acid leucine, which is a component of A-beta.
Over the course of several hours, cells in the brain picked up the labeled leucine and incorporated it into the new copies made of A-beta and other proteins. The scientists took periodic samples of the subjects' cerebrospinal fluid to determine how much of the A-beta included altered leucine.
Tracking the rise of the percentage of labeled A-beta over time reveals the A-beta production rate. Scientists then stop the leucine labeling but continue analyzing spinal fluid samples. As the body removed old A-beta and made new A-beta, the percentage of A-beta containing altered leucine dropped, revealing the A-beta clearance rate.
The results suggest a dose-dependent drop in A-beta production, with an 84 percent reduction in A-beta production being measured with the highest study drug dose.
The SILK procedure takes 36 hours, but provides scientists a more detailed assessment of amyloid beta production and clearance levels than they can obtain through conventional methods.
"You could use a spinal tap to look directly at the amount of A-beta present in the cerebrospinal fluid, but we've shown that natural processes cause A-beta levels to change dynamically," says Bateman. "Such changes make it more difficult to assess the effects of a drug in that fashion."
Notes:
The study was funded through a Lilly grant from a funding program that allowed Bateman to propose the research and retain control of it. Five of the paper's 12 authors are Eli Lilly employees.
Washington University in St. Louis licensed its pending patents on SILK to C2N Diagnostics, LLC, a St. Louis diagnostics company started by Bateman and senior author David Holtzman, M.D., the Andrew and Gretchen Jones Professor and Chair of Neurology. Bateman and Holtzman's financial interests in the company are governed by the university's conflict-of-interest policies.
Bateman RJ, Siemers E, Mawuenyega KG, Wen G, Bronwing KR, Sigurdson, WC, Yarasheski KE, Friedrich SW, DeMattos RB, May PC, Paul SM, Holtzman DM. A gamma-secretase inhibitor decreases amyloid-beta production in the central nervous system. Annals of Neurology, online April 10.
Funding from Eli Lilly and Company supported this research.
Washington University School of Medicine's 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children's hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked third in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children's hospitals, the School of Medicine is linked to BJC HealthCare.
Source:
Michael C. Purdy
Washington University in St. Louis
Scientists used the test to show that an Alzheimer's drug given to healthy volunteers reduced production of a substance known as amyloid beta (A-beta), a normal byproduct of human metabolism that builds to unhealthy levels forming brain plaques in Alzheimer's patients. The drug candidate, LY450139, which is also known as semagacestat, is being studied in clinical trials by Eli Lilly and Company.
Ongoing clinical trials are studying the effect that semagacestat may have on cognitive function and biochemical and brain imaging biomarkers in patients with Alzheimer's disease. Washington University researchers wanted to see whether the new measurement technique, stable isotope-linked kinetics (SILK), could detect the study drug's impact on A-beta synthesis in healthy volunteers.
"Bringing an Alzheimer's disease drug into clinical trials from tests in animal models has always been challenging," says study director Randall Bateman, M.D., a Washington University neurologist who treats patients at Barnes-Jewish Hospital. "We haven't had a way to quickly and accurately assess a drug's effects, and that meant there always had to be some degree of educated guesswork when it came to setting the optimal dosage for humans. SILK may help to eliminate much of that guesswork."
The results appear online in Annals of Neurology on April 10.
Scientists are unsure whether increased A-beta production, reduced clearance or a combination of the two lead to the A-beta buildup in the brain, a process that many believe triggers Alzheimer's disease. Bateman and his colleagues are currently using SILK to try to answer this question.
Until SILK, there has not been a way to directly measure the production or clearance of A-beta. The efficacy of potential new Alzheimer's drug candidates has been assessed by monitoring the cognitive functions of patients with the disease for extended periods of time, which require large, lengthy and expensive studies.
In their double-blind study, scientists gave 20 healthy volunteers varying doses of either a study drug or a placebo. At the start of the SILK test, volunteers were connected to an intravenous drip that gave them a slightly altered form of the amino acid leucine, which is a component of A-beta.
Over the course of several hours, cells in the brain picked up the labeled leucine and incorporated it into the new copies made of A-beta and other proteins. The scientists took periodic samples of the subjects' cerebrospinal fluid to determine how much of the A-beta included altered leucine.
Tracking the rise of the percentage of labeled A-beta over time reveals the A-beta production rate. Scientists then stop the leucine labeling but continue analyzing spinal fluid samples. As the body removed old A-beta and made new A-beta, the percentage of A-beta containing altered leucine dropped, revealing the A-beta clearance rate.
The results suggest a dose-dependent drop in A-beta production, with an 84 percent reduction in A-beta production being measured with the highest study drug dose.
The SILK procedure takes 36 hours, but provides scientists a more detailed assessment of amyloid beta production and clearance levels than they can obtain through conventional methods.
"You could use a spinal tap to look directly at the amount of A-beta present in the cerebrospinal fluid, but we've shown that natural processes cause A-beta levels to change dynamically," says Bateman. "Such changes make it more difficult to assess the effects of a drug in that fashion."
Notes:
The study was funded through a Lilly grant from a funding program that allowed Bateman to propose the research and retain control of it. Five of the paper's 12 authors are Eli Lilly employees.
Washington University in St. Louis licensed its pending patents on SILK to C2N Diagnostics, LLC, a St. Louis diagnostics company started by Bateman and senior author David Holtzman, M.D., the Andrew and Gretchen Jones Professor and Chair of Neurology. Bateman and Holtzman's financial interests in the company are governed by the university's conflict-of-interest policies.
Bateman RJ, Siemers E, Mawuenyega KG, Wen G, Bronwing KR, Sigurdson, WC, Yarasheski KE, Friedrich SW, DeMattos RB, May PC, Paul SM, Holtzman DM. A gamma-secretase inhibitor decreases amyloid-beta production in the central nervous system. Annals of Neurology, online April 10.
Funding from Eli Lilly and Company supported this research.
Washington University School of Medicine's 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children's hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked third in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children's hospitals, the School of Medicine is linked to BJC HealthCare.
Source:
Michael C. Purdy
Washington University in St. Louis
четверг, 16 июня 2011 г.
Promising Therapies With Adult Stem Cells
New findings on the transformation potential of adult stem cells will be highlighted. Researchers will discuss possible alternatives to embryonic stem cells in the treatment of diabetes, Alzheimer's disease, spinal cord injury and other catastrophic conditions.
Panelists:
* E. Terry Papoutsakis, Ph.D., Professor, Northwestern University
* Dennis Discher, Ph.D., Professor, University of Pennsylvania
* Kyle Kurpinski, Doctoral Student, University of California, Berkeley
American Chemical Society 232nd National Meeting San Francisco, Sept. 10-14, 2006
Wednesday, Sept. 13, 2006 10 A.M. -- Promising therapies with adult stem cells
Contact: Charmayne Marsh or Michael Bernstein
American Chemical Society
Panelists:
* E. Terry Papoutsakis, Ph.D., Professor, Northwestern University
* Dennis Discher, Ph.D., Professor, University of Pennsylvania
* Kyle Kurpinski, Doctoral Student, University of California, Berkeley
American Chemical Society 232nd National Meeting San Francisco, Sept. 10-14, 2006
Wednesday, Sept. 13, 2006 10 A.M. -- Promising therapies with adult stem cells
Contact: Charmayne Marsh or Michael Bernstein
American Chemical Society
Study Investigates Immune System Alterations In Brain; May Shed Light On Alzheimer's Disease-like Changes
What
Using laboratory mice that had been bred to have brain changes similar to Alzheimer's disease, scientists were able to reduce two characteristic features of the disease by modifying the mice's immune systems with a special peptide (MOG45D) related to the myelin sheath that insulates nerve cells and nerve fibers. As a result, anti-inflammatory cells were recruited from the blood into the brain, dampening the local inflammatory response.
An article published online by the Journal of Neurochemistry describes the immune intervention, its cellular and molecular mechanisms of action, and the effects on disease pathology.
Who
The study was conducted by scientists at the Maxine Dunitz Neurosurgical Institute at Cedars-Sinai Medical Center and the Weizmann Institute of Science in Rehovot, Israel. Michal Schwartz, Ph.D., the article's senior author, and Maya Koronyo-Hamaoui, Ph.D., first author, are available to provide additional details.
Schwartz is visiting professor at the Center of Neuroimmunology and Neurogenesis in the Department of Neurosurgery at Cedars-Sinai Medical Center and professor of neuroimmunology at the Weizmann Institute in Rehovot, Israel. Koronyo-Hamaoui is assistant professor and principal investigator in the Neuroimmunology Laboratory in the Department of Neurosurgery at Cedars-Sinai.
Details
The most frequent cause of senile dementia, Alzheimer's disease is associated with the overproduction of beta-amyloid peptides - molecules that accumulate as sticky deposits in the brain. These "extra-cellular" plaques (accumulating on the exterior of neurons) damage the cells and interrupt cell-to-cell signaling. Abnormal protein tangles (neurofibrillary tangles) inside neurons also lead to cell dysfunction and death.
Researchers seek to defeat the disease in several ways: by preventing plaque formation; treating existing plaque deposits; and repairing or replacing injured neurons.
In this study, scientists modified the cellular and molecular immune environment in the brains of laboratory mice bred to model Alzheimer's disease with an altered myelin-derived peptide. This recruited anti-inflammatory cells into the brain, which diminished the effects of local inflammatory cells and boosted the action of an enzyme that degrades plaque and is associated with glial scar formation.
This study was supported in part by the Maxine Dunitz Neurosurgical Institute in the Cedars-Sinai Department of Neurosurgery and by the Burns & Allen Research Institute at Cedars-Sinai.
Source
Cedars-Sinai Medical Center
Using laboratory mice that had been bred to have brain changes similar to Alzheimer's disease, scientists were able to reduce two characteristic features of the disease by modifying the mice's immune systems with a special peptide (MOG45D) related to the myelin sheath that insulates nerve cells and nerve fibers. As a result, anti-inflammatory cells were recruited from the blood into the brain, dampening the local inflammatory response.
An article published online by the Journal of Neurochemistry describes the immune intervention, its cellular and molecular mechanisms of action, and the effects on disease pathology.
Who
The study was conducted by scientists at the Maxine Dunitz Neurosurgical Institute at Cedars-Sinai Medical Center and the Weizmann Institute of Science in Rehovot, Israel. Michal Schwartz, Ph.D., the article's senior author, and Maya Koronyo-Hamaoui, Ph.D., first author, are available to provide additional details.
Schwartz is visiting professor at the Center of Neuroimmunology and Neurogenesis in the Department of Neurosurgery at Cedars-Sinai Medical Center and professor of neuroimmunology at the Weizmann Institute in Rehovot, Israel. Koronyo-Hamaoui is assistant professor and principal investigator in the Neuroimmunology Laboratory in the Department of Neurosurgery at Cedars-Sinai.
Details
The most frequent cause of senile dementia, Alzheimer's disease is associated with the overproduction of beta-amyloid peptides - molecules that accumulate as sticky deposits in the brain. These "extra-cellular" plaques (accumulating on the exterior of neurons) damage the cells and interrupt cell-to-cell signaling. Abnormal protein tangles (neurofibrillary tangles) inside neurons also lead to cell dysfunction and death.
Researchers seek to defeat the disease in several ways: by preventing plaque formation; treating existing plaque deposits; and repairing or replacing injured neurons.
In this study, scientists modified the cellular and molecular immune environment in the brains of laboratory mice bred to model Alzheimer's disease with an altered myelin-derived peptide. This recruited anti-inflammatory cells into the brain, which diminished the effects of local inflammatory cells and boosted the action of an enzyme that degrades plaque and is associated with glial scar formation.
This study was supported in part by the Maxine Dunitz Neurosurgical Institute in the Cedars-Sinai Department of Neurosurgery and by the Burns & Allen Research Institute at Cedars-Sinai.
Source
Cedars-Sinai Medical Center
среда, 15 июня 2011 г.
New Method To Study Key Targets In Alzheimer's Disease And Prostate Cancer
When designing a drug against a disease, chemists often used detailed plans of the proteins affected and against which the drugs must act. However, about a third of the proteins of our bodies have not yet been "photographed" because they generally vary in form, are in constant movements and have very little structure. This lack of "photographs" hinders the design of drugs against diseases involving proteins that are structurally "evasive", such as those in Alzheimer's disease and in prostate cancer that does not respond to conventional drugs. The group headed by Xavier Salvatella, ICREA researcher with the Chemistry and Molecular Pharmacology Programme at the Institute for Research in Biomedicine (IRB Barcelona), has developed a method to obtain structural information about intrinsically disordered proteins. The study appears in this week's Journal of the American Chemical Society, one of the most important journals in this field.
Proteins are combinations of amino acids that fold in tri-dimensional forms that determine their function. The particularity of intrinsically disordered proteins is that because they are so dynamic and have little folded structure it is almost impossible to determine the variety of shapes that they adopt and consequently the functions they exert. Classical techniques, such as crystallography and nuclear magnetic resonance, do not work with these proteins. The researcher Xavier Salvatella, who left Cambridge to join IRB Barcelona a little over a year ago, develops methods to study the movements of proteins through combining laboratory experiments and computational predictions, an approach used by very few groups in the world. The researchers have simultaneously used a thousand processors of the supercomputer MareNostrum to study a single protein model and develop a new programme for structural calculation, named ERIDU. They then checked that the calculated structures agreed with lab data measured independently. The researchers will make ERIDU available to the international scientific community.
Objective: Alzheimer's disease and prostate cancer
With this new methodology, the group at IRB Barcelona, in collaboration with the University of Cambridge, will study why beta-amyloid plaques develop in Alzheimer's disease. They will examine the variety of forms that this protein adopts before and during accumulation. In another project, Salvatella will address the androgen receptor, the target protein in Kennedy's disease, a rare neurodegenerative disorder that causes muscular atrophy, as well in prostate cancer. "Oncologists are calling for new strategies to stop the growth of prostate tumours", explains Salvatella. The drugs currently available inhibit a part of the androgen receptor that is well known but in later stages of the disease these drugs can stop working. This protein has another important part that is intrinsically disordered and about which there is no structural information. "If our method is as reliable as we think, we could start to decipher the variety of structural forms that this other active part adopts in order to design drugs in the future".
In only ten years intrinsically disordered proteins have become one of the most interesting fields of research for biomedicine. "We have seen that the greater the complexity of the organism, the more proteins of this kind it has; however, although these proteins are highly relevant we still know very little about them because, among other things, it is very difficult to study their structures", comments Salvatella. Next October, IRB Barcelona, jointly with the BBVA Foundation, is organising a Barcelona BioMed Conference on intrinsically disordered proteins. This event will bring together experts in this field to discuss the most relevant breakthroughs made in pioneering labs worldwide.
Reference article:
Refinement of ensembles describing unstructured proteins using Residual Dipolar Couplings.
Esteban-Mart?n, E.; Fenwick, R.; Salvatella, X.
Journal of the American Chemical Society 132, 4626-4632(2010)
Source:
S??nia Armengou
Institute for Research in Biomedicine (IRB Barcelona)
Proteins are combinations of amino acids that fold in tri-dimensional forms that determine their function. The particularity of intrinsically disordered proteins is that because they are so dynamic and have little folded structure it is almost impossible to determine the variety of shapes that they adopt and consequently the functions they exert. Classical techniques, such as crystallography and nuclear magnetic resonance, do not work with these proteins. The researcher Xavier Salvatella, who left Cambridge to join IRB Barcelona a little over a year ago, develops methods to study the movements of proteins through combining laboratory experiments and computational predictions, an approach used by very few groups in the world. The researchers have simultaneously used a thousand processors of the supercomputer MareNostrum to study a single protein model and develop a new programme for structural calculation, named ERIDU. They then checked that the calculated structures agreed with lab data measured independently. The researchers will make ERIDU available to the international scientific community.
Objective: Alzheimer's disease and prostate cancer
With this new methodology, the group at IRB Barcelona, in collaboration with the University of Cambridge, will study why beta-amyloid plaques develop in Alzheimer's disease. They will examine the variety of forms that this protein adopts before and during accumulation. In another project, Salvatella will address the androgen receptor, the target protein in Kennedy's disease, a rare neurodegenerative disorder that causes muscular atrophy, as well in prostate cancer. "Oncologists are calling for new strategies to stop the growth of prostate tumours", explains Salvatella. The drugs currently available inhibit a part of the androgen receptor that is well known but in later stages of the disease these drugs can stop working. This protein has another important part that is intrinsically disordered and about which there is no structural information. "If our method is as reliable as we think, we could start to decipher the variety of structural forms that this other active part adopts in order to design drugs in the future".
In only ten years intrinsically disordered proteins have become one of the most interesting fields of research for biomedicine. "We have seen that the greater the complexity of the organism, the more proteins of this kind it has; however, although these proteins are highly relevant we still know very little about them because, among other things, it is very difficult to study their structures", comments Salvatella. Next October, IRB Barcelona, jointly with the BBVA Foundation, is organising a Barcelona BioMed Conference on intrinsically disordered proteins. This event will bring together experts in this field to discuss the most relevant breakthroughs made in pioneering labs worldwide.
Reference article:
Refinement of ensembles describing unstructured proteins using Residual Dipolar Couplings.
Esteban-Mart?n, E.; Fenwick, R.; Salvatella, X.
Journal of the American Chemical Society 132, 4626-4632(2010)
Source:
S??nia Armengou
Institute for Research in Biomedicine (IRB Barcelona)
вторник, 14 июня 2011 г.
Four Researchers Given Lifetime Achievement Awards By The Alzheimer's Association
The Alzheimer's Association recognized four scientists for their extraordinary achievements in advancing Alzheimer research at the Alzheimer's Association International Conference on Alzheimer's Disease 2010 (AAICAD 2010) in Honolulu, Hawaii.
Honorees for their professional and scientific contributions to Alzheimer research are:
- Takeshi Iwatsubo, MD, Department of Neuropathology, Graduate School of Medicine at the University of Tokyo.
- Karen H. Ashe, MD, PhD, Department of Neurology and Neuroscience Director at the University of Minnesota.
- Marsel Mesulam, MD, Dunbar Professor of Neurology and Psychiatry and Director of the Cognitive Neurology and Alzheimer's Disease Center at Northwestern University.
- Marilyn Albert, PhD, Director of the Division of Cognitive Neuroscience in the Department of Neurology at Johns Hopkins University School of Medicine.
"We are beginning to reap the benefits of Alzheimer's scientific advancements made in the last two decades, including a robust pipeline of anti-dementia drug therapies and advances in early detection," said William Thies, PhD, Chief Medical and Scientific Officer at the Alzheimer's Association. "These leading researchers, who have been in the vanguard of scientific advancements in Alzheimer's disease, have devoted their professional careers to greater understanding of this disease. Their dedication and commitment will help us defeat Alzheimer's - the public health threat of the 21st century - and create a world where future generations will not have to experience this progressive and fatal disease."
Lifetime Achievement Awards in Alzheimer's Disease Research
Henry Wisniewski, MD, PhD; Khalid Iqbal, PhD; and Bengt Winblad, MD, PhD, founded AAICAD in 1988. Lifetime Achievement Awards named in their honor are given to three outstanding scientists who have dedicated their careers to helping millions around the world through their research.
At AAICAD 2010, the 2010 Henry Wisniewski Lifetime Achievement Award was presented to Dr. Takehsi Iwatsubo, whose significant research with the Japanese Alzheimer's Disease Neuroimaging Initiative (J-ADNI) is creating a longitudinal workup of standardized neuroimaging, biomarker and clinico-psychological surveys. Designed to maximize compatibility with US-ADNI, it is hoped that this work along with other global ADNI efforts will establish rigorous, quantitative descriptions of the natural course of Alzheimer's in its very early stages.
The 2010 Khalid Iqbal Lifetime Achievement Award was presented to Dr. Karen Ashe, whose research focuses on animal and cellular models of Alzheimer's. These transgenic animal models enhance understanding of how amyloid and tau proteins - thought to be the keys to the cause and progression of Alzheimer's - impact memory and cognition. Transgenic mice have been a mainstay in the preclinical investigation of new treatments for Alzheimer's.
The 2010 Bengt Winblad Lifetime Achievement Award was presented to Dr. Marsel Mesulam. His research addresses the connectivity of the monkey brain, the organization of human cholinergic pathways, the representation of cognitive functions by large-scale neurocognitive networks, and the neurobiology of dementias. Dr. Mesulam's work on cholinergic pathways has been groundbreaking in understanding Alzheimer's. He is a world expert in Primary Progressive Aphasia.
Zaven Khachaturian Award
In addition to these three awards, Dr. Marilyn Albert was recipient of the 2010 Zaven Khachaturian Award at AAICAD. Named in honor of noted scientist, administrator, consultant, lecturer and author, Zaven Khachaturian, PhD, this award recognizes an individual whose compelling vision, selfless dedication, and extraordinary achievement has significantly advanced the field of Alzheimer science.
Dr. Albert's distinguished career includes more than two decades as a faculty member at Harvard University Medical School. Her research has primarily focused on the cognitive and brain changes associated with aging and Alzheimer's. The scope has also encompassed investigating potential methods of early identification of Alzheimer's and lifestyle factors that may maintain mental abilities with advancing age.
Source:
Alzheimer's Association
Honorees for their professional and scientific contributions to Alzheimer research are:
- Takeshi Iwatsubo, MD, Department of Neuropathology, Graduate School of Medicine at the University of Tokyo.
- Karen H. Ashe, MD, PhD, Department of Neurology and Neuroscience Director at the University of Minnesota.
- Marsel Mesulam, MD, Dunbar Professor of Neurology and Psychiatry and Director of the Cognitive Neurology and Alzheimer's Disease Center at Northwestern University.
- Marilyn Albert, PhD, Director of the Division of Cognitive Neuroscience in the Department of Neurology at Johns Hopkins University School of Medicine.
"We are beginning to reap the benefits of Alzheimer's scientific advancements made in the last two decades, including a robust pipeline of anti-dementia drug therapies and advances in early detection," said William Thies, PhD, Chief Medical and Scientific Officer at the Alzheimer's Association. "These leading researchers, who have been in the vanguard of scientific advancements in Alzheimer's disease, have devoted their professional careers to greater understanding of this disease. Their dedication and commitment will help us defeat Alzheimer's - the public health threat of the 21st century - and create a world where future generations will not have to experience this progressive and fatal disease."
Lifetime Achievement Awards in Alzheimer's Disease Research
Henry Wisniewski, MD, PhD; Khalid Iqbal, PhD; and Bengt Winblad, MD, PhD, founded AAICAD in 1988. Lifetime Achievement Awards named in their honor are given to three outstanding scientists who have dedicated their careers to helping millions around the world through their research.
At AAICAD 2010, the 2010 Henry Wisniewski Lifetime Achievement Award was presented to Dr. Takehsi Iwatsubo, whose significant research with the Japanese Alzheimer's Disease Neuroimaging Initiative (J-ADNI) is creating a longitudinal workup of standardized neuroimaging, biomarker and clinico-psychological surveys. Designed to maximize compatibility with US-ADNI, it is hoped that this work along with other global ADNI efforts will establish rigorous, quantitative descriptions of the natural course of Alzheimer's in its very early stages.
The 2010 Khalid Iqbal Lifetime Achievement Award was presented to Dr. Karen Ashe, whose research focuses on animal and cellular models of Alzheimer's. These transgenic animal models enhance understanding of how amyloid and tau proteins - thought to be the keys to the cause and progression of Alzheimer's - impact memory and cognition. Transgenic mice have been a mainstay in the preclinical investigation of new treatments for Alzheimer's.
The 2010 Bengt Winblad Lifetime Achievement Award was presented to Dr. Marsel Mesulam. His research addresses the connectivity of the monkey brain, the organization of human cholinergic pathways, the representation of cognitive functions by large-scale neurocognitive networks, and the neurobiology of dementias. Dr. Mesulam's work on cholinergic pathways has been groundbreaking in understanding Alzheimer's. He is a world expert in Primary Progressive Aphasia.
Zaven Khachaturian Award
In addition to these three awards, Dr. Marilyn Albert was recipient of the 2010 Zaven Khachaturian Award at AAICAD. Named in honor of noted scientist, administrator, consultant, lecturer and author, Zaven Khachaturian, PhD, this award recognizes an individual whose compelling vision, selfless dedication, and extraordinary achievement has significantly advanced the field of Alzheimer science.
Dr. Albert's distinguished career includes more than two decades as a faculty member at Harvard University Medical School. Her research has primarily focused on the cognitive and brain changes associated with aging and Alzheimer's. The scope has also encompassed investigating potential methods of early identification of Alzheimer's and lifestyle factors that may maintain mental abilities with advancing age.
Source:
Alzheimer's Association
понедельник, 13 июня 2011 г.
New Alzheimer's Study Seeks To Find Earliest Clues To Disease Progression
Today, 5.3 million Americans are suffering from Alzheimer's disease (AD), and every 70 seconds, another person develops this devastating disease. These numbers will continue to increase with our aging population unless new prevention and treatment strategies are discovered. A study funded by the National Institute on Aging (NIA) at the National Institutes of Health (NIH) may help provide some answers. This two-year, $24 million study -- the Alzheimer's Disease Neuroimaging Initiative Grand Opportunity (ADNI GO) -- focuses for the first time on people experiencing the very earliest complaints of memory problems that affect their daily activities. ADNI GO expands on the groundbreaking Alzheimer's Disease Neuroimaging Initiative (ADNI) and will continue efforts to identify biomarkers that can help build a greater understanding of the progression of AD.
"ADNI GO is helping us determine the sequence and timing of events at the initial onset of mild symptoms," said Paul Aisen, M.D., director of the Alzheimer's Disease Cooperative Study (ADCS). "It is our hope that this research will enable us to better identify who is at risk, as well as the effectiveness of potential prevention and treatment strategies."
Many people view memory loss as an unavoidable aspect of aging, but memory loss that disrupts daily life is not a normal part of growing older. ADNI GO researchers are looking for participants between the ages of 55 and 90 who are otherwise healthy, but may be experiencing signs of early stage of amnestic mild cognitive impairment (aMCI), a condition that may lead to Alzheimer's disease.
"We cannot end this terrible disease unless we know more about it," said Dr. Aisen. "That is where the amazing volunteers, their friends and their families can make the difference in our success."
Source:
ADNI GO
"ADNI GO is helping us determine the sequence and timing of events at the initial onset of mild symptoms," said Paul Aisen, M.D., director of the Alzheimer's Disease Cooperative Study (ADCS). "It is our hope that this research will enable us to better identify who is at risk, as well as the effectiveness of potential prevention and treatment strategies."
Many people view memory loss as an unavoidable aspect of aging, but memory loss that disrupts daily life is not a normal part of growing older. ADNI GO researchers are looking for participants between the ages of 55 and 90 who are otherwise healthy, but may be experiencing signs of early stage of amnestic mild cognitive impairment (aMCI), a condition that may lead to Alzheimer's disease.
"We cannot end this terrible disease unless we know more about it," said Dr. Aisen. "That is where the amazing volunteers, their friends and their families can make the difference in our success."
Source:
ADNI GO
Caregivers May Benefit From Adult Day Care
Caring for an elderly family member can be stressful and can pose health threats to caregivers. Steven Zarit, professor and head, Department of Human Development and Family Studies, Penn State, received a $3 million grant from the National Institute on Aging to study the effects of caregiving on familial caregivers. He will look at people who care for family members with dementia and how adult day care impacts the stress levels of all individuals involved.
People with dementia experience progressive memory loss, which can lead them to act out in ways that are not always easy to handle. They may try to leave the house, struggle with dressing, reject help and become agitated. This erratic behavior requires constant surveillance and any lapses in vigilance could lead to danger. Trained professionals are more prepared to deal with these types of behaviors and often experience less stress than family members.
"Using adult day care can reduce stress for family members by lifting the burden of responsibility from them for a few hours," said Zarit. "At the same time, day care provides stimulating activities that promote sleep and well-being in those being cared for."
Zarit will interview and collect saliva samples from caregivers on eight consecutive days to test both self-perceptions of stress and physiological stress. Because adult day care is typically used only three or four days a week, he will be able to assess how stress levels fluctuate when day care is used or not used.
"In many studies that test stress in individuals, the subjects might only have one day that they experience high stress," said Zarit. "In this experiment, though, participants will experience several days of high stress. This should give us a better understanding of the mechanism through which stress affects our health and it will be able to tell us what happens physiologically when someone reports having a good or bad day."
Through his research, Zarit will be able to assess whether or not using day care truly improves the health of people suffering from dementia and their family members. He will work with 180 participants over three years, primarily with adult day care centers in New Jersey, which are known for providing excellent day care service.
Source:
A'ndrea Elyse Messer
Penn State
People with dementia experience progressive memory loss, which can lead them to act out in ways that are not always easy to handle. They may try to leave the house, struggle with dressing, reject help and become agitated. This erratic behavior requires constant surveillance and any lapses in vigilance could lead to danger. Trained professionals are more prepared to deal with these types of behaviors and often experience less stress than family members.
"Using adult day care can reduce stress for family members by lifting the burden of responsibility from them for a few hours," said Zarit. "At the same time, day care provides stimulating activities that promote sleep and well-being in those being cared for."
Zarit will interview and collect saliva samples from caregivers on eight consecutive days to test both self-perceptions of stress and physiological stress. Because adult day care is typically used only three or four days a week, he will be able to assess how stress levels fluctuate when day care is used or not used.
"In many studies that test stress in individuals, the subjects might only have one day that they experience high stress," said Zarit. "In this experiment, though, participants will experience several days of high stress. This should give us a better understanding of the mechanism through which stress affects our health and it will be able to tell us what happens physiologically when someone reports having a good or bad day."
Through his research, Zarit will be able to assess whether or not using day care truly improves the health of people suffering from dementia and their family members. He will work with 180 participants over three years, primarily with adult day care centers in New Jersey, which are known for providing excellent day care service.
Source:
A'ndrea Elyse Messer
Penn State
воскресенье, 12 июня 2011 г.
Many Newly Diagnosed Alzheimer's Disease Patients Do Not Receive Alzheimer's Drugs As First-Line Therapy
Decision Resources, one of the world's leading research and advisory firms focusing on pharmaceutical and healthcare issues, finds that while approximately 70 percent of surveyed physicians' newly diagnosed patients have mild-to-moderate Alzheimer's disease, only 52.2 percent of first-line patients are prescribed an acetylcholinesterase inhibitor (AChEI). Instead, 28.1 percent of first-line patients are prescribed an antidepressant. The new report entitled Treatment Algorithms in Alzheimer's Disease finds that 65.8 percent of these patients take antidepressants as a monotherapy in this line.
First-line prescribing of antidepressants is largely driven by primary care physicians; 45 percent of surveyed primary care physicians indicate they prescribe antidepressants first line as a monotherapy, compared with only 27 percent of surveyed neurologists.
"The prescribing of antidepressants as first line therapy for Alzheimer's disease not only underscores the relatively high rate of comorbidity between Alzheimer's disease and depression, but more importantly indicates that physicians and/or patients prioritize the treatment of depression in newly diagnosed Alzheimer's disease patients," said Matthew Winton, Ph.D., analyst with Decision Resources. "This is likely because physicians perceive that effective treatments exist for depression, but not for cognitive decline."
The report also finds that relatively long delays separate a patient's first diagnosis for Alzheimer's disease and the start of treatment. Patient-level claims data show that only 34.9 percent of patients begin first-line treatment for the disease within a year of their first diagnosis. Slow treatment initiation of newly diagnosed patients can be attributed to the unwillingness of patients to receive treatment.
About Treatment Algorithm Insight Series
Decision Resources combines in-depth primary research with the most extensive claims-based longitudinal patient-level data from IMS Lifelink: Health Plans Claims database to provide exceptional insight into physicians' prescribing trends and the factors that drive therapy product choice, from diagnosis through multiple courses of treatment, for a specific disease.
About Decision Resources, Inc.
Decision Resources, Inc. is a cohesive portfolio of companies that offers best-in-class, high-value information and insights on important sectors of the healthcare industry. Clients rely on this analysis and data to make informed decisions.
All company, brand or product names contained in this document may be trademarks or registered trademarks of their respective holders.
Source: Decision Resources
First-line prescribing of antidepressants is largely driven by primary care physicians; 45 percent of surveyed primary care physicians indicate they prescribe antidepressants first line as a monotherapy, compared with only 27 percent of surveyed neurologists.
"The prescribing of antidepressants as first line therapy for Alzheimer's disease not only underscores the relatively high rate of comorbidity between Alzheimer's disease and depression, but more importantly indicates that physicians and/or patients prioritize the treatment of depression in newly diagnosed Alzheimer's disease patients," said Matthew Winton, Ph.D., analyst with Decision Resources. "This is likely because physicians perceive that effective treatments exist for depression, but not for cognitive decline."
The report also finds that relatively long delays separate a patient's first diagnosis for Alzheimer's disease and the start of treatment. Patient-level claims data show that only 34.9 percent of patients begin first-line treatment for the disease within a year of their first diagnosis. Slow treatment initiation of newly diagnosed patients can be attributed to the unwillingness of patients to receive treatment.
About Treatment Algorithm Insight Series
Decision Resources combines in-depth primary research with the most extensive claims-based longitudinal patient-level data from IMS Lifelink: Health Plans Claims database to provide exceptional insight into physicians' prescribing trends and the factors that drive therapy product choice, from diagnosis through multiple courses of treatment, for a specific disease.
About Decision Resources, Inc.
Decision Resources, Inc. is a cohesive portfolio of companies that offers best-in-class, high-value information and insights on important sectors of the healthcare industry. Clients rely on this analysis and data to make informed decisions.
All company, brand or product names contained in this document may be trademarks or registered trademarks of their respective holders.
Source: Decision Resources
суббота, 11 июня 2011 г.
Better Care For Dementia Patients Through New Funding, Australia
With Australia's ageing population, diseases like dementia are on the rise. And, thanks to $1.7 million in recent grants, The University of Queensland will be at the forefront of research dealing with a range of dementia-related issues.
Three UQ research teams have won National Health and Medical Research Council (NHMRC) funding for studies into dementia, spanning care in hospitals, transitions to residential care and ascertaining the capacity of people with dementia to make decisions about their finances.
The UQ researchers who have obtained funding are Associate Professor Nancy Pachana ($547,250), Professor Len Gray ($516,698) and Professor Helen Chenery ($648,360), each leading teams combining health and social science expertise.
Dr Pachana's research deals with developing a proven method to help the Office of the Adult Guardian determine financial capacity in people with dementia, particularly where there are allegations of fiscal abuse.
"This process is often stressful for the older person, and having family members manage the older person's assets may result in family conflict," Dr Pachana said.
The outcome of the research would aid health and legal professionals, guardianship boards and tribunals, as well as people with dementia and their family members, she said.
Professor Gray's project will investigate issues surrounding acute hospital care of people with dementia, to identify the specific needs of patients with dementia to inform better hospital design and treatment.
He said people with dementia were more prone to acute illnesses due to falls, strokes, heart failures and infections but they traditionally did not do well in clinical environments.
"Hospitals appear to be unfriendly environments for these people, exposing them to the risk of anxiety, delirium, disturbed behaviour and injury. They therefore require specialist care," Professor Gray said.
"This study will examine the current use of hospitals by people with dementia, including the frequency of cases, their outcomes and the staff and carers' perspectives of the issues, with a view to designing better future care."
Focusing on the potentially traumatic transition of dementia patients from home to residential care, Professor Chenery and her colleagues aim to develop an intervention program for dementia patients in both metropolitan and rural Queensland that focuses on positive communication and memory strategies.
The program would maximise dementia patients' ability to learn and retain functional skills to preserve the health and wellbeing of both people with dementia and their caregivers, she said.
"Previous models of care in dementia have tended to focus on single skill areas," Professor Chenery said.
"The key innovation in this project is that it brings together researchers from speech pathology, psychology, nursing and psychiatry to develop an interdisciplinary intervention targeted at the intersection between memory and language."
These three grants take to four the number of NHMRC Dementia Research Grants awarded to UQ researchers. UQ was awarded a first-round dementia grant of $530,000 in 2007 for a study led by Associate Professor Gerard Byrne into anxiety and depression in dementia patients.
The University of Queensland, Brisbane Australia
Three UQ research teams have won National Health and Medical Research Council (NHMRC) funding for studies into dementia, spanning care in hospitals, transitions to residential care and ascertaining the capacity of people with dementia to make decisions about their finances.
The UQ researchers who have obtained funding are Associate Professor Nancy Pachana ($547,250), Professor Len Gray ($516,698) and Professor Helen Chenery ($648,360), each leading teams combining health and social science expertise.
Dr Pachana's research deals with developing a proven method to help the Office of the Adult Guardian determine financial capacity in people with dementia, particularly where there are allegations of fiscal abuse.
"This process is often stressful for the older person, and having family members manage the older person's assets may result in family conflict," Dr Pachana said.
The outcome of the research would aid health and legal professionals, guardianship boards and tribunals, as well as people with dementia and their family members, she said.
Professor Gray's project will investigate issues surrounding acute hospital care of people with dementia, to identify the specific needs of patients with dementia to inform better hospital design and treatment.
He said people with dementia were more prone to acute illnesses due to falls, strokes, heart failures and infections but they traditionally did not do well in clinical environments.
"Hospitals appear to be unfriendly environments for these people, exposing them to the risk of anxiety, delirium, disturbed behaviour and injury. They therefore require specialist care," Professor Gray said.
"This study will examine the current use of hospitals by people with dementia, including the frequency of cases, their outcomes and the staff and carers' perspectives of the issues, with a view to designing better future care."
Focusing on the potentially traumatic transition of dementia patients from home to residential care, Professor Chenery and her colleagues aim to develop an intervention program for dementia patients in both metropolitan and rural Queensland that focuses on positive communication and memory strategies.
The program would maximise dementia patients' ability to learn and retain functional skills to preserve the health and wellbeing of both people with dementia and their caregivers, she said.
"Previous models of care in dementia have tended to focus on single skill areas," Professor Chenery said.
"The key innovation in this project is that it brings together researchers from speech pathology, psychology, nursing and psychiatry to develop an interdisciplinary intervention targeted at the intersection between memory and language."
These three grants take to four the number of NHMRC Dementia Research Grants awarded to UQ researchers. UQ was awarded a first-round dementia grant of $530,000 in 2007 for a study led by Associate Professor Gerard Byrne into anxiety and depression in dementia patients.
The University of Queensland, Brisbane Australia
пятница, 10 июня 2011 г.
Alzheimer's Society Comment On Genetic Risk Factors Of Alzheimer's Disease
Scientists have been aware for some time that the genes we inherit from our parents may partly determine whether we will develop specific diseases.
However, the role of genetics in the development of dementia is still not fully understood. This is an important study following families affected by dementia over a long period of time.
For the majority of people the effect of inheritance seems to be small. If a parent or other relative has dementia your own chances of developing it are only a little higher than if there were no cases of dementia in the family. This study suggests that this risk is increased if both of your parents have had dementia.
We also know that there are a small number of families where there is a very clear inheritance of dementia from one generation to the next.
We are still learning what causes Alzheimer's disease and other forms of dementia.
It is clear that genes do play a role but the largest risk factor remains your age. As one in three people who live to over 65 will die with dementia it is vital that more research is carried out to fight this devastating condition.
Notes:
The Alzheimer's Society is the leading care and research charity for people with all forms dementia and their carers. It provides information and education, support for carers, and quality day and home care. It funds medical and scientific research and campaigns for improved health and social services and greater public understanding of dementia.
The Alzheimer's Society provides a national help line on 0845 3000 336 and website alzheimers.uk.
Alzheimer's Society
However, the role of genetics in the development of dementia is still not fully understood. This is an important study following families affected by dementia over a long period of time.
For the majority of people the effect of inheritance seems to be small. If a parent or other relative has dementia your own chances of developing it are only a little higher than if there were no cases of dementia in the family. This study suggests that this risk is increased if both of your parents have had dementia.
We also know that there are a small number of families where there is a very clear inheritance of dementia from one generation to the next.
We are still learning what causes Alzheimer's disease and other forms of dementia.
It is clear that genes do play a role but the largest risk factor remains your age. As one in three people who live to over 65 will die with dementia it is vital that more research is carried out to fight this devastating condition.
Notes:
The Alzheimer's Society is the leading care and research charity for people with all forms dementia and their carers. It provides information and education, support for carers, and quality day and home care. It funds medical and scientific research and campaigns for improved health and social services and greater public understanding of dementia.
The Alzheimer's Society provides a national help line on 0845 3000 336 and website alzheimers.uk.
Alzheimer's Society
Alzheimer's Drug Discovery Foundation Funds Development Of Clinical Tests For Alzheimer's Disease
The Alzheimer's Drug
Discovery Foundation (ADDF) awarded the British firm of Cambridge
Cognition Ltd. a grant of $200,000 to assist in their development of
a clinical cognitive assessment product for Alzheimer's disease. ADDF
made this award as part of its effort to advance early detection and
the reliable assessment of cognitive function in patients with
Alzheimer's disease and related dementias in clinical care, as well as
accelerate drug development and clinical monitoring of therapy.
Cambridge Cognition is a world leader in the development of
computerized cognitive tests, with its CANTAB battery, which are now
in use in over 500 research departments in over 60 countries. Their
Paired Associate Learning (PAL) test is widely recognized as being
the most accurate current test for the detection of early stage
dementia and Mild Cognitive Impairment, as well as accurately
differentiating between demented and normal patients and those
suffering from depression. This test will form the basis for the
future clinical assessment of AD.
"The market for computerized cognitive tests in diseases such as
Alzheimer's is expanding, maturing and gaining recognition," remarked
Howard Fillit, MD and Executive Director of ADDF.? "The device and
tests being developed by Cambridge Cognition will enable the
clinician to accurately identify patients with cognitive impairment
due to early dementia. The device will also enable clinicians to
objectively measure the ongoing effects of disease modifying drugs
currently in development and promote their effective use.? We
assessed Cambridge Cognition both on the quality of their science and
for commercial due diligence.? Their scientific base is outstanding
with over 600 quality peer reviewed papers and we believe that their
'stand alone' device has clinical merit."
Ian Harris, The CEO of Cambridge Cognition, welcomed the grant as
"this will really speed up our time to market and is an enormous vote
of confidence in both our science and our business model by a highly
respected independent charity.? This test when in clinical use will
make a real difference to patient outcomes."
About the Alzheimer's Drug Discovery Foundation (ADDF)
ADDF is the only public charity whose sole mission is to accelerate
the discovery and development of drugs to prevent, treat and cure
Alzheimer's disease, related dementias and cognitive aging. We award
grants to leading scientists conducting breakthrough drug discovery
research.
ADDF uses a venture philanthropy model to bridge the worldwide
funding gap between basic research and later-stage development, using
any return on investment to support new research. Since 1998, we have
received over 1,600 requests to fund new ideas for Alzheimer's drugs.
For all, we provided expert reviews and recommendations to advance
their programs. We granted more than $35M to fund over 240
Alzheimer's drug discovery programs in academic centers and
biotechnology companies in 12 countries. For more information, visit
our website at alzdiscovery.
About Cambridge Cognition Ltd.
Cambridge Cognition develops and markets CANTAB(R), the world's
leading cognitive testing product for the diagnosis and assessment of
important mental health diseases including Alzheimer's, Depression,
Schizophrenia and ADHD. The computerised neuropsychological tests in
CANTAB(R) are outstandingly sensitive and extensively validated, with
a bibliography of over 600 peer-reviewed journal papers. Based in
Cambridge, England, and Cambridge, Massachusetts, Cambridge Cognition
Ltd supplies its products and services to the pharmaceutical industry
and academic researchers across the globe.
Alzheimer's Drug Discovery Foundation
Discovery Foundation (ADDF) awarded the British firm of Cambridge
Cognition Ltd. a grant of $200,000 to assist in their development of
a clinical cognitive assessment product for Alzheimer's disease. ADDF
made this award as part of its effort to advance early detection and
the reliable assessment of cognitive function in patients with
Alzheimer's disease and related dementias in clinical care, as well as
accelerate drug development and clinical monitoring of therapy.
Cambridge Cognition is a world leader in the development of
computerized cognitive tests, with its CANTAB battery, which are now
in use in over 500 research departments in over 60 countries. Their
Paired Associate Learning (PAL) test is widely recognized as being
the most accurate current test for the detection of early stage
dementia and Mild Cognitive Impairment, as well as accurately
differentiating between demented and normal patients and those
suffering from depression. This test will form the basis for the
future clinical assessment of AD.
"The market for computerized cognitive tests in diseases such as
Alzheimer's is expanding, maturing and gaining recognition," remarked
Howard Fillit, MD and Executive Director of ADDF.? "The device and
tests being developed by Cambridge Cognition will enable the
clinician to accurately identify patients with cognitive impairment
due to early dementia. The device will also enable clinicians to
objectively measure the ongoing effects of disease modifying drugs
currently in development and promote their effective use.? We
assessed Cambridge Cognition both on the quality of their science and
for commercial due diligence.? Their scientific base is outstanding
with over 600 quality peer reviewed papers and we believe that their
'stand alone' device has clinical merit."
Ian Harris, The CEO of Cambridge Cognition, welcomed the grant as
"this will really speed up our time to market and is an enormous vote
of confidence in both our science and our business model by a highly
respected independent charity.? This test when in clinical use will
make a real difference to patient outcomes."
About the Alzheimer's Drug Discovery Foundation (ADDF)
ADDF is the only public charity whose sole mission is to accelerate
the discovery and development of drugs to prevent, treat and cure
Alzheimer's disease, related dementias and cognitive aging. We award
grants to leading scientists conducting breakthrough drug discovery
research.
ADDF uses a venture philanthropy model to bridge the worldwide
funding gap between basic research and later-stage development, using
any return on investment to support new research. Since 1998, we have
received over 1,600 requests to fund new ideas for Alzheimer's drugs.
For all, we provided expert reviews and recommendations to advance
their programs. We granted more than $35M to fund over 240
Alzheimer's drug discovery programs in academic centers and
biotechnology companies in 12 countries. For more information, visit
our website at alzdiscovery.
About Cambridge Cognition Ltd.
Cambridge Cognition develops and markets CANTAB(R), the world's
leading cognitive testing product for the diagnosis and assessment of
important mental health diseases including Alzheimer's, Depression,
Schizophrenia and ADHD. The computerised neuropsychological tests in
CANTAB(R) are outstandingly sensitive and extensively validated, with
a bibliography of over 600 peer-reviewed journal papers. Based in
Cambridge, England, and Cambridge, Massachusetts, Cambridge Cognition
Ltd supplies its products and services to the pharmaceutical industry
and academic researchers across the globe.
Alzheimer's Drug Discovery Foundation
четверг, 9 июня 2011 г.
New trial drug with older drug helps memory of Alzheimers
An experimental drug combined with an already-popular memory-enhancing compound may further delay memory loss in patients
with Alzheimer's disease and other dementias, Johns Hopkins University scientists, in collaboration with researchers from
University of North Carolina, have found.
The findings, described in the June issue of Neuropsychopharmacology, also indicate that the experimental treatment in
question - a compound known as SGS742 - works by blocking certain chemicals that interfere with memory formation.
"The findings in laboratory animals - both improved memory in our tests and evidence that the drug targets the biology for
making memories in the brain - places this drug on solid footing as a candidate therapeutic agent," said the study's lead
author, Michela Gallagher.
SGS742, previously shown to improve memory in animals, is an experimental treatment for memory disorders. It is currently in
human clinical trials led by California-based Saegis Pharmaceuticals Inc., which holds a worldwide exclusive license granted
by the drug's developer.
Gallagher, a Krieger-Eisenhower Professor and the chair of the Department of Psychological and Brain Sciences in the
university's Zanvyl Krieger School of Arts and Sciences, said these studies did not address SGS742's potential as a cure or
preventive treatment for Alzheimer's disease itself. They were intended, rather, to assess its potential as a treatment for
the disease's key symptom: memory loss.
"Memory impairment occurs early in the disease and worsens as the disease progresses. However, until the later stages of the
disease, memory is impaired but not entirely gone," Gallagher said. "By augmenting the brain's memory-making ability, drugs
could be used to treat this symptom and to improve the quality of life for patients who have a disease that has a slow
progression over years."
SGS742 has been found in clinical trials to be beneficial to humans with mild cognitive impairment. The Johns Hopkins team
investigated how the compound works. The team compared SGS742 with Aricept ® (generic name: donepezil), an approved and
frequently used treatment for Alzheimer's disease manufactured by Eisai Inc. Ltd. The Johns Hopkins researchers found in
animal studies that a combination of SGS742 and Aricept ® improved memory to a larger degree than either drug alone, implying
a potential for future combination therapy protocols.
The research team conducted this study on 60 normal young male rats who were not memory-impaired. Each rat was given at
various times SGS742, Aricept ®, a combination of the two drugs or no drugs at all, and was tested on its skill navigating a
series of mazes that placed increasing demands on its memory.
"The mazes were designed to take advantage of the rats' natural foraging instincts," explains Rebecca Haberman, an associate
research scientist at Johns Hopkins who is a co-author on the study. "Rats will not readily return to the place where they
previously ate all the available food. So we asked the rats to remember where they had found treats in the 'information'
session, and to look for food in new places during the recall tests."
It quickly became apparent that the rodents performed better when they were given either SGS742 or Aricept ® rather than no
drug at all. What's more, those rats given both SGS742 and Aricept ® were able to both acquire and retain information more
quickly and for a longer period of time than when they had not been thus treated.
Researchers also analyzed the interaction of the compound with the biological mechanisms involved in the creation of
long-term memory. They learned that SGS742 alters the activity of gene control machinery that is important for memory
consolidation.
They focused on a molecule, CREB2, that is believed to block memory formation by binding to a specific gene sequence.
Analysis of the brains of the rats revealed that those who had been treated with SGS742 had less CREB2 bound to this
important gene sequence than did the rats that had not been treated.
"This indicates that SGS742-treated rats had an easier time activating the appropriate genes necessary for memory
consolidation," Haberman said. "The fact that SGS742 improved memory even when it was given after the rats were exposed to
information further supports that the drug is important for retaining information, and not just for obtaining it."
Funding for this research was provided by Saegis Pharmaceuticals Inc. Authors on the paper include A. Helm, R.P. Haberman,
S.L. Dean, and M. Gallagher of the Department of Psychological and Brain Sciences of The Johns Hopkins University, E.C. Hoyt,
P.K. Lund of the Department of Cell and Molecular Physiology, University of North Carolina at Chapel Hill, and T. Melcher of
Saegis Pharmaceuticals Inc., Half Moon Bay, Calif.
Gallagher is a scientific consultant to Saegis Pharmaceuticals and has an equity interest in the company. Under a licensing
arrangement between The Johns Hopkins University and Saegis, Gallagher is entitled to a share of royalties received by the
university on sales of products resulting from this research.
Related links:
Michela Gallagher: psy.jhu/fs/faculty/gallagher.htm
Department of Psychological and Brain Sciences: psy.jhu
Johns Hopkins University
jhu
View drug information on ARICEPT.
with Alzheimer's disease and other dementias, Johns Hopkins University scientists, in collaboration with researchers from
University of North Carolina, have found.
The findings, described in the June issue of Neuropsychopharmacology, also indicate that the experimental treatment in
question - a compound known as SGS742 - works by blocking certain chemicals that interfere with memory formation.
"The findings in laboratory animals - both improved memory in our tests and evidence that the drug targets the biology for
making memories in the brain - places this drug on solid footing as a candidate therapeutic agent," said the study's lead
author, Michela Gallagher.
SGS742, previously shown to improve memory in animals, is an experimental treatment for memory disorders. It is currently in
human clinical trials led by California-based Saegis Pharmaceuticals Inc., which holds a worldwide exclusive license granted
by the drug's developer.
Gallagher, a Krieger-Eisenhower Professor and the chair of the Department of Psychological and Brain Sciences in the
university's Zanvyl Krieger School of Arts and Sciences, said these studies did not address SGS742's potential as a cure or
preventive treatment for Alzheimer's disease itself. They were intended, rather, to assess its potential as a treatment for
the disease's key symptom: memory loss.
"Memory impairment occurs early in the disease and worsens as the disease progresses. However, until the later stages of the
disease, memory is impaired but not entirely gone," Gallagher said. "By augmenting the brain's memory-making ability, drugs
could be used to treat this symptom and to improve the quality of life for patients who have a disease that has a slow
progression over years."
SGS742 has been found in clinical trials to be beneficial to humans with mild cognitive impairment. The Johns Hopkins team
investigated how the compound works. The team compared SGS742 with Aricept ® (generic name: donepezil), an approved and
frequently used treatment for Alzheimer's disease manufactured by Eisai Inc. Ltd. The Johns Hopkins researchers found in
animal studies that a combination of SGS742 and Aricept ® improved memory to a larger degree than either drug alone, implying
a potential for future combination therapy protocols.
The research team conducted this study on 60 normal young male rats who were not memory-impaired. Each rat was given at
various times SGS742, Aricept ®, a combination of the two drugs or no drugs at all, and was tested on its skill navigating a
series of mazes that placed increasing demands on its memory.
"The mazes were designed to take advantage of the rats' natural foraging instincts," explains Rebecca Haberman, an associate
research scientist at Johns Hopkins who is a co-author on the study. "Rats will not readily return to the place where they
previously ate all the available food. So we asked the rats to remember where they had found treats in the 'information'
session, and to look for food in new places during the recall tests."
It quickly became apparent that the rodents performed better when they were given either SGS742 or Aricept ® rather than no
drug at all. What's more, those rats given both SGS742 and Aricept ® were able to both acquire and retain information more
quickly and for a longer period of time than when they had not been thus treated.
Researchers also analyzed the interaction of the compound with the biological mechanisms involved in the creation of
long-term memory. They learned that SGS742 alters the activity of gene control machinery that is important for memory
consolidation.
They focused on a molecule, CREB2, that is believed to block memory formation by binding to a specific gene sequence.
Analysis of the brains of the rats revealed that those who had been treated with SGS742 had less CREB2 bound to this
important gene sequence than did the rats that had not been treated.
"This indicates that SGS742-treated rats had an easier time activating the appropriate genes necessary for memory
consolidation," Haberman said. "The fact that SGS742 improved memory even when it was given after the rats were exposed to
information further supports that the drug is important for retaining information, and not just for obtaining it."
Funding for this research was provided by Saegis Pharmaceuticals Inc. Authors on the paper include A. Helm, R.P. Haberman,
S.L. Dean, and M. Gallagher of the Department of Psychological and Brain Sciences of The Johns Hopkins University, E.C. Hoyt,
P.K. Lund of the Department of Cell and Molecular Physiology, University of North Carolina at Chapel Hill, and T. Melcher of
Saegis Pharmaceuticals Inc., Half Moon Bay, Calif.
Gallagher is a scientific consultant to Saegis Pharmaceuticals and has an equity interest in the company. Under a licensing
arrangement between The Johns Hopkins University and Saegis, Gallagher is entitled to a share of royalties received by the
university on sales of products resulting from this research.
Related links:
Michela Gallagher: psy.jhu/fs/faculty/gallagher.htm
Department of Psychological and Brain Sciences: psy.jhu
Johns Hopkins University
jhu
View drug information on ARICEPT.
среда, 8 июня 2011 г.
UNC Co-Leads Study To Identify Risks For Dementia, Cognitive Decline
University of North Carolina at Chapel Hill researchers are co-leading a national study to examine whether middle-aged people's physical health influences their risk of dementia later in life.
The study aims to determine what role vascular risk factors- including hypertension, diabetes and lifestyle - experienced in middle age may play in the development of dementia (vascular or due to Alzheimer's disease) and cognitive decline in the elderly.
UNC's Gillings School of Global Public Health's Collaborative Studies Coordinating Center will lead the neurocognitive study, which builds on its Atherosclerosis Risk in Communities (ARIC) study, a large epidemiologic investigation of the risk factors for heart disease and stroke that has been collecting data for more than 20 years.
The new neurocognitive study is funded through a $26 million grant over four years from the National Institutes of Health to five collaborating institutions: UNC, the University of Mississippi Medical Center, the University of Minnesota, along with Johns Hopkins and Wake Forest universities. UNC receives $4.6 million from the grant.
The study, a comprehensive examination of thousands of patients, will include detailed neurocognitive testing and brain imaging, said Diane Catellier, Dr.P.H., research associate professor of biostatistics and the principle investigator from UNC.
"Using the new exam data and the wealth of information collected during ARIC's 20-plus years, we expect to find out more about the causes of dementia and less severe symptoms of mild cognitive impairment," Catellier said. "We hope to get a unique view into early physiological changes that eventually culminate in dementia. The findings may help identify at-risk individuals who may benefit from early interventions targeting modifiable risk factors."
The original study has followed a group of roughly 16,000 participants for more than 20 years, from middle age into late life. Over the years, participants have been extensively evaluated for diseases and factors including heart disease, hypertension and cognitive function.
"The new ARIC Neurocognitive Study will be one of the most comprehensive investigations to date into the role of vascular and related mid-life risk factors in Alzheimer's and cognitive decline," said Thomas Mosley, M.D., University of Mississippi Medical Center professor of geriatric medicine and one of the new study's lead investigators.
Mosley said he believes Alzheimer's disease likely isn't caused by a single factor, but rather by a complex process involving multiple factors interacting and accumulating over decades.
"Understanding the risk factors involved in this complex process may lead to new targets for treatment," he said. "It could also allow us to intervene at an earlier point with people who are at high risk for dementia, a time when preventive treatments may be most effective."
Recent research has found African Americans may have a twofold or greater risk for Alzheimer's compared to whites. With one of the largest and most extensively evaluated African-American study subgroups, the study will help illuminate the role of ethnic differences in relative risk for dementia.
Previous findings from the long-term study have indicated the importance of vascular risk factors in predicting decline in cognitive functions such as memory and processing speed. Using brain imaging, researchers have also shown brain changes, such as atrophy and silent strokes, are surprisingly common, even in middle-age adults. They have also found that these brain abnormalities begin to affect cognitive functions as early as middle age.
The new neurocognitive study is co-funded by three NIH institutes: the National Heart, Lung and Blood Institute; the National Institute of Neurological Disorders and Stroke; and the National Eye Institute.
Source:
University of North Carolina at Chapel Hill
The study aims to determine what role vascular risk factors- including hypertension, diabetes and lifestyle - experienced in middle age may play in the development of dementia (vascular or due to Alzheimer's disease) and cognitive decline in the elderly.
UNC's Gillings School of Global Public Health's Collaborative Studies Coordinating Center will lead the neurocognitive study, which builds on its Atherosclerosis Risk in Communities (ARIC) study, a large epidemiologic investigation of the risk factors for heart disease and stroke that has been collecting data for more than 20 years.
The new neurocognitive study is funded through a $26 million grant over four years from the National Institutes of Health to five collaborating institutions: UNC, the University of Mississippi Medical Center, the University of Minnesota, along with Johns Hopkins and Wake Forest universities. UNC receives $4.6 million from the grant.
The study, a comprehensive examination of thousands of patients, will include detailed neurocognitive testing and brain imaging, said Diane Catellier, Dr.P.H., research associate professor of biostatistics and the principle investigator from UNC.
"Using the new exam data and the wealth of information collected during ARIC's 20-plus years, we expect to find out more about the causes of dementia and less severe symptoms of mild cognitive impairment," Catellier said. "We hope to get a unique view into early physiological changes that eventually culminate in dementia. The findings may help identify at-risk individuals who may benefit from early interventions targeting modifiable risk factors."
The original study has followed a group of roughly 16,000 participants for more than 20 years, from middle age into late life. Over the years, participants have been extensively evaluated for diseases and factors including heart disease, hypertension and cognitive function.
"The new ARIC Neurocognitive Study will be one of the most comprehensive investigations to date into the role of vascular and related mid-life risk factors in Alzheimer's and cognitive decline," said Thomas Mosley, M.D., University of Mississippi Medical Center professor of geriatric medicine and one of the new study's lead investigators.
Mosley said he believes Alzheimer's disease likely isn't caused by a single factor, but rather by a complex process involving multiple factors interacting and accumulating over decades.
"Understanding the risk factors involved in this complex process may lead to new targets for treatment," he said. "It could also allow us to intervene at an earlier point with people who are at high risk for dementia, a time when preventive treatments may be most effective."
Recent research has found African Americans may have a twofold or greater risk for Alzheimer's compared to whites. With one of the largest and most extensively evaluated African-American study subgroups, the study will help illuminate the role of ethnic differences in relative risk for dementia.
Previous findings from the long-term study have indicated the importance of vascular risk factors in predicting decline in cognitive functions such as memory and processing speed. Using brain imaging, researchers have also shown brain changes, such as atrophy and silent strokes, are surprisingly common, even in middle-age adults. They have also found that these brain abnormalities begin to affect cognitive functions as early as middle age.
The new neurocognitive study is co-funded by three NIH institutes: the National Heart, Lung and Blood Institute; the National Institute of Neurological Disorders and Stroke; and the National Eye Institute.
Source:
University of North Carolina at Chapel Hill
вторник, 7 июня 2011 г.
Neuronal Function May Be Impaired By High Doses Of Lithium-Like Drugs
New laboratory research suggests that lithium and other drugs that inhibit a particular enzyme, GSK-3 beta, should be used with caution in treating Alzheimer's disease because too high a dose can impair, rather than enhance, neuronal function.
Lithium is currently in clinical trials for treating Alzheimer's. Pharmaceutical companies are interested in producing other GSK-3 beta inhibitors for the disease because these drugs are relatively easy to make and lithium has been shown to be safe in low doses in treating people with manic-depressive illness, said Dr. William D. Snider, professor of neurology, cell and molecular physiology at the University of North Carolina at Chapel Hill's School of Medicine.
"People might think that if you make the inhibitor stronger and stronger, that would be better. Our in-vitro experiments show that you will have to be careful with how you use GSK-3 beta inhibitors, because if you use too much, it will interfere with and possibly kill neurons," said Snider, who also is director of UNC's Neuroscience Center
The results, published online in the journal Neuron, were surprising because GSK-3 beta inhibitors have been shown at some doses to improve neuronal function. "It's known that when GSK-3 beta is inactivated that tends to allow the processes inside the cell it regulates to function normally," Snider said.
But when the researchers strongly inhibited GSK-3 beta in mouse neurons in cell culture, the growth of axons, which carry messages between nerve cells, was markedly reduced.
The researchers inhibited GSK-3 beta using RNA silencing. "RNA silencing allows you to specifically knock down the level of a particular protein inside the cell," Snider said.
In a second set of experiments, the researchers treated mouse neurons with a low dose and a high dose of a GSK-3 beta inhibitor similar to lithium. The high dose impaired neuronal function, while the low dose improved it.
Snider's group plans to further investigate the effect of inhibiting GSK-3 beta in a whole-mouse model. "We will take a conditional mutagenesis approach in mice to knock out the GSK-3 beta in the nervous system," Snider said. "We'll be able to find out if we get the same effect in the whole animal that we got using RNA silencing in the culture dish."
The researchers will also work to understand how GSK-3 operates in relation to a protein called Tau, which is implicated in Alzheimer's.
Note: School of Medicine contact: Tom Hughes
In addition to Snider, other authors are lead author Dr. Woo-Yang Kim, Drs. Jiang Zhou and Yan-Min Wang, all of UNC's Neuroscience Center; Drs. Eva Anton and Yukako Yokota, both of the Neuroscience Center and UNC's department of cell and molecular physiology; Dr. Feng-Quan Zhou of the Johns Hopkins University School of Medicine; Drs. Takeshi Yoshimura and Kozo Kaibuchi of Nagoya University, Japan; and Dr. James R. Woodgett of Ontario Cancer Institute, Toronto.
The study was funded by the National Institute of Neurological Disorders and Stroke, part of the National Institutes of Health.
Contact: Les Lang
University of North Carolina School of Medicine
Lithium is currently in clinical trials for treating Alzheimer's. Pharmaceutical companies are interested in producing other GSK-3 beta inhibitors for the disease because these drugs are relatively easy to make and lithium has been shown to be safe in low doses in treating people with manic-depressive illness, said Dr. William D. Snider, professor of neurology, cell and molecular physiology at the University of North Carolina at Chapel Hill's School of Medicine.
"People might think that if you make the inhibitor stronger and stronger, that would be better. Our in-vitro experiments show that you will have to be careful with how you use GSK-3 beta inhibitors, because if you use too much, it will interfere with and possibly kill neurons," said Snider, who also is director of UNC's Neuroscience Center
The results, published online in the journal Neuron, were surprising because GSK-3 beta inhibitors have been shown at some doses to improve neuronal function. "It's known that when GSK-3 beta is inactivated that tends to allow the processes inside the cell it regulates to function normally," Snider said.
But when the researchers strongly inhibited GSK-3 beta in mouse neurons in cell culture, the growth of axons, which carry messages between nerve cells, was markedly reduced.
The researchers inhibited GSK-3 beta using RNA silencing. "RNA silencing allows you to specifically knock down the level of a particular protein inside the cell," Snider said.
In a second set of experiments, the researchers treated mouse neurons with a low dose and a high dose of a GSK-3 beta inhibitor similar to lithium. The high dose impaired neuronal function, while the low dose improved it.
Snider's group plans to further investigate the effect of inhibiting GSK-3 beta in a whole-mouse model. "We will take a conditional mutagenesis approach in mice to knock out the GSK-3 beta in the nervous system," Snider said. "We'll be able to find out if we get the same effect in the whole animal that we got using RNA silencing in the culture dish."
The researchers will also work to understand how GSK-3 operates in relation to a protein called Tau, which is implicated in Alzheimer's.
Note: School of Medicine contact: Tom Hughes
In addition to Snider, other authors are lead author Dr. Woo-Yang Kim, Drs. Jiang Zhou and Yan-Min Wang, all of UNC's Neuroscience Center; Drs. Eva Anton and Yukako Yokota, both of the Neuroscience Center and UNC's department of cell and molecular physiology; Dr. Feng-Quan Zhou of the Johns Hopkins University School of Medicine; Drs. Takeshi Yoshimura and Kozo Kaibuchi of Nagoya University, Japan; and Dr. James R. Woodgett of Ontario Cancer Institute, Toronto.
The study was funded by the National Institute of Neurological Disorders and Stroke, part of the National Institutes of Health.
Contact: Les Lang
University of North Carolina School of Medicine
High Fruit And Vegetable Intake Positively Correlated With Antioxidant Status, Cognitive Performance
Researchers at the Institute of Biochemistry and Molecular Biology I of the Heinrich-Heine University, D??sseldorf, Germany, investigated the relationship between fruit and vegetable intake, plasma antioxidant micronutrient status and cognitive performance in healthy subjects aged 45 to 102 years. Their results, published in the August issue of the Journal of Alzheimer's Disease, indicated higher cognitive performance in individuals with high daily intake of fruits and vegetables.
Subjects with a high daily intake (about 400 g) of fruits and vegetables had higher antioxidant levels, lower indicators of free radical-induced damage against lipids as well as better cognitive performance compared to healthy subjects of any age consuming low amounts (< 100 g/day) of fruits and vegetables. Modification of nutritional habits aimed at increasing intake of fruits and vegetables, therefore, should be encouraged to lower the prevalence of cognitive impairment.
The work was performed in collaboration with the Department of Pharmacology at Temple University in Philadelphia, Pennsylvania, the Department of Geriatrics at Perugia University, Italy, and the Department of Neurology of the St. Elisabeth Hospital in Cologne, Germany.
Dr. M. Cristina Polidori, currently at the Department of Geriatrics, Marienhospital Herne, Ruhr-University of Bochum, Germany, explains: "It is known that there is a strong association between fruit and vegetable intake and the natural antioxidant defenses of the body against free radicals. It is also known that bad nutritional habits increase the risk of developing cognitive impairment with and without dementia. With this work we show a multiple link between fruit and vegetable intake, antioxidant defenses and cognitive performance, in the absence of disease and independent of age. Among other lifestyle habits, it is recommended to improve nutrition in general and fruit and vegetable intake in particular at any age, beginning as early as possible. This may increase our chances to remain free of dementia in advanced age."
These findings are independentof age, gender, body mass index, level of education, lipid profile and albumin levels, all factors able to influence cognitive and antioxidant status. The relevance of the findings is also strengthened by the large sample that included 193 healthy subjects.
Further studies are planned that will include larger subject cohorts, patients with Alzheimer's disease at different stages and patients with mild cognitive impairment without dementia.
Reference: Polidori MC, Pratico D, Mangialasche F, Mariani E, Aust O, Anlasik T, Mang N, Pientka L, Stahl W, Sies H, Nelles G. High fruit and vegetable intake is positively correlated with antioxidant status and cognitive performance in healthy subjects. J Alzheimers Dis 17:4 (August 2009).
Source:
Esther Mateike
IOS Press
Subjects with a high daily intake (about 400 g) of fruits and vegetables had higher antioxidant levels, lower indicators of free radical-induced damage against lipids as well as better cognitive performance compared to healthy subjects of any age consuming low amounts (< 100 g/day) of fruits and vegetables. Modification of nutritional habits aimed at increasing intake of fruits and vegetables, therefore, should be encouraged to lower the prevalence of cognitive impairment.
The work was performed in collaboration with the Department of Pharmacology at Temple University in Philadelphia, Pennsylvania, the Department of Geriatrics at Perugia University, Italy, and the Department of Neurology of the St. Elisabeth Hospital in Cologne, Germany.
Dr. M. Cristina Polidori, currently at the Department of Geriatrics, Marienhospital Herne, Ruhr-University of Bochum, Germany, explains: "It is known that there is a strong association between fruit and vegetable intake and the natural antioxidant defenses of the body against free radicals. It is also known that bad nutritional habits increase the risk of developing cognitive impairment with and without dementia. With this work we show a multiple link between fruit and vegetable intake, antioxidant defenses and cognitive performance, in the absence of disease and independent of age. Among other lifestyle habits, it is recommended to improve nutrition in general and fruit and vegetable intake in particular at any age, beginning as early as possible. This may increase our chances to remain free of dementia in advanced age."
These findings are independentof age, gender, body mass index, level of education, lipid profile and albumin levels, all factors able to influence cognitive and antioxidant status. The relevance of the findings is also strengthened by the large sample that included 193 healthy subjects.
Further studies are planned that will include larger subject cohorts, patients with Alzheimer's disease at different stages and patients with mild cognitive impairment without dementia.
Reference: Polidori MC, Pratico D, Mangialasche F, Mariani E, Aust O, Anlasik T, Mang N, Pientka L, Stahl W, Sies H, Nelles G. High fruit and vegetable intake is positively correlated with antioxidant status and cognitive performance in healthy subjects. J Alzheimers Dis 17:4 (August 2009).
Source:
Esther Mateike
IOS Press
понедельник, 6 июня 2011 г.
Blocking Stress Protein Decreases Alzheimer's Peptide In Mice
Scientists revealed in November 2006 that stress increases production in mice of a brain peptide critical to Alzheimer's disease. Now the same group has shown that blocking a different brain peptide slows the stress-induced increase, opening a new door to treatment. Researchers from Washington University School of Medicine in St. Louis report the results online this week in the Proceedings of the National Academy of Sciences.
Studies of humans and animals have suggested that stress may increase risk of Alzheimer's disease, but the new research is among the first studies to elaborate the basic biomolecular mechanisms that may underlie this increased risk.
The results build on earlier findings from coauthors John G. Csernansky, M.D., the Gregory B. Couch Professor of Psychiatry and professor of neurobiology, and Hongxin Dong, Ph.D., instructor in psychiatry. Using mice genetically modified to model human Alzheimer's disease, Csernansky and Dong showed that raising them under isolated conditions in smaller cages accelerated the deposition of brain plaques and declines in cognitive ability.
Brain plaques are believed to be a primary cause of the memory loss and other mental damage inflicted by Alzheimer's disease. They are mostly comprised of a peptide known as amyloid beta, so researchers immediately suspected that stress was increasing amyloid beta levels. But because there are other factors that can accelerate plaque build-up, they needed to test the link.
For that new test, scientists used a technique known as microdialysis to monitor amyloid beta levels in the brains of mice exposed to the same stressors: isolation and smaller cages.
"Stress remarkably elevated soluble amyloid beta levels in the spaces between brain cells," says senior author David Holtzman, M.D., the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology. "But we didn't know based on those initial experiments if it was a chronic effect or a much more immediate effect. If it was more immediate, we thought we might be able to identify some of the brain molecules involved in increasing the levels."
Lead author Jea-Eun Kang, a graduate student in the Holtzman lab, utilized a quicker way to cause stress: temporarily restrain mice from moving. Three hours of restraint led to a 30 percent increase in amyloid beta levels.
The spike in amyloid beta encouraged researchers to start looking for molecules that might be enabling this rapid change. Stress hormones produced by the adrenal gland were natural suspects. In mice, that meant corticosterone, the mouse equivalent of the human hormone cortisol. But a large dose of corticosterone didn't cause a similar rapid change in amyloid beta levels.
When they widened their search for molecules released in the mouse brain by stress, the scientists identified one called corticotropin-releasing factor (CRF), which is linked to increased levels of brain cell communication. In 2005, Holtzman, John Cirrito, Ph.D., a postdoctoral research associate in neurology and psychiatry, and colleagues showed that increased communication between brain cells also contributed to increased amyloid beta.
When they directly placed CRF in the mouse brain, amyloid beta levels rose immediately. Mice given a CRF blocker and then stressed did not display increased amyloid beta.
"There are very few known environmental risk factors for Alzheimer's disease," Holtzman notes. "Head trauma increases risk, higher education lowers it. Stress may be another environmental factor that increases risk."
Holtzman, Csernansky and their colleagues are intrigued by the possibility that drugs that block CRF or reduce anxiety may provide a new way to decrease amyloid beta and eventually delay or prevent Alzheimer's disease. Holtzman and his colleagues are also continuing to explore connections between brain cell activity and amyloid beta levels.
The studies were carried out in the Hope Center for Neurological Disorders and in conjunction with the Alzheimer's Disease Research Center, both at Washington University School of Medicine.
Kang J-E, Cirrito JR, Dong H, Csernansky JG, Holtzman DM. Acute stress increases interstitial fluid amyloid-beta via corticotropin-releasing factor and neuronal activity. Proceedings of the National Academy of Science, electronic edition, June 4, 2007.
Funding from the National Institute on Aging of the National Institutes of Health, the Alzheimer's Association, the Cure Alzheimer's Fund and Eli Lilly supported this research.
Washington University School of Medicine's full-time and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children's hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked fourth in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children's hospitals, the School of Medicine is linked to BJC HealthCare.
Contact: Jim Dryden
Washington University School of Medicine
Studies of humans and animals have suggested that stress may increase risk of Alzheimer's disease, but the new research is among the first studies to elaborate the basic biomolecular mechanisms that may underlie this increased risk.
The results build on earlier findings from coauthors John G. Csernansky, M.D., the Gregory B. Couch Professor of Psychiatry and professor of neurobiology, and Hongxin Dong, Ph.D., instructor in psychiatry. Using mice genetically modified to model human Alzheimer's disease, Csernansky and Dong showed that raising them under isolated conditions in smaller cages accelerated the deposition of brain plaques and declines in cognitive ability.
Brain plaques are believed to be a primary cause of the memory loss and other mental damage inflicted by Alzheimer's disease. They are mostly comprised of a peptide known as amyloid beta, so researchers immediately suspected that stress was increasing amyloid beta levels. But because there are other factors that can accelerate plaque build-up, they needed to test the link.
For that new test, scientists used a technique known as microdialysis to monitor amyloid beta levels in the brains of mice exposed to the same stressors: isolation and smaller cages.
"Stress remarkably elevated soluble amyloid beta levels in the spaces between brain cells," says senior author David Holtzman, M.D., the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology. "But we didn't know based on those initial experiments if it was a chronic effect or a much more immediate effect. If it was more immediate, we thought we might be able to identify some of the brain molecules involved in increasing the levels."
Lead author Jea-Eun Kang, a graduate student in the Holtzman lab, utilized a quicker way to cause stress: temporarily restrain mice from moving. Three hours of restraint led to a 30 percent increase in amyloid beta levels.
The spike in amyloid beta encouraged researchers to start looking for molecules that might be enabling this rapid change. Stress hormones produced by the adrenal gland were natural suspects. In mice, that meant corticosterone, the mouse equivalent of the human hormone cortisol. But a large dose of corticosterone didn't cause a similar rapid change in amyloid beta levels.
When they widened their search for molecules released in the mouse brain by stress, the scientists identified one called corticotropin-releasing factor (CRF), which is linked to increased levels of brain cell communication. In 2005, Holtzman, John Cirrito, Ph.D., a postdoctoral research associate in neurology and psychiatry, and colleagues showed that increased communication between brain cells also contributed to increased amyloid beta.
When they directly placed CRF in the mouse brain, amyloid beta levels rose immediately. Mice given a CRF blocker and then stressed did not display increased amyloid beta.
"There are very few known environmental risk factors for Alzheimer's disease," Holtzman notes. "Head trauma increases risk, higher education lowers it. Stress may be another environmental factor that increases risk."
Holtzman, Csernansky and their colleagues are intrigued by the possibility that drugs that block CRF or reduce anxiety may provide a new way to decrease amyloid beta and eventually delay or prevent Alzheimer's disease. Holtzman and his colleagues are also continuing to explore connections between brain cell activity and amyloid beta levels.
The studies were carried out in the Hope Center for Neurological Disorders and in conjunction with the Alzheimer's Disease Research Center, both at Washington University School of Medicine.
Kang J-E, Cirrito JR, Dong H, Csernansky JG, Holtzman DM. Acute stress increases interstitial fluid amyloid-beta via corticotropin-releasing factor and neuronal activity. Proceedings of the National Academy of Science, electronic edition, June 4, 2007.
Funding from the National Institute on Aging of the National Institutes of Health, the Alzheimer's Association, the Cure Alzheimer's Fund and Eli Lilly supported this research.
Washington University School of Medicine's full-time and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children's hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked fourth in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children's hospitals, the School of Medicine is linked to BJC HealthCare.
Contact: Jim Dryden
Washington University School of Medicine
воскресенье, 5 июня 2011 г.
Adult ADHD Significantly Increases Risk Of Common Form Of Dementia
Adults who suffer from attention-deficit and hyperactivity disorder (ADHD) are more than three times as likely to develop a common form of degenerative dementia than those without, according to research in the January issue of the European Journal of Neurology.
Researchers from Argentina confirmed the link during a study of 360 patients with degenerative dementia and 149 healthy controls, matched by age, sex and education. The dementia patients comprised 109 people with dementia with Lewy bodies (DLB) and 251 with Alzheimer's.
"Our study showed that 48 per cent of patients with DLB - the second most common cause of degenerative dementia in the elderly after Alzheimer's - had previously suffered from adult ADHD" says lead author Dr Angel Golimstok. "This was more than three times the 15 per cent rate found in both the control group and the group with Alzheimer's.
"DLB is thought to account for around ten per cent of dementia cases in older people, but it tends to be under-diagnosed because it shares some characteristics with both Alzheimer's and Parkinson's.
"It is a degenerative neurological condition that has a progressive and disabling effect on a person's mental and physical skills. Other symptoms can include recurrent and realistic visual hallucinations, fluctuations in the person's everyday abilities and spontaneous movement problems similar to those observed in Parkinson's.
"ADHD is one of the most common behaviour disorders in child and adolescent psychiatry and the problems it causes, such as difficulty paying attention, hyperactivity and doing things impulsively, can continue into adulthood.
"It is believed that the same neurotransmitter pathway problems are involved in the development of both conditions, so our research set out to test the theory that adult ADHD often precedes DLB."
The average age of the study subjects was 75 in the DLB group and 74 in the Alzheimer's and control groups. Approximately two-third of the participants were female and length of education was very similar. None of the patients were taking psychostimulant drugs.
Patient selection was restricted to people with mild to moderate dementia, measuring 14 to 26 on the mini mental status examination scale and one to two on the clinical dementia rating scale.
In the healthy controls, previous ADHD symptoms were assessed using information from the subjects and direct informants. In patients with cognitive impairment, the assessment was based on symptoms described by direct informants who had known the patient for at least 10 years and had information obtained from a close relative who knew the patient in childhood.
Two neurologists, who were unaware of the objectives of the study, were independently asked to assess all the patients for adult ADHD using:
the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), which has been produced by the American Psychiatric Association to diagnose psychiatric disorders
the validated Wender Utah Rating Scale, which is specially designed to retrospectively assess ADHD.
This produced agreement levels of 98 per cent in the DLB group, 96 per cent in the Alzheimer's group and 97.5 per cent in the control group.
A third neurologist provided their judgement in the small number of cases where the first two disagreed and a diagnosis of ADHD was recorded if two out of the three neurologists agreed. The results were then checked by a fourth neurologist fully informed about the objectives of the study.
These results provided an overall diagnosis of previous adult ADHD for the two dementia groups and the control. They also showed that impulsivity and hyperactivity, which are major symptoms of ADHD, were significantly higher in the DLB group than the Alzheimer's group and the control group (measuring 14.7, 5.9 and 6.4 respectively on the Wender Utah Rating Scale).
"We believe that our study is the first of its kind to examine the clinical association between adult ADHD symptoms and DLB and that it has established a clear link between the two conditions" says Dr Golimstok.
"Our theory is that this association can be explained by the common neurotransmitter dysfunction present in both conditions. There is clearly a common process involved in both illnesses and it appears that ADHD often develops into DLB as the patient ages."
Notes:
Previous adult attention-deficit and hyperactivity disorder symptoms and risk of dementia with Lewy bodies: a case-control study. Golimstok et al. European Journal of Neurology. 18, pp78-84. (January 2011). DOI: 10.1111/j.1468-1331.2010.03064.x
Source:
Annette Whibley
Wiley-Blackwell
Researchers from Argentina confirmed the link during a study of 360 patients with degenerative dementia and 149 healthy controls, matched by age, sex and education. The dementia patients comprised 109 people with dementia with Lewy bodies (DLB) and 251 with Alzheimer's.
"Our study showed that 48 per cent of patients with DLB - the second most common cause of degenerative dementia in the elderly after Alzheimer's - had previously suffered from adult ADHD" says lead author Dr Angel Golimstok. "This was more than three times the 15 per cent rate found in both the control group and the group with Alzheimer's.
"DLB is thought to account for around ten per cent of dementia cases in older people, but it tends to be under-diagnosed because it shares some characteristics with both Alzheimer's and Parkinson's.
"It is a degenerative neurological condition that has a progressive and disabling effect on a person's mental and physical skills. Other symptoms can include recurrent and realistic visual hallucinations, fluctuations in the person's everyday abilities and spontaneous movement problems similar to those observed in Parkinson's.
"ADHD is one of the most common behaviour disorders in child and adolescent psychiatry and the problems it causes, such as difficulty paying attention, hyperactivity and doing things impulsively, can continue into adulthood.
"It is believed that the same neurotransmitter pathway problems are involved in the development of both conditions, so our research set out to test the theory that adult ADHD often precedes DLB."
The average age of the study subjects was 75 in the DLB group and 74 in the Alzheimer's and control groups. Approximately two-third of the participants were female and length of education was very similar. None of the patients were taking psychostimulant drugs.
Patient selection was restricted to people with mild to moderate dementia, measuring 14 to 26 on the mini mental status examination scale and one to two on the clinical dementia rating scale.
In the healthy controls, previous ADHD symptoms were assessed using information from the subjects and direct informants. In patients with cognitive impairment, the assessment was based on symptoms described by direct informants who had known the patient for at least 10 years and had information obtained from a close relative who knew the patient in childhood.
Two neurologists, who were unaware of the objectives of the study, were independently asked to assess all the patients for adult ADHD using:
the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), which has been produced by the American Psychiatric Association to diagnose psychiatric disorders
the validated Wender Utah Rating Scale, which is specially designed to retrospectively assess ADHD.
This produced agreement levels of 98 per cent in the DLB group, 96 per cent in the Alzheimer's group and 97.5 per cent in the control group.
A third neurologist provided their judgement in the small number of cases where the first two disagreed and a diagnosis of ADHD was recorded if two out of the three neurologists agreed. The results were then checked by a fourth neurologist fully informed about the objectives of the study.
These results provided an overall diagnosis of previous adult ADHD for the two dementia groups and the control. They also showed that impulsivity and hyperactivity, which are major symptoms of ADHD, were significantly higher in the DLB group than the Alzheimer's group and the control group (measuring 14.7, 5.9 and 6.4 respectively on the Wender Utah Rating Scale).
"We believe that our study is the first of its kind to examine the clinical association between adult ADHD symptoms and DLB and that it has established a clear link between the two conditions" says Dr Golimstok.
"Our theory is that this association can be explained by the common neurotransmitter dysfunction present in both conditions. There is clearly a common process involved in both illnesses and it appears that ADHD often develops into DLB as the patient ages."
Notes:
Previous adult attention-deficit and hyperactivity disorder symptoms and risk of dementia with Lewy bodies: a case-control study. Golimstok et al. European Journal of Neurology. 18, pp78-84. (January 2011). DOI: 10.1111/j.1468-1331.2010.03064.x
Source:
Annette Whibley
Wiley-Blackwell
суббота, 4 июня 2011 г.
Gammaglobulin Treatment For Alzheimer's Disease To Be Tested By University Hospitals Case Medical Center
Researchers from the Memory and Cognition Center at University Hospitals Case Medical Center will begin testing an intriguing new approach to slowing down the progression of Alzheimer's Disease (AD) using Intravenous Immune Globulin (IGIV), also known as gammaglobulin. IGIV is traditionally used to treat primary immunodeficiency disorders, but is not currently approved for treating AD, which is one of the leading causes of dementia in the elderly.
Initial research in experimental models and patients suggests that immunotherapy targeting beta amyloid (the protein that forms the core of plaques in the brain) may provide a more effective way to treat AD. Antibodies that bind to beta amyloid are present in IGIV, which is made from the blood of several thousand healthy adults.
One of the hallmarks of AD pathology is an abundance of beta-amyloid deposits in the brain. While it is not yet known if beta amyloid plaques cause AD or are a byproduct of the disease, scientists are interested in finding ways to reduce the toxic effects of beta amyloid on the brain. Antibodies against beta amyloid may do so by binding to toxic forms of beta amyloid, thereby neutralizing them and/or promoting their elimination.
"We are investigating whether IGIV, which contains naturally occurring human anti-amyloid antibodies, will defend the brain of AD patients against the damaging effects of beta amyloid. If it does, giving IGIV to patients with mild to moderate Alzheimer's may potentially slow the rate of progression of the disease," says Alan Lerner, M.D., principal investigator for the study in Cleveland and director of the Memory and Cognition Center.
"In our initial studies in AD patients, IGIV provided significant cognitive benefits, improved brain metabolism and reduced beta amyloid levels in the spinal fluid," says Norman Relkin, M.D., project director and director of the Weill Cornell Alzheimer's Disease and Memory Disorders Program. In a Phase II trial at Weill Cornell, Dr. Relkin reported that participants undergoing several months of continuous IGIV therapy also demonstrated improvement in their activities of daily living. He added, "These findings, as well as IGIV's long established record of safe use for treating other diseases, provide a strong rationale for further study in AD patients on a larger scale."
The GAP (Gammaglobulin Alzheimer's Partnership) Study will examine the safety, effectiveness and tolerability of IGIV in patients with mild to moderate AD. GAP is recruiting 360 participants at 36 sites nationwide. This large Phase III clinical trial expands on earlier testing, is one of two Phase III trials and is part of the final phase in studying IGIV as a potential treatment for AD before seeking regulatory approval.
The trial is being conducted by the Alzheimer's Disease Cooperative Study (ADCS), a nationwide consortium of research centers and clinics coordinated by the University of California at San Diego and directed by Paul Aisen, M.D.
"As many as five million Americans may be afflicted now and with the numbers growing rapidly, ADCS clinical trials such as the GAP study are essential to finding new and more effective treatments for Alzheimer's disease," Aisen commented.
The ADCS is primarily supported by the National Institute on Aging (NIA), part of the National Institutes of Health. The GAP study is jointly funded by Baxter International Inc. and the NIA.
Source:
George Stamatis
University Hospitals Case Medical Center
Initial research in experimental models and patients suggests that immunotherapy targeting beta amyloid (the protein that forms the core of plaques in the brain) may provide a more effective way to treat AD. Antibodies that bind to beta amyloid are present in IGIV, which is made from the blood of several thousand healthy adults.
One of the hallmarks of AD pathology is an abundance of beta-amyloid deposits in the brain. While it is not yet known if beta amyloid plaques cause AD or are a byproduct of the disease, scientists are interested in finding ways to reduce the toxic effects of beta amyloid on the brain. Antibodies against beta amyloid may do so by binding to toxic forms of beta amyloid, thereby neutralizing them and/or promoting their elimination.
"We are investigating whether IGIV, which contains naturally occurring human anti-amyloid antibodies, will defend the brain of AD patients against the damaging effects of beta amyloid. If it does, giving IGIV to patients with mild to moderate Alzheimer's may potentially slow the rate of progression of the disease," says Alan Lerner, M.D., principal investigator for the study in Cleveland and director of the Memory and Cognition Center.
"In our initial studies in AD patients, IGIV provided significant cognitive benefits, improved brain metabolism and reduced beta amyloid levels in the spinal fluid," says Norman Relkin, M.D., project director and director of the Weill Cornell Alzheimer's Disease and Memory Disorders Program. In a Phase II trial at Weill Cornell, Dr. Relkin reported that participants undergoing several months of continuous IGIV therapy also demonstrated improvement in their activities of daily living. He added, "These findings, as well as IGIV's long established record of safe use for treating other diseases, provide a strong rationale for further study in AD patients on a larger scale."
The GAP (Gammaglobulin Alzheimer's Partnership) Study will examine the safety, effectiveness and tolerability of IGIV in patients with mild to moderate AD. GAP is recruiting 360 participants at 36 sites nationwide. This large Phase III clinical trial expands on earlier testing, is one of two Phase III trials and is part of the final phase in studying IGIV as a potential treatment for AD before seeking regulatory approval.
The trial is being conducted by the Alzheimer's Disease Cooperative Study (ADCS), a nationwide consortium of research centers and clinics coordinated by the University of California at San Diego and directed by Paul Aisen, M.D.
"As many as five million Americans may be afflicted now and with the numbers growing rapidly, ADCS clinical trials such as the GAP study are essential to finding new and more effective treatments for Alzheimer's disease," Aisen commented.
The ADCS is primarily supported by the National Institute on Aging (NIA), part of the National Institutes of Health. The GAP study is jointly funded by Baxter International Inc. and the NIA.
Source:
George Stamatis
University Hospitals Case Medical Center
Yin And Yang -- Balance Could Play Key Role In Progression Of Alzheimer's Disease
Researchers at Rensselaer Polytechnic Institute are challenging current thinking on the causes and prevention of Alzheimer's disease, offering a new hypothesis that could be the key to preventing this form of dementia. The researchers have found that a specific imbalance between two peptides may be the cause of the fatal neurological disease that affects more than five million people in the United States.
"We have found that two peptides, AB42 and AB40, must be in balance for normal function," said Chunyu Wang, lead researcher and assistant professor of biology at Rensselaer. "They are like the Yin and Yang in Taiji, an ancient Chinese philosophy. When the peptides are produced in the correct proportions, the brain is healthy; but when that delicate balance is changed, pathological changes will occur in the brain and the person's memories become hazy, leading to eventual dementia."
Wang expects that this imbalance could be the main factor in the progression of Alzheimer's disease. If correct, the addition of AB40 may stop the disease's development. Wang notes that further research is needed, but his preliminary results challenge the current mode of thinking about how these peptides contribute to the progression of the disease.
The research will be published in the June edition of the Journal of Molecular Biology.
Peptides are formed by the linking of different amino acids. The two peptides that Wang investigated were both Amyloid B-peptides (AB) - specifically those composed of 40 and 42 amino acids, called AB40 and AB42. These two peptides have been previously found in deposits, called senile plaques or amyloid plaques, in brains afflicted with Alzheimer-s disease. These plaques, mainly composed of AB42 fibrils, are a hallmark of Alzheimer-s disease.
Prior research has uncovered that increased levels of AB42 become toxic to brain cells when individual molecules of AB42, or monomers, combine to form oligomer or fibril chains. This process is called aggregation. But the role of AB40, which is also found in senile plaques and generated from the same protein as AB42, has not been clearly established. Wang set out to determine what role this peptide played in the generation of AB42 aggregates.
Wang used the advanced Nuclear Magnetic Resonance (NMR) machines within Rensselaer-s Center for Biotechnology and Interdisciplinary Studies to monitor the formation of harmful AB42 fibrils in the presence of different levels of AB40. NMR is an extremely powerful research tool capable of characterizing the three-dimensional structure and dynamics of biological molecules.
Using NMR data, Wang found that as AB40 levels increased, the aggregation of AB42 fibrils sharply decreased, protecting benign AB42 monomers.
"We have found that the ratio of AB40 to AB42 plays a key role in AB42 aggregation," Wang said. "The current mode of thinking in Alzheimer-s emphasizes the toxic role of AB42 but neglects the protective role of AB40. Combined with previous work on AB40 by many other groups, our data suggest that AB40 has an equally important, protective role in Alzheimer-s. Thus AB42, the bad molecule, and AB40, the good molecule, are like Yin and Yang in Taiji. The brain can only function normally when they are in balance."
Wang-s experiments show that when there is 15 times more AB40 than AB42, the formation of AB42 fibrils is almost completely stopped. "This means that the introduction of AB40 to tip the peptide balance toward AB40 could potentially halt or slow down the progression of the Alzheimer-s in the human brain," Wang said.
Wang plans to continue investigating how AB40 halts the formation of AB42 fibrils, and he already sees vast implications for this change in thinking about the progression of the disease.
"This has the potential to become a simple therapy to prevent the formation of toxic AB42 species," he said. "I plan to continue my research on the role of AB40 and hope that we can test this theory on human neurons, animal models, and someday in clinical trials. One critical advantage of using AB40 for the prevention or therapy for Alzheimer-s is that AB40 is already known to be largely free of side effects at near physiological concentration."
The research was funded by the Alzheimer-s Association and a New York State Office of Science, Technology, and Academic Research (NYSTAR) James D. Watson Investigator Program Award.
Rensselaer graduate student Yilin Yan worked with Wang on the research project.
About Rensselaer
Rensselaer Polytechnic Institute, founded in 1824, is the nation-s oldest technological university. The university offers bachelor-s, master-s, and doctoral degrees in engineering, the sciences, information technology, architecture, management, and the humanities and social sciences. Institute programs serve undergraduates, graduate students, and working professionals around the world. Rensselaer faculty are known for pre-eminence in research conducted in a wide range of fields, with particular emphasis in biotechnology, nanotechnology, information technology, and the media arts and technology. The Institute is well known for its success in the transfer of technology from the laboratory to the marketplace so that new discoveries and inventions benefit human life, protect the environment, and strengthen economic development.
Contact: Gabrielle DeMarco
Rensselaer Polytechnic Institute
"We have found that two peptides, AB42 and AB40, must be in balance for normal function," said Chunyu Wang, lead researcher and assistant professor of biology at Rensselaer. "They are like the Yin and Yang in Taiji, an ancient Chinese philosophy. When the peptides are produced in the correct proportions, the brain is healthy; but when that delicate balance is changed, pathological changes will occur in the brain and the person's memories become hazy, leading to eventual dementia."
Wang expects that this imbalance could be the main factor in the progression of Alzheimer's disease. If correct, the addition of AB40 may stop the disease's development. Wang notes that further research is needed, but his preliminary results challenge the current mode of thinking about how these peptides contribute to the progression of the disease.
The research will be published in the June edition of the Journal of Molecular Biology.
Peptides are formed by the linking of different amino acids. The two peptides that Wang investigated were both Amyloid B-peptides (AB) - specifically those composed of 40 and 42 amino acids, called AB40 and AB42. These two peptides have been previously found in deposits, called senile plaques or amyloid plaques, in brains afflicted with Alzheimer-s disease. These plaques, mainly composed of AB42 fibrils, are a hallmark of Alzheimer-s disease.
Prior research has uncovered that increased levels of AB42 become toxic to brain cells when individual molecules of AB42, or monomers, combine to form oligomer or fibril chains. This process is called aggregation. But the role of AB40, which is also found in senile plaques and generated from the same protein as AB42, has not been clearly established. Wang set out to determine what role this peptide played in the generation of AB42 aggregates.
Wang used the advanced Nuclear Magnetic Resonance (NMR) machines within Rensselaer-s Center for Biotechnology and Interdisciplinary Studies to monitor the formation of harmful AB42 fibrils in the presence of different levels of AB40. NMR is an extremely powerful research tool capable of characterizing the three-dimensional structure and dynamics of biological molecules.
Using NMR data, Wang found that as AB40 levels increased, the aggregation of AB42 fibrils sharply decreased, protecting benign AB42 monomers.
"We have found that the ratio of AB40 to AB42 plays a key role in AB42 aggregation," Wang said. "The current mode of thinking in Alzheimer-s emphasizes the toxic role of AB42 but neglects the protective role of AB40. Combined with previous work on AB40 by many other groups, our data suggest that AB40 has an equally important, protective role in Alzheimer-s. Thus AB42, the bad molecule, and AB40, the good molecule, are like Yin and Yang in Taiji. The brain can only function normally when they are in balance."
Wang-s experiments show that when there is 15 times more AB40 than AB42, the formation of AB42 fibrils is almost completely stopped. "This means that the introduction of AB40 to tip the peptide balance toward AB40 could potentially halt or slow down the progression of the Alzheimer-s in the human brain," Wang said.
Wang plans to continue investigating how AB40 halts the formation of AB42 fibrils, and he already sees vast implications for this change in thinking about the progression of the disease.
"This has the potential to become a simple therapy to prevent the formation of toxic AB42 species," he said. "I plan to continue my research on the role of AB40 and hope that we can test this theory on human neurons, animal models, and someday in clinical trials. One critical advantage of using AB40 for the prevention or therapy for Alzheimer-s is that AB40 is already known to be largely free of side effects at near physiological concentration."
The research was funded by the Alzheimer-s Association and a New York State Office of Science, Technology, and Academic Research (NYSTAR) James D. Watson Investigator Program Award.
Rensselaer graduate student Yilin Yan worked with Wang on the research project.
About Rensselaer
Rensselaer Polytechnic Institute, founded in 1824, is the nation-s oldest technological university. The university offers bachelor-s, master-s, and doctoral degrees in engineering, the sciences, information technology, architecture, management, and the humanities and social sciences. Institute programs serve undergraduates, graduate students, and working professionals around the world. Rensselaer faculty are known for pre-eminence in research conducted in a wide range of fields, with particular emphasis in biotechnology, nanotechnology, information technology, and the media arts and technology. The Institute is well known for its success in the transfer of technology from the laboratory to the marketplace so that new discoveries and inventions benefit human life, protect the environment, and strengthen economic development.
Contact: Gabrielle DeMarco
Rensselaer Polytechnic Institute
пятница, 3 июня 2011 г.
Common Medication Associated With Cognitive Decline In Elderly
A study published in Journal of the American Geriatrics Society suggested that the use of certain medications in elderly populations may be associated with cognitive decline. The study examined the effects of exposure to anticholinergic medications, a type of drug used to treat a variety of disorders that include respiratory and gastrointestinal problems, on over 500 relatively healthy men aged 65 years or older with high blood pressure.
Older people often take several drugs to treat multiple health conditions. As some of these drugs also have properties that affect neurotransmitters in the brain that are important to overall brain function, the researchers examined the total effects of all medications taken by the patients, both prescription and over-the-counter, that were believed to affect the function of a particular neurotransmitter, acetylcholine.
The findings show that chronic use of medications with anticholinergic properties may have detrimental effects on memory and the ability to perform daily living tasks, such as shopping and managing finances. Participants showed deficits in both memory and daily function when they took these medications over the course of a year. The degree of memory difficulty and impairment in daily living tasks also increased proportionally to the total amount of drug exposure, based on a rating scale the authors developed to assess anticholinergicity of the drugs.
According to study co-author Dr. Ling Han of the Yale University Department of Internal Medicine, elderly patients may be more vulnerable to these types of medications due to neurological and pharmacokinetical changes related to aging..
"This study extends our previous findings on acute cognitive impairment following recent anticholinergic exposure in older medical inpatients," says Han. "Prescribing for older adults who take multiple prescription and over-the-counter medications requires careful attention to minimize the risk of potential harms of the drugs while maximizing their health benefits."
The Journal of the American Geriatrics Society is a comprehensive and reliable source of monthly research and information about common diseases and disorders of older adults. For more information, please visit blackwellpublishing/jgs.
Wiley-Blackwell was formed in February 2007 as a result of the acquisition of Blackwell Publishing Ltd. by John Wiley & Sons, Inc., and its merger with Wiley's Scientific, Technical, and Medical business. Together, the companies have created a global publishing business with deep strength in every major academic and professional field. Wiley-Blackwell publishes approximately 1,400 scholarly peer-reviewed journals and an extensive collection of books with global appeal. For more information on Wiley-Blackwell, please visit wiley-blackwell or interscience.wiley.
Wiley-Blackwell
Older people often take several drugs to treat multiple health conditions. As some of these drugs also have properties that affect neurotransmitters in the brain that are important to overall brain function, the researchers examined the total effects of all medications taken by the patients, both prescription and over-the-counter, that were believed to affect the function of a particular neurotransmitter, acetylcholine.
The findings show that chronic use of medications with anticholinergic properties may have detrimental effects on memory and the ability to perform daily living tasks, such as shopping and managing finances. Participants showed deficits in both memory and daily function when they took these medications over the course of a year. The degree of memory difficulty and impairment in daily living tasks also increased proportionally to the total amount of drug exposure, based on a rating scale the authors developed to assess anticholinergicity of the drugs.
According to study co-author Dr. Ling Han of the Yale University Department of Internal Medicine, elderly patients may be more vulnerable to these types of medications due to neurological and pharmacokinetical changes related to aging..
"This study extends our previous findings on acute cognitive impairment following recent anticholinergic exposure in older medical inpatients," says Han. "Prescribing for older adults who take multiple prescription and over-the-counter medications requires careful attention to minimize the risk of potential harms of the drugs while maximizing their health benefits."
The Journal of the American Geriatrics Society is a comprehensive and reliable source of monthly research and information about common diseases and disorders of older adults. For more information, please visit blackwellpublishing/jgs.
Wiley-Blackwell was formed in February 2007 as a result of the acquisition of Blackwell Publishing Ltd. by John Wiley & Sons, Inc., and its merger with Wiley's Scientific, Technical, and Medical business. Together, the companies have created a global publishing business with deep strength in every major academic and professional field. Wiley-Blackwell publishes approximately 1,400 scholarly peer-reviewed journals and an extensive collection of books with global appeal. For more information on Wiley-Blackwell, please visit wiley-blackwell or interscience.wiley.
Wiley-Blackwell
четверг, 2 июня 2011 г.
Alzheimer's - more sensitive tests for predicting
Two recent studies may help clinicians and researchers better predict and understand dementia of the Alzheimer's type early in its history. Both studies appear in the September issue of Neuropsychology, which is published by the American Psychological Association (APA). Psychologists focus on early detection in part because current medications are useful only when given very early in the course of the disease.
In the first study, psychologists Pauline Spaan, PhD, and Jeroen Raaijmakers, PhD, from the University of Amsterdam in collaboration with neurologist Cees Jonker, MD, PhD, from the Vrije Universiteit in Amsterdam analyzed the data on 119 participants in the Longitudinal Aging Study Amsterdam, a large, population-based study of older people. The researchers visited older people in their homes and gave them memory tests loaded on laptop computers. Two years later, they compared the test scores of people who went on to develop Alzheimer's with the scores of those who stayed healthy.
The researchers analyzed memory components that included episodic (what happened; what did you hear or read); semantic (vocabulary, facts); and implicit (learning without awareness of learning, "priming"). Three tests were very good at predicting who would develop Alzheimer's by two years later. Participants for whom "priming" information didn't aid memory or whose learning wasn't aided by semantic knowledge -- were significantly more likely to develop Alzheimer's.
The strongly predictive tests were, in order of their power, a Paired-Associate Learning Test, which cued participants to recall five semantically related and five semantically unrelated pairs of words; and a Perceptual Identification Task, which measured how fast participants read aloud words briefly presented on a computer screen. To test implicit memory, experimenters repeated some words to see whether "priming" took place, which would help participants read those words faster. The researchers also gave a Visual Association Test, which cued participants to recall six line drawings of common objects that had been presented earlier in an illogical interaction with another object or cue.
On the word-pair memory test, people destined to develop Alzheimer's disease didn't do any better when words were related than when they weren't. The authors think these participants may already have lost key knowledge of word attributes that normally help people to more easily remember words by means of their semantic associations. Sometimes, at-risk participants reported a vague sense that one word had something to do with another, but they couldn't say exactly what. The authors suspect they couldn't encode the word pairs at a sufficiently deep level because they'd lost the semantic knowledge that stays intact in normally aging people.
On the word-reading test, word repetition (to measure priming) didn't help high-risk participants to perform better, a sign that they weren't learning implicitly as well as the people who would stay healthy. The authors speculate that because high-risk participants drew less benefit from word repetition, they did not encode the words properly.
These tests remained sensitive to the risk of developing Alzheimer's disease even within a more homogeneous subset of the broader study population, people with mild cognitive impairment. For both the whole and subset study groups, these tests predicted future Alzheimer's diagnosis as much as two years early.
Equally important, the popular Mini Mental Status Exam (MMSE), a test mainly sensitive to episodic memory, was not as good a predictor. Although clinicians use it for quick, easy-to-administer screening, the authors found it to be "less predictive [than the tests sensitive to semantic and implicit memory]. These [MMSE and other purely episodic memory] tasks may only differentiate between pathological and normal aging when dementia has progressed to a more advanced stage."
In the second Neuropsychology study, an established psychological test has picked up early-warning signs of Alzheimer's disease. A new study in the September issue of Neuropsychology explains how the dichotic listening task, which measures how well people process information when they hear one thing in the left ear and another in the right ear, confirms that very early in the disease, people have problems with selective attention. This problem, although not as obvious as memory loss, may also explain why early-stage patients start to struggle with everyday tasks that call for processing a lot of information - such as driving.
At the Alzheimer's Disease Research Center at Washington University in St. Louis, Janet Duchek, PhD and David Balota, PhD, studied 94 participants in their early to mid-70s with healthy, very mild, or mild dementia of the Alzheimer's type. They looked for information-processing breakdowns suspected to happen early in the disease, before the appearance of language and visuospatial problems. Problems with attention, the authors say, could "underlie the difficulty with daily activities often seen in the early stages of the disease."
Duchek and Balota used a dichotic listening task, presenting information to participants via headphones. One stream of information - computer-generated speech naming three digits (such as 4, 3, 1) - went to the left ear; a different stream (such as 9, 2, 5) went to the right ear. The psychologists measured how well participants recalled the digits presented to each ear.
As predicted, people with early dementia remembered the digits presented to the right ear far better than they recalled the digits presented to the left ear. When the researchers controlled for overall recall performance, the mild dementia group recalled 21.7% more information from their right ear vs. left ear, and even the very mildly affected group recalled 11.3% more from the right ear. The control participants only recalled 5.8% more from the right vs. left.
Clearly, people with mild or very mild Alzheimer's relied more heavily on the default pathway for processing information, which for language would be the left side of the brain. In other words, these patients had a harder time switching their attention and reporting what they heard in the left ear, which sent information to the right half of the brain.
The right-ear advantage increased with dementia severity. People farther along in the disease relied even more on the dominant left-side channel; in other words, they found it even harder to override the usual path to process what went through the left ear to the right brain. The study confirms that attentional processing, like other cognitive processes, is affected early in Alzheimer's disease. Poor attentional controls can leave people falling back on familiar, "pre-programmed" information pathways. Write the authors, "One can speculate about the importance of attentional control in everyday tasks, such as driving." Their speculation is supported by prior findings that performance on dichotic listening predicts accident rates in commercial bus drivers.
Article 1: "Early Assessment of Dementia: The Contribution of Different Memory Components," Pauline E.J. Spaan, PhD, and Jeroen G.W. Raaijmakers, PhD, University of Amsterdam, and Cees Jonker, PhD, MD, Vrije Universiteit; Neuropsychology, 2005, Vol. 19, No. 5.
Article 2: "Failure to Control Prepotent Pathways in Early Stage Dementia of the Alzheimer's Type: Evidence from Dichotic Listening," Janet M. Duchek, PhD, and David A. Balota, PhD, Washington University; Neuropsychology, 2005, Vol. 19, No. 5.
(Full text of the both articles is available from the APA Public Affairs Office click here for Article 1
and
Article 2
The American Psychological Association (APA), in Washington, DC, is the largest scientific and professional organization representing psychology in the United States and is the world's largest association of psychologists. APA's membership includes more than 150,000 researchers, educators, clinicians, consultants and students. Through its divisions in 53 subfields of psychology and affiliations with 60 state, territorial and Canadian provincial associations, APA works to advance psychology as a science, as a profession and as a means of promoting human welfare.
Pam Willenz
pwillenzapa
American Psychological Association
apa
In the first study, psychologists Pauline Spaan, PhD, and Jeroen Raaijmakers, PhD, from the University of Amsterdam in collaboration with neurologist Cees Jonker, MD, PhD, from the Vrije Universiteit in Amsterdam analyzed the data on 119 participants in the Longitudinal Aging Study Amsterdam, a large, population-based study of older people. The researchers visited older people in their homes and gave them memory tests loaded on laptop computers. Two years later, they compared the test scores of people who went on to develop Alzheimer's with the scores of those who stayed healthy.
The researchers analyzed memory components that included episodic (what happened; what did you hear or read); semantic (vocabulary, facts); and implicit (learning without awareness of learning, "priming"). Three tests were very good at predicting who would develop Alzheimer's by two years later. Participants for whom "priming" information didn't aid memory or whose learning wasn't aided by semantic knowledge -- were significantly more likely to develop Alzheimer's.
The strongly predictive tests were, in order of their power, a Paired-Associate Learning Test, which cued participants to recall five semantically related and five semantically unrelated pairs of words; and a Perceptual Identification Task, which measured how fast participants read aloud words briefly presented on a computer screen. To test implicit memory, experimenters repeated some words to see whether "priming" took place, which would help participants read those words faster. The researchers also gave a Visual Association Test, which cued participants to recall six line drawings of common objects that had been presented earlier in an illogical interaction with another object or cue.
On the word-pair memory test, people destined to develop Alzheimer's disease didn't do any better when words were related than when they weren't. The authors think these participants may already have lost key knowledge of word attributes that normally help people to more easily remember words by means of their semantic associations. Sometimes, at-risk participants reported a vague sense that one word had something to do with another, but they couldn't say exactly what. The authors suspect they couldn't encode the word pairs at a sufficiently deep level because they'd lost the semantic knowledge that stays intact in normally aging people.
On the word-reading test, word repetition (to measure priming) didn't help high-risk participants to perform better, a sign that they weren't learning implicitly as well as the people who would stay healthy. The authors speculate that because high-risk participants drew less benefit from word repetition, they did not encode the words properly.
These tests remained sensitive to the risk of developing Alzheimer's disease even within a more homogeneous subset of the broader study population, people with mild cognitive impairment. For both the whole and subset study groups, these tests predicted future Alzheimer's diagnosis as much as two years early.
Equally important, the popular Mini Mental Status Exam (MMSE), a test mainly sensitive to episodic memory, was not as good a predictor. Although clinicians use it for quick, easy-to-administer screening, the authors found it to be "less predictive [than the tests sensitive to semantic and implicit memory]. These [MMSE and other purely episodic memory] tasks may only differentiate between pathological and normal aging when dementia has progressed to a more advanced stage."
In the second Neuropsychology study, an established psychological test has picked up early-warning signs of Alzheimer's disease. A new study in the September issue of Neuropsychology explains how the dichotic listening task, which measures how well people process information when they hear one thing in the left ear and another in the right ear, confirms that very early in the disease, people have problems with selective attention. This problem, although not as obvious as memory loss, may also explain why early-stage patients start to struggle with everyday tasks that call for processing a lot of information - such as driving.
At the Alzheimer's Disease Research Center at Washington University in St. Louis, Janet Duchek, PhD and David Balota, PhD, studied 94 participants in their early to mid-70s with healthy, very mild, or mild dementia of the Alzheimer's type. They looked for information-processing breakdowns suspected to happen early in the disease, before the appearance of language and visuospatial problems. Problems with attention, the authors say, could "underlie the difficulty with daily activities often seen in the early stages of the disease."
Duchek and Balota used a dichotic listening task, presenting information to participants via headphones. One stream of information - computer-generated speech naming three digits (such as 4, 3, 1) - went to the left ear; a different stream (such as 9, 2, 5) went to the right ear. The psychologists measured how well participants recalled the digits presented to each ear.
As predicted, people with early dementia remembered the digits presented to the right ear far better than they recalled the digits presented to the left ear. When the researchers controlled for overall recall performance, the mild dementia group recalled 21.7% more information from their right ear vs. left ear, and even the very mildly affected group recalled 11.3% more from the right ear. The control participants only recalled 5.8% more from the right vs. left.
Clearly, people with mild or very mild Alzheimer's relied more heavily on the default pathway for processing information, which for language would be the left side of the brain. In other words, these patients had a harder time switching their attention and reporting what they heard in the left ear, which sent information to the right half of the brain.
The right-ear advantage increased with dementia severity. People farther along in the disease relied even more on the dominant left-side channel; in other words, they found it even harder to override the usual path to process what went through the left ear to the right brain. The study confirms that attentional processing, like other cognitive processes, is affected early in Alzheimer's disease. Poor attentional controls can leave people falling back on familiar, "pre-programmed" information pathways. Write the authors, "One can speculate about the importance of attentional control in everyday tasks, such as driving." Their speculation is supported by prior findings that performance on dichotic listening predicts accident rates in commercial bus drivers.
Article 1: "Early Assessment of Dementia: The Contribution of Different Memory Components," Pauline E.J. Spaan, PhD, and Jeroen G.W. Raaijmakers, PhD, University of Amsterdam, and Cees Jonker, PhD, MD, Vrije Universiteit; Neuropsychology, 2005, Vol. 19, No. 5.
Article 2: "Failure to Control Prepotent Pathways in Early Stage Dementia of the Alzheimer's Type: Evidence from Dichotic Listening," Janet M. Duchek, PhD, and David A. Balota, PhD, Washington University; Neuropsychology, 2005, Vol. 19, No. 5.
(Full text of the both articles is available from the APA Public Affairs Office click here for Article 1
and
Article 2
The American Psychological Association (APA), in Washington, DC, is the largest scientific and professional organization representing psychology in the United States and is the world's largest association of psychologists. APA's membership includes more than 150,000 researchers, educators, clinicians, consultants and students. Through its divisions in 53 subfields of psychology and affiliations with 60 state, territorial and Canadian provincial associations, APA works to advance psychology as a science, as a profession and as a means of promoting human welfare.
Pam Willenz
pwillenzapa
American Psychological Association
apa
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