A bizarre disease that caused sufferers to fall into a deep 'sleep' while still being aware
of their surroundings can offer us insight into the nature of Parkinson's disease.
Dr Paul Foley from Neuroscience Research Australia says the pandemic of encephalitis
lethargica, which swept the world in the 1920s, caused Parkinson's-like symptoms in
many sufferers, most of whom were less than 30 years old.
"While we don't know for sure what caused encephalitis lethargica, there is strong
evidence that it was a virus that ultimately caused neurological symptoms to appear
many years after the initial infection," says Dr Foley.
"We can use this as a model to investigate the notion that there may be an
infectious involvement in other brain diseases, such as Parkinson's disease, and
even Alzheimer's disease and multiple sclerosis," he says.
Encephalitis lethargica had two distinct phases. During the first, acute phase, victims
seemed to fall asleep, but often maintained an awareness of their environment.
"They would close their eyes, and just didn't have the will power to move themselves,"
says Dr Foley. As many as one third of sufferers died during this initial phase.
In the second, chronic phase, which often commenced after a healthy interval of many
years, most victims developed incurable neurological symptoms resembling Parkinson's
disease. People in this stage were depicted in Oliver Sacks' book, 'Awakenings'.
Dr Foley says his research indicates that around 30% of those who developed chronic
symptoms did not experience any acute phase symptoms.
"This suggests that it is possible an infection can have long term consequences for
brain function, even where the initial infection is mild or even negligible," he says.
Dr Foley says that encephalitis lethargica can help us investigate other infections that
cause neurological symptoms after a long lag time, and can possibly help us
understand the cause of some brain diseases.
"The idea of an infectious involvement in diseases like schizophrenia and Parkinson's
disease is controversial today, just as it was in the 1920s," he says. "But by the end of
the 1920s, researchers had built up evidence with regards to encephalitis lethargica to
show an infection can have serious psychiatric and neurological outcomes."
"I'm hoping that putting these facts out there may help researchers piece together the
puzzle with regards to other brain diseases," says Dr Foley.
Dr Foley is currently completing a book on encephalitis lethargica, and will be giving a
talk at the Australian Museum on Tuesday, 29th of March 2011, at 7pm.
Source:
Neuroscience Research Australia (NeuRA)
вторник, 31 мая 2011 г.
понедельник, 30 мая 2011 г.
More Education, Less Dementia Risk
A team of researchers from the UK and Finland has discovered why people who stay in education longer have a lower risk of developing dementia - a question that has puzzled scientists for the past decade.
Examining the brains of 872 people who had been part of three large ageing studies, and who before their deaths had completed questionnaires about their education, the researchers found that more education makes people better able to cope with changes in the brain associated with dementia.
Over the past decade, studies on dementia have consistently showed that the more time you spend in education, the lower your risk of dementia. For each additional year of education there is an 11% decrease in risk of developing dementia, this study reports.
However, these studies have been unable to determine whether or not education - which is linked to higher socioeconomic status and healthier lifestyles - protects the brain against dementia.
This is not the case, the new study lead by Professor Carol Brayne of the University of Cambridge has found. Instead, the study shows people with different levels of education have similar brain pathology but that those with more education are better able to compensate for the effects of dementia.
According to co-author Dr Hannah Keage of the University of Cambridge: "Previous research has shown that there is not a one-to-one relationship between being diagnosed with dementia during life and changes seen in the brain at death. One person may show lots of pathology in their brain while another shows very little, yet both may have had dementia. Our study shows education in early life appears to enable some people to cope with a lot of changes in their brain before showing dementia symptoms."
Compared with previous research, this study was able to answer the question because of its large size and statistical power.
The researchers used data from the EClipSE collaboration, which combines the three European population-based longitudinal studies of ageing (the Medical Research Council Cognitive Function and Ageing Study, the Cambridge City Over-75s Cohort Study and Vantaa 85+, a Finnish study).
The studies have assessed participants for up to 20 years and are three of only six such studies in the world.
The results have important implications for public health at a time when populations in many countries are ageing.
"Education is known to be good for population health and equity. This study provides strong support for investment in early life factors which should have an impact on society and the whole lifespan. This is hugely relevant to policy decisions about the importance of resource allocation between health and education," says Professor Brayne.
The results are published today in the journal Brain. The study was funded by the BUPA Foundation, the European Union and the Medical Research Council.
The paper:
Carol Brayne et al, 'Education, the brain and dementia: neuroprotection or compensation' is published in Brain on 26 July 2010.
Source:
Becky Allen
University of Cambridge
Examining the brains of 872 people who had been part of three large ageing studies, and who before their deaths had completed questionnaires about their education, the researchers found that more education makes people better able to cope with changes in the brain associated with dementia.
Over the past decade, studies on dementia have consistently showed that the more time you spend in education, the lower your risk of dementia. For each additional year of education there is an 11% decrease in risk of developing dementia, this study reports.
However, these studies have been unable to determine whether or not education - which is linked to higher socioeconomic status and healthier lifestyles - protects the brain against dementia.
This is not the case, the new study lead by Professor Carol Brayne of the University of Cambridge has found. Instead, the study shows people with different levels of education have similar brain pathology but that those with more education are better able to compensate for the effects of dementia.
According to co-author Dr Hannah Keage of the University of Cambridge: "Previous research has shown that there is not a one-to-one relationship between being diagnosed with dementia during life and changes seen in the brain at death. One person may show lots of pathology in their brain while another shows very little, yet both may have had dementia. Our study shows education in early life appears to enable some people to cope with a lot of changes in their brain before showing dementia symptoms."
Compared with previous research, this study was able to answer the question because of its large size and statistical power.
The researchers used data from the EClipSE collaboration, which combines the three European population-based longitudinal studies of ageing (the Medical Research Council Cognitive Function and Ageing Study, the Cambridge City Over-75s Cohort Study and Vantaa 85+, a Finnish study).
The studies have assessed participants for up to 20 years and are three of only six such studies in the world.
The results have important implications for public health at a time when populations in many countries are ageing.
"Education is known to be good for population health and equity. This study provides strong support for investment in early life factors which should have an impact on society and the whole lifespan. This is hugely relevant to policy decisions about the importance of resource allocation between health and education," says Professor Brayne.
The results are published today in the journal Brain. The study was funded by the BUPA Foundation, the European Union and the Medical Research Council.
The paper:
Carol Brayne et al, 'Education, the brain and dementia: neuroprotection or compensation' is published in Brain on 26 July 2010.
Source:
Becky Allen
University of Cambridge
воскресенье, 29 мая 2011 г.
Alzheimer's Society's Response To The General Medical Council's 'Tomorrow's Doctors' Guidance
The General Medical Council will this week publish its latest 'Tomorrow's Doctors' guidance calling for a more 'hands on' approach to medical training.
The review says medical students should be able to carry out a range of skills including filling out a prescription form before they leave university.
It follows a survey of 2,400 medical students and junior doctors last year which found that three quarters felt they had put patients at risk because they had not been trained to prescribe drugs properly.
'It is vitally important that hospital staff who prescribe drugs are properly trained and confident to do this. Alzheimer's Society welcomes the news that the General Medical Council is addressing this in its new standards for 'tomorrow's doctors'.
'We estimate around 100,000 people with dementia are inappropriately prescribed antipsychotics at any one time. These drugs have limited benefits for people with dementia, can cause serious side effects and increase the risk of death. Better training is needed to inform staff about these dangers and to equip them to deal with challenging behaviour in other ways.
'The government is also reviewing the use of antipsychotic drugs. This is a crucial opportunity to address this serious issue and must be published as soon as possible.'
Neil Hunt
Chief Executive
Alzheimer's Society
The review says medical students should be able to carry out a range of skills including filling out a prescription form before they leave university.
It follows a survey of 2,400 medical students and junior doctors last year which found that three quarters felt they had put patients at risk because they had not been trained to prescribe drugs properly.
'It is vitally important that hospital staff who prescribe drugs are properly trained and confident to do this. Alzheimer's Society welcomes the news that the General Medical Council is addressing this in its new standards for 'tomorrow's doctors'.
'We estimate around 100,000 people with dementia are inappropriately prescribed antipsychotics at any one time. These drugs have limited benefits for people with dementia, can cause serious side effects and increase the risk of death. Better training is needed to inform staff about these dangers and to equip them to deal with challenging behaviour in other ways.
'The government is also reviewing the use of antipsychotic drugs. This is a crucial opportunity to address this serious issue and must be published as soon as possible.'
Neil Hunt
Chief Executive
Alzheimer's Society
Alzheimer's Society Comment On New Research Showing Antipsychotics Double Risk Of Stroke In People With Dementia, Published In The BMJ
This comprehensive study highlights the detrimental affect all types of antipsychotics have on people with dementia.
It confirms previous research that these drugs vastly increase risk of stroke and death.
Care home staff need specialist dementia training to effectively care for people with dementia. Alzheimer's Society research shows that specialist training could reduce antipsychotic use by 50% and save the UK ??35 million a year, if it was mandatory.
The over-prescription of antipsychotics is a serious breach of human rights, these drugs should only be a last resort. The forthcoming National Dementia Strategy is a crucial opportunity stop this dangerous over-prescription and we look forward to its launch in the autumn.
Neil Hunt
Chief Executive
Alzheimer's Society
Notes
Spokespeople available: please contact the press office on 0207 423 3595. Information and facts on dementia available on request.
- Over 70% of people with dementia experience challenging behavior at some point during illness. More often than not this is an expression of unmet need, not a symptom of dementia.
- 1 in 3 people over 65 will die with dementia.
- 700,000 people in the UK have a form of dementia, more than half have Alzheimer's disease. In less than 20 years nearly a million people will be living with dementia. This will soar to 1.7 million people by 2051. 1 in 6 people over 80 have dementia.
- Alzheimer's Society campaigns for and champions the rights of people living with dementia and the millions who care for them. Alzheimer's Society works in England, Wales and Northern Ireland.
- As a charity, Alzheimer's Society needs to raise money to care for people today and to find a cure for tomorrow.
Alzheimer's Society
It confirms previous research that these drugs vastly increase risk of stroke and death.
Care home staff need specialist dementia training to effectively care for people with dementia. Alzheimer's Society research shows that specialist training could reduce antipsychotic use by 50% and save the UK ??35 million a year, if it was mandatory.
The over-prescription of antipsychotics is a serious breach of human rights, these drugs should only be a last resort. The forthcoming National Dementia Strategy is a crucial opportunity stop this dangerous over-prescription and we look forward to its launch in the autumn.
Neil Hunt
Chief Executive
Alzheimer's Society
Notes
Spokespeople available: please contact the press office on 0207 423 3595. Information and facts on dementia available on request.
- Over 70% of people with dementia experience challenging behavior at some point during illness. More often than not this is an expression of unmet need, not a symptom of dementia.
- 1 in 3 people over 65 will die with dementia.
- 700,000 people in the UK have a form of dementia, more than half have Alzheimer's disease. In less than 20 years nearly a million people will be living with dementia. This will soar to 1.7 million people by 2051. 1 in 6 people over 80 have dementia.
- Alzheimer's Society campaigns for and champions the rights of people living with dementia and the millions who care for them. Alzheimer's Society works in England, Wales and Northern Ireland.
- As a charity, Alzheimer's Society needs to raise money to care for people today and to find a cure for tomorrow.
Alzheimer's Society
суббота, 28 мая 2011 г.
Universit?© De Montr?©al Research On Semantic Memory
Famous mugs do more than prompt us into buying magazines, according to new Universit?© de Montr?©al research. In the December issue of the Canadian Journal on Aging, a team of scientists explain how the ability to name famous faces or access biographical knowledge about celebrities holds clues that could help in early Alzheimer's detection.
"Semantic memory for people - triggered through name, voice or face - is knowledge we have gathered over the course of our lifetime on a person which enables us to recognize this person," says senior author Sven Joubert, a professor at the Universit?© de Montr?©al Department of Psychology and a researcher at the Centre de recherche de l'Institut universitaire de g?©riatrie de Montr?©al.
The goal of semantic study was to determine whether the ability to recall names of famous people decreases with age, since the condition named anomia ranks among the most common complaints from the elderly. To investigate, Dr. Joubert collaborated with first author Roxane Langlois to divide 117 healthy elderly, aged 60 to 91 years old, into three groups who were submitted to two semantic memory tests.
In a first test, subjects were shown the faces of 30 famous people such as Albert Einstein, C?©line Dion, Catherine Deneuve, Pierre Elliott Trudeau, Wayne Gretzky. They were first asked to name these famous faces, and then questioned on their professions, nationality and specific life events. In a second test a few weeks later, subjects were shown the names of the same 30 celebrities and were questioned again on biographical knowledge.
The result? Our ability to recall the name of someone we know upon seeing their face declines steadily in normal aging. Semantic memory for people however seems unaffected by age. For instance, even if a subject couldn't name George W. Bush they still knew he was a politician or president of the United States. Another finding is that healthy elderly are better at accessing biographical knowledge about famous people from their names than from their faces. A person's name provides direct access to semantic memory because it is invariant, contrarily to visual stimuli.
These findings motived Dr. Joubert to conduct a second study, in press in Neuropsychologia, on elderly people suffering from mild cognitive impairment and another group in the initial phase of Alzheimer's.
"Our hypothesis was that contrary to the healthy subjects, both these groups should show difficulties finding the names of people, but that they should also show signs of a depleting semantic memory," says Dr. Joubert, adding that since 50 to 80 percent of people with mild cognitive problems develop Alzheimer's over the course of several years.
This semantic memory test could become an essential clinical tool to identify people at risk of developing the disease. Results show that the ability to remember names is even more pronounced in mild cognitive impairment and in early Alzheimer's disease than in normal aging. Contrary to normal aging, however, a decline in semantic memory for famous people was also observed.
Partners in research:
The study on normal aging was supported by the Natural Sciences and Engineering Research Council of Canada. The study on mild cognitive impairment and Alzheimer's disease was supported by the Alzheimer Society of Canada, the, the Centre de recherche de l'Institut universitaire de g?©riatrie de Montr?©al and the Fonds de la recherche en sant?© du Qu?©bec.
About the study:
The paper, "Manque du nom propre et effet de la modalit?© sur la capacit?© ? reconna?®tre des personnes connues au cours du vieillissement normal," published in the Canadian Journal on Aging, was authored by Roxane Langlois, Francine Fontaine, Caroline Hamel and Sven Joubert of the Universit?© de Montr?©al / Centre de recherche de l'Institut universitaire de g?©riatrie de Montr?©al.
Source: Sylvain-Jacques Desjardins
University of Montreal
"Semantic memory for people - triggered through name, voice or face - is knowledge we have gathered over the course of our lifetime on a person which enables us to recognize this person," says senior author Sven Joubert, a professor at the Universit?© de Montr?©al Department of Psychology and a researcher at the Centre de recherche de l'Institut universitaire de g?©riatrie de Montr?©al.
The goal of semantic study was to determine whether the ability to recall names of famous people decreases with age, since the condition named anomia ranks among the most common complaints from the elderly. To investigate, Dr. Joubert collaborated with first author Roxane Langlois to divide 117 healthy elderly, aged 60 to 91 years old, into three groups who were submitted to two semantic memory tests.
In a first test, subjects were shown the faces of 30 famous people such as Albert Einstein, C?©line Dion, Catherine Deneuve, Pierre Elliott Trudeau, Wayne Gretzky. They were first asked to name these famous faces, and then questioned on their professions, nationality and specific life events. In a second test a few weeks later, subjects were shown the names of the same 30 celebrities and were questioned again on biographical knowledge.
The result? Our ability to recall the name of someone we know upon seeing their face declines steadily in normal aging. Semantic memory for people however seems unaffected by age. For instance, even if a subject couldn't name George W. Bush they still knew he was a politician or president of the United States. Another finding is that healthy elderly are better at accessing biographical knowledge about famous people from their names than from their faces. A person's name provides direct access to semantic memory because it is invariant, contrarily to visual stimuli.
These findings motived Dr. Joubert to conduct a second study, in press in Neuropsychologia, on elderly people suffering from mild cognitive impairment and another group in the initial phase of Alzheimer's.
"Our hypothesis was that contrary to the healthy subjects, both these groups should show difficulties finding the names of people, but that they should also show signs of a depleting semantic memory," says Dr. Joubert, adding that since 50 to 80 percent of people with mild cognitive problems develop Alzheimer's over the course of several years.
This semantic memory test could become an essential clinical tool to identify people at risk of developing the disease. Results show that the ability to remember names is even more pronounced in mild cognitive impairment and in early Alzheimer's disease than in normal aging. Contrary to normal aging, however, a decline in semantic memory for famous people was also observed.
Partners in research:
The study on normal aging was supported by the Natural Sciences and Engineering Research Council of Canada. The study on mild cognitive impairment and Alzheimer's disease was supported by the Alzheimer Society of Canada, the, the Centre de recherche de l'Institut universitaire de g?©riatrie de Montr?©al and the Fonds de la recherche en sant?© du Qu?©bec.
About the study:
The paper, "Manque du nom propre et effet de la modalit?© sur la capacit?© ? reconna?®tre des personnes connues au cours du vieillissement normal," published in the Canadian Journal on Aging, was authored by Roxane Langlois, Francine Fontaine, Caroline Hamel and Sven Joubert of the Universit?© de Montr?©al / Centre de recherche de l'Institut universitaire de g?©riatrie de Montr?©al.
Source: Sylvain-Jacques Desjardins
University of Montreal
пятница, 27 мая 2011 г.
The Emerging Role Of Infection In Alzheimer's Disease
A number of chronic diseases are in fact caused by one or more infectious agents. For example, stomach ulcers are caused by Helicobacter pylori, chronic lung disease in newborns and chronic asthma in adults are both caused by Mycoplasmas and Chlamydia pneumonia, while some other pathogens have been associated with atherosclerosis. The realization that pathogens can produce slowly progressive chronic diseases has opened new lines of research into Alzheimer's disease.
In a special issue of the Journal of Alzheimer's Disease published May 2008, guest editors Judith Miklossy, from The University of British Columbia, and Ralph N. Martins, from Edith Cowan University and Hollywood Private Hospital, Perth, Western Australia, and a group of experts explore this exciting topic.
Alzheimer's disease (AD), the most frequent cause of dementia, is a form of amyloidosis. It has been known for a century that dementia, brain atrophy and amyloidosis can be caused by chronic bacterial infections, namely by Treponema pallidum in the atrophic form of general paresis in syphilis. Bacteria and viruses are powerful stimulators of inflammation. It was suggested by Alois Alzheimer and his colleagues a century ago that microorganisms may be contributors in the generation of senile plaques in AD.
The fact that pathogens may suppress, subvert or evade host defenses and establish chronic or latent infection has received little attention in the past. During infection, active oxygen and nitrogen species generated by inflammatory cells may cause DNA damage, induce apoptosis, and modulate enzyme activities and gene expression. Depending upon the biology of the pathogen and the host defense mechanisms the organism can persist in the infected tissues and cause chronic inflammation and amyloid deposition. The outcome of infection is as much determined by the genetic predisposition of the patient as by the virulence and biology of the infecting agent. Environmental factors and nutrition are critical determinants of disease expression as well.
In this special issue a series of reviews draws attention to both historic and recent observations related to this emerging field of AD research. The first review shows the importance of chronic inflammation in AD, followed by three articles presenting evidence on the involvement of spirochetes, Chlamydia pneumoniae and Herpes simplex virus type 1 in AD. These are followed by a review of amyloid proteins, which occur in many cellular forms in Eukaryotes and Prokaryotes.
The link between several viral and bacterial infections and the most significant genetic factor for AD, APOE a4, is discussed in the next review. The link between excessive or misplaced iron and a variety of neurodegenerative diseases and infection is reviewed in the final article.
According to Miklossy and Martins, "The historic and new observations reviewed in this special issue clearly show that high priority should be given for further research in this field as it may have major implications for public health, treatment, and prevention as adequate anti-bacterial and anti-viral drugs are available. Treatment of a bacterial infection and associated viral infection may result in regression and, if started early, prevention of disease. The impact on reducing healthcare costs would be substantial."
Source: Astrid Engelen
IOS Press
In a special issue of the Journal of Alzheimer's Disease published May 2008, guest editors Judith Miklossy, from The University of British Columbia, and Ralph N. Martins, from Edith Cowan University and Hollywood Private Hospital, Perth, Western Australia, and a group of experts explore this exciting topic.
Alzheimer's disease (AD), the most frequent cause of dementia, is a form of amyloidosis. It has been known for a century that dementia, brain atrophy and amyloidosis can be caused by chronic bacterial infections, namely by Treponema pallidum in the atrophic form of general paresis in syphilis. Bacteria and viruses are powerful stimulators of inflammation. It was suggested by Alois Alzheimer and his colleagues a century ago that microorganisms may be contributors in the generation of senile plaques in AD.
The fact that pathogens may suppress, subvert or evade host defenses and establish chronic or latent infection has received little attention in the past. During infection, active oxygen and nitrogen species generated by inflammatory cells may cause DNA damage, induce apoptosis, and modulate enzyme activities and gene expression. Depending upon the biology of the pathogen and the host defense mechanisms the organism can persist in the infected tissues and cause chronic inflammation and amyloid deposition. The outcome of infection is as much determined by the genetic predisposition of the patient as by the virulence and biology of the infecting agent. Environmental factors and nutrition are critical determinants of disease expression as well.
In this special issue a series of reviews draws attention to both historic and recent observations related to this emerging field of AD research. The first review shows the importance of chronic inflammation in AD, followed by three articles presenting evidence on the involvement of spirochetes, Chlamydia pneumoniae and Herpes simplex virus type 1 in AD. These are followed by a review of amyloid proteins, which occur in many cellular forms in Eukaryotes and Prokaryotes.
The link between several viral and bacterial infections and the most significant genetic factor for AD, APOE a4, is discussed in the next review. The link between excessive or misplaced iron and a variety of neurodegenerative diseases and infection is reviewed in the final article.
According to Miklossy and Martins, "The historic and new observations reviewed in this special issue clearly show that high priority should be given for further research in this field as it may have major implications for public health, treatment, and prevention as adequate anti-bacterial and anti-viral drugs are available. Treatment of a bacterial infection and associated viral infection may result in regression and, if started early, prevention of disease. The impact on reducing healthcare costs would be substantial."
Source: Astrid Engelen
IOS Press
четверг, 26 мая 2011 г.
National Dementia Strategy Must Be 'Bold And Ambitious', UK
In advance of the publication of the Government's consultation on the National Dementia Strategy tomorrow, Help the Aged has called on the Government to be 'bold and ambitious'
Elizabeth McLennan, Policy Officer at Help the Aged said:
'Research conducted by Help the Aged has revealed that the UK public rank mental decline higher than any other worry about ageing - more important even than money worries. With the number of people suffering from the disease expected to rise by two thirds in the next 20 years, this comes as no surprise.
'Unless we get to grips with this condition, we will face not only spiralling economic costs but also rising levels of unmet need.
'It's vital that that the dementia strategy paves the way for much higher levels of research into the disease - tackling the causes of the condition is the first step. The Government must also ensure that those living with dementia are given the best possible care, both at home and in care homes.
'Every care home should have a recognised expert on dementia on their staff, and all staff must have training in how best to provide care for people with dementia. Care homes must also provide constructive activities to enable people who have dementia, to keep their brain's active, so potentially reducing decline in mental ability.
'Dementia robs victims of their identities as memory, speech and understanding are lost. Failure to fund much higher levels of research into the condition means condemning many more people to an older age affected by increasing mental incapacity.'
Notes
The Disconnected Mind is a major scientific study into early mental decline funded by Help the Aged. The study takes unique data from the 1947 Scottish Mental Survey and combines it with a decade of new research using the latest techniques, such as MRI scanning. By revisiting 1,000 of the original participants from 1947, who are now in their 70's, the study will span 60 years and 1,000 lives to unlock the secrets of mental decline. The goal is to produce essential new understanding that will lead to medical solutions or suggest lifestyle changes that can help reduce the condition.
Help the Aged is running The Disconnected Mind study and is currently appealing for the donations it needs to support this vital research through to its conclusion in 2015. For more information visit disconnectedmind.uk
Right care, Right deal' is the new national campaign launched to build public awareness and support for the need for brave and innovative solutions for the social care system. With the Government indicating that social care is an urgent political priority, and in advance of the expected green paper later in 2008, the campaign combines three of the UK's largest charities working with and for older people and their families and carers, and will urge the government to renew its vision for the future of social care in England. Visit rightcare.uk
Help the Aged is the charity fighting to free disadvantaged older people in the UK and overseas from poverty, isolation, neglect and ageism. It campaigns to raise public awareness of the issues affecting older people and to bring about policy change. The Charity delivers a range of services: information and advice, home support and community living, including international development work. These are supported by its paid-for services and fundraising activities - which aim to increase funding in the future to respond to the growing unmet needs of disadvantaged older people. Help the Aged also funds vital research into the health issues and experiences of older people to improve the quality of later life.
Help the Aged urgently needs donations and support to help it in the increasingly challenging fight to free disadvantaged older people from poverty, isolation and neglect.
Help the Aged
Elizabeth McLennan, Policy Officer at Help the Aged said:
'Research conducted by Help the Aged has revealed that the UK public rank mental decline higher than any other worry about ageing - more important even than money worries. With the number of people suffering from the disease expected to rise by two thirds in the next 20 years, this comes as no surprise.
'Unless we get to grips with this condition, we will face not only spiralling economic costs but also rising levels of unmet need.
'It's vital that that the dementia strategy paves the way for much higher levels of research into the disease - tackling the causes of the condition is the first step. The Government must also ensure that those living with dementia are given the best possible care, both at home and in care homes.
'Every care home should have a recognised expert on dementia on their staff, and all staff must have training in how best to provide care for people with dementia. Care homes must also provide constructive activities to enable people who have dementia, to keep their brain's active, so potentially reducing decline in mental ability.
'Dementia robs victims of their identities as memory, speech and understanding are lost. Failure to fund much higher levels of research into the condition means condemning many more people to an older age affected by increasing mental incapacity.'
Notes
The Disconnected Mind is a major scientific study into early mental decline funded by Help the Aged. The study takes unique data from the 1947 Scottish Mental Survey and combines it with a decade of new research using the latest techniques, such as MRI scanning. By revisiting 1,000 of the original participants from 1947, who are now in their 70's, the study will span 60 years and 1,000 lives to unlock the secrets of mental decline. The goal is to produce essential new understanding that will lead to medical solutions or suggest lifestyle changes that can help reduce the condition.
Help the Aged is running The Disconnected Mind study and is currently appealing for the donations it needs to support this vital research through to its conclusion in 2015. For more information visit disconnectedmind.uk
Right care, Right deal' is the new national campaign launched to build public awareness and support for the need for brave and innovative solutions for the social care system. With the Government indicating that social care is an urgent political priority, and in advance of the expected green paper later in 2008, the campaign combines three of the UK's largest charities working with and for older people and their families and carers, and will urge the government to renew its vision for the future of social care in England. Visit rightcare.uk
Help the Aged is the charity fighting to free disadvantaged older people in the UK and overseas from poverty, isolation, neglect and ageism. It campaigns to raise public awareness of the issues affecting older people and to bring about policy change. The Charity delivers a range of services: information and advice, home support and community living, including international development work. These are supported by its paid-for services and fundraising activities - which aim to increase funding in the future to respond to the growing unmet needs of disadvantaged older people. Help the Aged also funds vital research into the health issues and experiences of older people to improve the quality of later life.
Help the Aged urgently needs donations and support to help it in the increasingly challenging fight to free disadvantaged older people from poverty, isolation and neglect.
Help the Aged
UCLA Scientists Identify How Immune Cells May Help Predict Alzheimer's Risk; MP Biomedicals Granted Rights To Further Develop Screening Tool
UCLA scientists have discovered a way to measure the amount of amyloid beta that is being absorbed by immune cells in the blood. Amyloid beta forms the plaques considered the hallmark of Alzheimer's disease, and if the immune system isn't adequately clearing amyloid beta, it may indicate Alzheimer's risk, according to the researchers.
MP Biomedicals LLC, a global life sciences and diagnostics company dedicated to Alzheimer's disease research, has received an exclusive, worldwide license to commercialize the UCLA technology and create a diagnostic blood test for public use to screen for Alzheimer's risk.
"Early diagnosis is the cornerstone of preventive approaches to Alzheimer's disease," said Dr. Milan Fiala, lead author of the UCLA study and a researcher at the David Geffen School of Medicine at UCLA and the Veterans Affairs Greater Los Angeles Healthcare System. "We are pleased that the process we've identified using immune cells to help predict Alzheimer's risk will be further developed by MP Biomedicals."
"We are excited by the opportunity to forward the UCLA science in creating a cost-effective blood test to screen for Alzheimer's risk that could be used in any hospital or lab," said Milan Panic, CEO of MP Biomedicals.
Dr. Miodrag Micic, vice president of research and development for MP Biomedicals, noted that other blood tests for Alzheimer's diagnosis measure factors such as inflammation and infection, which are also present in other diseases like atherosclerosis and may complicate the interpretation of results.
The recently published study on the process identified by UCLA, which uses the "innate" immune system present at birth, appeared in the May issue of the Journal of Neuroimmunology.
In the study, researchers took blood samples and isolated monocytes, which from birth act as the immune system's janitors, traveling through the brain and body and gobbling up waste products - including amyloid beta. The monocytes were incubated overnight with amyloid beta, which was labeled with a fluorescent marker. Using a common laboratory method known as flow cytometry, researchers then measured the amount of amyloid beta ingested by the immune cells by assessing how much fluorescence was being emitted from each monocyte cell.
The 18 Alzheimer's disease patients in the study showed the least uptake of amyloid beta; the healthy control group, which consisted of 14 university professors, demonstrated the highest uptake. The method was able to distinguish with adequate sensitivity and specificity the Alzheimer's disease patients.
The results were found to be positive in 94 percent of the Alzheimer's patients and negative in 100 percent of the university professor control group. In addition, the results were found to be positive in 60 percent of study participants who suffered from mild cognitive impairment, a condition that increases the risk of developing Alzheimer's.
"Patients and control subjects were also tracked over time to see if their immune response changed," Fiala said. For example, an Alzheimer's disease patient over time showed declining results, while a university professor continued to demonstrate a high uptake of amyloid beta.
Micic noted that the new method could be a flag for further testing and interventions.
"Similar to screening patients for heart disease risk by a cholesterol test, a positive result for Alzheimer's risk in some patients may suggest further interventions and advanced diagnostics, such as a brain PET scan and neurocognitive testing."
The study was funded in part by MP Biomedicals LLC. Fiala is a consultant for the company and also served in the company's speakers bureau.
Source
The David Geffen School of Medicine at UCLA
MP Biomedicals LLC, a global life sciences and diagnostics company dedicated to Alzheimer's disease research, has received an exclusive, worldwide license to commercialize the UCLA technology and create a diagnostic blood test for public use to screen for Alzheimer's risk.
"Early diagnosis is the cornerstone of preventive approaches to Alzheimer's disease," said Dr. Milan Fiala, lead author of the UCLA study and a researcher at the David Geffen School of Medicine at UCLA and the Veterans Affairs Greater Los Angeles Healthcare System. "We are pleased that the process we've identified using immune cells to help predict Alzheimer's risk will be further developed by MP Biomedicals."
"We are excited by the opportunity to forward the UCLA science in creating a cost-effective blood test to screen for Alzheimer's risk that could be used in any hospital or lab," said Milan Panic, CEO of MP Biomedicals.
Dr. Miodrag Micic, vice president of research and development for MP Biomedicals, noted that other blood tests for Alzheimer's diagnosis measure factors such as inflammation and infection, which are also present in other diseases like atherosclerosis and may complicate the interpretation of results.
The recently published study on the process identified by UCLA, which uses the "innate" immune system present at birth, appeared in the May issue of the Journal of Neuroimmunology.
In the study, researchers took blood samples and isolated monocytes, which from birth act as the immune system's janitors, traveling through the brain and body and gobbling up waste products - including amyloid beta. The monocytes were incubated overnight with amyloid beta, which was labeled with a fluorescent marker. Using a common laboratory method known as flow cytometry, researchers then measured the amount of amyloid beta ingested by the immune cells by assessing how much fluorescence was being emitted from each monocyte cell.
The 18 Alzheimer's disease patients in the study showed the least uptake of amyloid beta; the healthy control group, which consisted of 14 university professors, demonstrated the highest uptake. The method was able to distinguish with adequate sensitivity and specificity the Alzheimer's disease patients.
The results were found to be positive in 94 percent of the Alzheimer's patients and negative in 100 percent of the university professor control group. In addition, the results were found to be positive in 60 percent of study participants who suffered from mild cognitive impairment, a condition that increases the risk of developing Alzheimer's.
"Patients and control subjects were also tracked over time to see if their immune response changed," Fiala said. For example, an Alzheimer's disease patient over time showed declining results, while a university professor continued to demonstrate a high uptake of amyloid beta.
Micic noted that the new method could be a flag for further testing and interventions.
"Similar to screening patients for heart disease risk by a cholesterol test, a positive result for Alzheimer's risk in some patients may suggest further interventions and advanced diagnostics, such as a brain PET scan and neurocognitive testing."
The study was funded in part by MP Biomedicals LLC. Fiala is a consultant for the company and also served in the company's speakers bureau.
Source
The David Geffen School of Medicine at UCLA
среда, 25 мая 2011 г.
Alva Is On The Ball With New Day Care Centre, Scotland
A new Alzheimer Scotland day care centre was officially opened this month by Scottish football legend and famous TV pundit Alan Hansen. The centre has been in operation since January 2007, but the official unveiling coincided with the completion of the picturesque garden (which owes much to the green fingers of Falkirk Service Manager, Fay Godfrey) to the rear of the building.
The Viewfield Day Care Centre has been converted from a one-storey residential building in the heart of a quiet Alva neighbourhood, ensuring that its users remain
at the very heart of the local community. As well as hailing from the local area, Hansen has a personal link to the service at Viewfield Drive: his father has Alzheimer's and attends day care at the centre. Hansen said, "This place is fantastic, it really is; the people do such a great job. It is a wonderful place to come to: there should be more like this."
Lesley Corr, assistant service manager with Alzheimer Scotland, said, "It is a lovely place to work, and there is so much space where we can work one-to-one when needed. I'm chuffed to bits; thanks to everyone who has helped us get this far."
Alzheimer Scotland
The Viewfield Day Care Centre has been converted from a one-storey residential building in the heart of a quiet Alva neighbourhood, ensuring that its users remain
at the very heart of the local community. As well as hailing from the local area, Hansen has a personal link to the service at Viewfield Drive: his father has Alzheimer's and attends day care at the centre. Hansen said, "This place is fantastic, it really is; the people do such a great job. It is a wonderful place to come to: there should be more like this."
Lesley Corr, assistant service manager with Alzheimer Scotland, said, "It is a lovely place to work, and there is so much space where we can work one-to-one when needed. I'm chuffed to bits; thanks to everyone who has helped us get this far."
Alzheimer Scotland
вторник, 24 мая 2011 г.
Human Antibodies In Blood Could Potentially Act As Specific Protection Against Toxic Form Of Beta Amyloid In Alzheimer's
In an important advance in the battle against Alzheimer's disease, physician-scientists at NewYork-Presbyterian Hospital/Weill Cornell Medical Center have identified naturally occurring antibodies in human blood that may help to defend against this form of dementia as well as other neurodegenerative diseases.
The newly found antibodies selectively target aggregates of beta amyloid proteins called "oligomers" that are toxic to brain cells, while ignoring the benign single-molecule forms of the same proteins. The existence of such antibodies was predicted by animal studies, but they were never previously demonstrated to be present in substantial quantities in blood from normal humans.
Lead researcher Dr. Norman Relkin, a behavioral neurologist and neuroscientist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center, presented the findings at the "2nd Alzheimer's Association International Conference on Prevention of Dementia," in Washington, DC.
Dr. Relkin is director of the Memory Disorders Program at NewYork-Presbyterian/Weill Cornell and associate professor of clinical neurology at Weill Cornell Medical College.
Dr. Relkin's team has been testing an antibody-based immunotherapy called Intravenous Immunoglobulin (IVIG) as a potential new treatment for Alzheimer's. IVIG is made from the blood of healthy donors and was previously reported to contain small quantities of antibodies against beta amyloid.
"The effects of IVIG in lowering beta amyloid levels in Alzheimer's patients in our Phase I clinical trial were much more profound than we expected," Dr. Relkin explains. "We couldn't readily explain this based on the low levels of anti-amyloid antibodies known to be present in IVIG. We suspected there might be another, unseen player."
His laboratory studies demonstrated that IVIG initially bound very little single-molecule ("monomer") beta amyloid in a test tube. However, it gathered up much more of the protein when the amyloid was "aged" in a way that allowed soluble aggregates to form.
These beta amyloid "oligomers" can grow into insoluble "fibrils" that cluster around brain cells and are a hallmark of Alzheimer's disease. While monomers are produced from birth and appear to be relatively benign, oligomers have been implicated as potent toxins responsible for Alzheimer's-linked memory loss and brain cell death. This has led many scientists to speculate that oligomers may be the main culprit in Alzheimer's and therefore a prime target for a new generation of disease-modifying treatments.
To further confirm that these natural antibodies bind with oligomers, Dr. Relkin and his colleagues collaborated with Drs. Charles Glabe and Rakez Kayed from the University of California at Irvine, who had previously created anti-oligomer antibodies in rabbits. Using techniques pioneered by Dr. Glabe's group, the NewYork-Presbyterian/Weill Cornell scientists were able to measure and extract the human version of anti-oligomer antibodies from IVIG and then demonstrate that these antibodies are present in the blood of normal individuals.
The basis for the selective recognition of oligomers by these antibodies appears to be their capacity to recognize the oligomer's misfolded shape.
"That was a surprise, because most antibodies work by recognizing some aspect of the chemical structure of their target -- not their shape," explains Weill Cornell Medical College molecular biologist and study co-author, Dr. Paul Szabo. "That means that even though beta amyloid monomers and oligomers have the same fundamental chemical makeup, human anti-oligomer antibodies can distinguish between them. The antibodies recognize a particular shape that proteins assume only when they become these toxic aggregates."
The ability of the antibodies to recognize toxic proteins based on their shape may have important implications for immune therapy of other neurologic disorders, the researchers explain.
"We were able to confirm that the antibodies we found not only recognize oligomers of beta amyloid but also unhealthy forms of other proteins that accumulate in a wide variety of diseases, such as Parkinson's, Lewy body dementia and Prion disease (the human form of 'Mad Cow' disease), to name a few," says Dr. Relkin.
Since beta amyloid oligomers are much less abundant in the body than the single-molecule variety, the relatively high amount of oligomer-specific antibody found in human blood suggests that the immune system recognizes these aggregates to be a particularly noxious threat.
"This could be part of an innate defense mechanism against Alzheimer's and other age-related neurodegenerative disorders," comments Dr. Marc Weksler, The Irving Wright Sherwood Professor of Geriatrics and professor of medicine at Weill Cornell Medical College, and senior investigator in the Phase I IVIG study that led to this discovery.
However, the clear demonstration of the relationship of these scientific findings to clinical benefit in patients requires much more study, the experts say.
NewYork-Presbyterian/Weill Cornell is currently leading a six-month Phase II study of IVIG in 24 patients with mild and moderate Alzheimer's disease, which is planned to be complete later this year. While this study may provide a signal of the effect of IVIG therapy to clinical outcomes, further investigation in larger controlled and longer-term trials will be needed to definitively demonstrate whether IVIG is useful in treating Alzheimer's.
Still, this discovery substantially boosts our understanding of Alzheimer's and other neurodegenerative illnesses, the experts say.
This work was funded by grants from Baxter Healthcare, which developed and produces GAMMAGARD IVIG; the Citigroup Foundation; and private philanthropy.
Other collaborators on the "Alzheimer's Association Prevention Conference" presentation include Drs. Marc Weksler, Diana Mujalli, Sushila Shenoy and Basia Adamiak -- all of NewYork-Presbyterian Hospital/Weill Cornell Medical Center.
NewYork-Presbyterian Hospital/Weill Cornell Medical Center
New York-Presbyterian Hospital/Weill Cornell Medical Center, located in New York City, is one of the leading academic medical centers in the world, comprising the teaching hospital New York-Presbyterian and its academic partner, Weill Cornell Medical College. NewYork-Presbyterian/Weill Cornell provides state-of-the-art inpatient, ambulatory and preventive care in all areas of medicine, and is committed to excellence in patient care, research, education and community service. New York-Presbyterian, which is ranked sixth on the U.S. News & World Report's list of top hospitals, also comprises NewYork-Presbyterian Hospital/Columbia University Medical Center.
Contact: Jonathan Weil
New York- Presbyterian Hospital/Columbia University Medical Center
The newly found antibodies selectively target aggregates of beta amyloid proteins called "oligomers" that are toxic to brain cells, while ignoring the benign single-molecule forms of the same proteins. The existence of such antibodies was predicted by animal studies, but they were never previously demonstrated to be present in substantial quantities in blood from normal humans.
Lead researcher Dr. Norman Relkin, a behavioral neurologist and neuroscientist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center, presented the findings at the "2nd Alzheimer's Association International Conference on Prevention of Dementia," in Washington, DC.
Dr. Relkin is director of the Memory Disorders Program at NewYork-Presbyterian/Weill Cornell and associate professor of clinical neurology at Weill Cornell Medical College.
Dr. Relkin's team has been testing an antibody-based immunotherapy called Intravenous Immunoglobulin (IVIG) as a potential new treatment for Alzheimer's. IVIG is made from the blood of healthy donors and was previously reported to contain small quantities of antibodies against beta amyloid.
"The effects of IVIG in lowering beta amyloid levels in Alzheimer's patients in our Phase I clinical trial were much more profound than we expected," Dr. Relkin explains. "We couldn't readily explain this based on the low levels of anti-amyloid antibodies known to be present in IVIG. We suspected there might be another, unseen player."
His laboratory studies demonstrated that IVIG initially bound very little single-molecule ("monomer") beta amyloid in a test tube. However, it gathered up much more of the protein when the amyloid was "aged" in a way that allowed soluble aggregates to form.
These beta amyloid "oligomers" can grow into insoluble "fibrils" that cluster around brain cells and are a hallmark of Alzheimer's disease. While monomers are produced from birth and appear to be relatively benign, oligomers have been implicated as potent toxins responsible for Alzheimer's-linked memory loss and brain cell death. This has led many scientists to speculate that oligomers may be the main culprit in Alzheimer's and therefore a prime target for a new generation of disease-modifying treatments.
To further confirm that these natural antibodies bind with oligomers, Dr. Relkin and his colleagues collaborated with Drs. Charles Glabe and Rakez Kayed from the University of California at Irvine, who had previously created anti-oligomer antibodies in rabbits. Using techniques pioneered by Dr. Glabe's group, the NewYork-Presbyterian/Weill Cornell scientists were able to measure and extract the human version of anti-oligomer antibodies from IVIG and then demonstrate that these antibodies are present in the blood of normal individuals.
The basis for the selective recognition of oligomers by these antibodies appears to be their capacity to recognize the oligomer's misfolded shape.
"That was a surprise, because most antibodies work by recognizing some aspect of the chemical structure of their target -- not their shape," explains Weill Cornell Medical College molecular biologist and study co-author, Dr. Paul Szabo. "That means that even though beta amyloid monomers and oligomers have the same fundamental chemical makeup, human anti-oligomer antibodies can distinguish between them. The antibodies recognize a particular shape that proteins assume only when they become these toxic aggregates."
The ability of the antibodies to recognize toxic proteins based on their shape may have important implications for immune therapy of other neurologic disorders, the researchers explain.
"We were able to confirm that the antibodies we found not only recognize oligomers of beta amyloid but also unhealthy forms of other proteins that accumulate in a wide variety of diseases, such as Parkinson's, Lewy body dementia and Prion disease (the human form of 'Mad Cow' disease), to name a few," says Dr. Relkin.
Since beta amyloid oligomers are much less abundant in the body than the single-molecule variety, the relatively high amount of oligomer-specific antibody found in human blood suggests that the immune system recognizes these aggregates to be a particularly noxious threat.
"This could be part of an innate defense mechanism against Alzheimer's and other age-related neurodegenerative disorders," comments Dr. Marc Weksler, The Irving Wright Sherwood Professor of Geriatrics and professor of medicine at Weill Cornell Medical College, and senior investigator in the Phase I IVIG study that led to this discovery.
However, the clear demonstration of the relationship of these scientific findings to clinical benefit in patients requires much more study, the experts say.
NewYork-Presbyterian/Weill Cornell is currently leading a six-month Phase II study of IVIG in 24 patients with mild and moderate Alzheimer's disease, which is planned to be complete later this year. While this study may provide a signal of the effect of IVIG therapy to clinical outcomes, further investigation in larger controlled and longer-term trials will be needed to definitively demonstrate whether IVIG is useful in treating Alzheimer's.
Still, this discovery substantially boosts our understanding of Alzheimer's and other neurodegenerative illnesses, the experts say.
This work was funded by grants from Baxter Healthcare, which developed and produces GAMMAGARD IVIG; the Citigroup Foundation; and private philanthropy.
Other collaborators on the "Alzheimer's Association Prevention Conference" presentation include Drs. Marc Weksler, Diana Mujalli, Sushila Shenoy and Basia Adamiak -- all of NewYork-Presbyterian Hospital/Weill Cornell Medical Center.
NewYork-Presbyterian Hospital/Weill Cornell Medical Center
New York-Presbyterian Hospital/Weill Cornell Medical Center, located in New York City, is one of the leading academic medical centers in the world, comprising the teaching hospital New York-Presbyterian and its academic partner, Weill Cornell Medical College. NewYork-Presbyterian/Weill Cornell provides state-of-the-art inpatient, ambulatory and preventive care in all areas of medicine, and is committed to excellence in patient care, research, education and community service. New York-Presbyterian, which is ranked sixth on the U.S. News & World Report's list of top hospitals, also comprises NewYork-Presbyterian Hospital/Columbia University Medical Center.
Contact: Jonathan Weil
New York- Presbyterian Hospital/Columbia University Medical Center
понедельник, 23 мая 2011 г.
Alzheimer's Association Releases Dementia Care Practice Recommendations For End-Of-Life Care
The Alzheimer's Association released its third set of Dementia Care Practice Recommendations for Assisted Living Residences and Nursing Homes. The Recommendations focus on improving the end of life experience for people with Alzheimer's and other dementias by offering concrete suggestions for addressing issues unique to people with dementia at the end of life.
The Recommendations were released at the Alzheimer's Association's 15th annual Dementia Care Conference, held in Chicago.
More than 50 percent of residents in assisted living and nursing homes have some form of dementia or cognitive impairment, including Alzheimer's. Available research indicates that about 67 percent of dementia-related deaths occur in nursing homes. The number of people with Alzheimer's is projected to sharply increase from more than 5 million today to as many as 16 million by 2050, as the 78 million Baby Boomers mature and reach the age of highest risk.
"Underlying the end-of-life care practice recommendations is a person-centered approach to dementia care, which involves tailoring care to the abilities and changing needs of each resident," said Peter Reed, Ph.D., Senior Director of Programs for the Alzheimer's Association.
The recommended care practices for end-of-life cover:
-- Communication and decision-making strategies, including residents and family members.
-- Assessment and care of behavioral and physical symptoms, including pain.
-- Psychosocial and spiritual support of residents and family.
-- Care provision, coordination and communication when residents choose hospice services.
-- Acknowledgment of resident death and bereavement services.
-- Staff training.
Key aspects of the wide ranging report include:
-- The need for advance planning for end of life as soon as possible after diagnosis of dementia. This includes documenting the person's wishes regarding medical treatments in advanced stages of dementia and designation of a proxy decision-maker.
-- Provision of person-centered palliative care to people with advanced dementia. Care should follow residents' wishes regarding end of life as closely as possible.
-- The importance of dementia-specific training for residential care workers on end of life issues - for example, signs of dying, pain management issues, and communicating with families.
The recommendations emphasize the importance of consistency in individualized and person-centered care approaches; development of relationships between staff and residents; and increasing staff knowledge of individual resident needs, abilities and preferences.
"Our highly collaborative, consensus-based process ensures that the Recommendations represent the best dementia care practices and, at the same time, are practical so that nursing homes and assisted living residences can incorporate them into the daily care routines of their residents," said Jane Tilly, Dr.PH., Director of Quality Care Advocacy for the Alzheimer's Association.
Two primary sources of research evidence were used to develop the Phase 3 Recommendations on end-of-life care. An Association-sponsored literature review, End-of-life Care for People with Dementia in Residential Care Settings, by Ladislav Volicer, M.D., Ph.D., summarizes current peer-reviewed research relevant to end-of-life care for residents with severe dementia. To extend the knowledge gained through this literature review, Dr. Tilly, with Abel Fok, wrote Quality End-of-life Care for Individuals with Dementia in Assisted Living and Nursing Homes and Public Policy Barriers to Delivering This Care, which describes what practitioners, providers, professionals and researchers believe constitutes high quality end-of-life care for residents with dementia.
Dementia care experts and professional staff from the Alzheimer's Association, representatives of more than 30 national associations and other experts used the evidence in a consensus-building process to translate the research into specific suggestions illustrated by "real world" examples based on the experience of the contributors.
To support implementation of the Recommendations and help ensure that staff is adequately trained, the Alzheimer's Association is developing classroom-style and online training programs based on the recommendations for all levels of care staff in assisted living residences and nursing homes. The Association is also advocating with direct care providers and working with federal and state policy makers to incorporate the recommendations into their quality assurance systems.
Alzheimer's Association Quality Care Campaign
In 2005, the Alzheimer's Association launched its Quality Care Campaign to improve the quality of care for residents with dementia in assisted living and nursing homes. To better respond to residents' needs, the Association joined with leaders in dementia care to develop the evidence-based Dementia Care Practice Recommendations for Assisted Living Residences and Nursing Homes. Phase 1 of the recommendations focuses on the basics of good dementia care, food and fluid consumption, pain management and social engagement. Phase 2 covers wandering, falls and physical restraints. Now, Phase 3 covers end-of-life care practices and issues.
All aspects of the Quality Care Campaign are based on the best available evidence on effective dementia care in residential settings. To date, more than 30 leading health and senior care organizations have expressed their support and acceptance of one or more phases of the Dementia Care Practice Recommendations.
Alzheimer's Association
The Alzheimer's Association is the first and largest voluntary health organization in Alzheimer care, support and research. Our mission is to eliminate Alzheimer's disease through the advancement of research, provide and enhance care and support for all affected, and reduce the risk of dementia through the promotion of brain health. Our vision is a world without Alzheimer's.
alz/
The Recommendations were released at the Alzheimer's Association's 15th annual Dementia Care Conference, held in Chicago.
More than 50 percent of residents in assisted living and nursing homes have some form of dementia or cognitive impairment, including Alzheimer's. Available research indicates that about 67 percent of dementia-related deaths occur in nursing homes. The number of people with Alzheimer's is projected to sharply increase from more than 5 million today to as many as 16 million by 2050, as the 78 million Baby Boomers mature and reach the age of highest risk.
"Underlying the end-of-life care practice recommendations is a person-centered approach to dementia care, which involves tailoring care to the abilities and changing needs of each resident," said Peter Reed, Ph.D., Senior Director of Programs for the Alzheimer's Association.
The recommended care practices for end-of-life cover:
-- Communication and decision-making strategies, including residents and family members.
-- Assessment and care of behavioral and physical symptoms, including pain.
-- Psychosocial and spiritual support of residents and family.
-- Care provision, coordination and communication when residents choose hospice services.
-- Acknowledgment of resident death and bereavement services.
-- Staff training.
Key aspects of the wide ranging report include:
-- The need for advance planning for end of life as soon as possible after diagnosis of dementia. This includes documenting the person's wishes regarding medical treatments in advanced stages of dementia and designation of a proxy decision-maker.
-- Provision of person-centered palliative care to people with advanced dementia. Care should follow residents' wishes regarding end of life as closely as possible.
-- The importance of dementia-specific training for residential care workers on end of life issues - for example, signs of dying, pain management issues, and communicating with families.
The recommendations emphasize the importance of consistency in individualized and person-centered care approaches; development of relationships between staff and residents; and increasing staff knowledge of individual resident needs, abilities and preferences.
"Our highly collaborative, consensus-based process ensures that the Recommendations represent the best dementia care practices and, at the same time, are practical so that nursing homes and assisted living residences can incorporate them into the daily care routines of their residents," said Jane Tilly, Dr.PH., Director of Quality Care Advocacy for the Alzheimer's Association.
Two primary sources of research evidence were used to develop the Phase 3 Recommendations on end-of-life care. An Association-sponsored literature review, End-of-life Care for People with Dementia in Residential Care Settings, by Ladislav Volicer, M.D., Ph.D., summarizes current peer-reviewed research relevant to end-of-life care for residents with severe dementia. To extend the knowledge gained through this literature review, Dr. Tilly, with Abel Fok, wrote Quality End-of-life Care for Individuals with Dementia in Assisted Living and Nursing Homes and Public Policy Barriers to Delivering This Care, which describes what practitioners, providers, professionals and researchers believe constitutes high quality end-of-life care for residents with dementia.
Dementia care experts and professional staff from the Alzheimer's Association, representatives of more than 30 national associations and other experts used the evidence in a consensus-building process to translate the research into specific suggestions illustrated by "real world" examples based on the experience of the contributors.
To support implementation of the Recommendations and help ensure that staff is adequately trained, the Alzheimer's Association is developing classroom-style and online training programs based on the recommendations for all levels of care staff in assisted living residences and nursing homes. The Association is also advocating with direct care providers and working with federal and state policy makers to incorporate the recommendations into their quality assurance systems.
Alzheimer's Association Quality Care Campaign
In 2005, the Alzheimer's Association launched its Quality Care Campaign to improve the quality of care for residents with dementia in assisted living and nursing homes. To better respond to residents' needs, the Association joined with leaders in dementia care to develop the evidence-based Dementia Care Practice Recommendations for Assisted Living Residences and Nursing Homes. Phase 1 of the recommendations focuses on the basics of good dementia care, food and fluid consumption, pain management and social engagement. Phase 2 covers wandering, falls and physical restraints. Now, Phase 3 covers end-of-life care practices and issues.
All aspects of the Quality Care Campaign are based on the best available evidence on effective dementia care in residential settings. To date, more than 30 leading health and senior care organizations have expressed their support and acceptance of one or more phases of the Dementia Care Practice Recommendations.
Alzheimer's Association
The Alzheimer's Association is the first and largest voluntary health organization in Alzheimer care, support and research. Our mission is to eliminate Alzheimer's disease through the advancement of research, provide and enhance care and support for all affected, and reduce the risk of dementia through the promotion of brain health. Our vision is a world without Alzheimer's.
alz/
воскресенье, 22 мая 2011 г.
Alzheimer's Society Comment On Annual Survey Of UK Local Authority Baseline Fee Rates 2009/10
Community Care Market News has conducted an annual survey of local authority fee rates for nursing and residential care.
Baseline fee rates for the 200,000 council supported elderly people in independent sector care homes across the UK have received an average uplift of 2.6% for financial year 2009/10, according to Laing & Buisson's annual survey published in the June edition of Community Care Market News. This is a slight fall compared to the 3% increase seen in last year's round of uplifts.
Alzheimer's Society comment:
'Everyday over 250, 000 people with dementia in care homes need care and support. Good care homes show us that good care can make a huge difference to people's quality of life but sadly there is a huge variation in the quality of care being delivered. Often the difference between good care and poor care is the amount of money invested in resources, training, support and staff.
'In these times of unprecedented fiscal stringency and low rises in baseline fee, councils and care homes must show extra vigilance when commissioning for quality care. The proposed green paper on Adult Funding of Social Care must also deliver a transparent, fair and sustainable system of who pays for care.'
Neil Hunt
Chief Executive
Alzheimer's Society
Notes
- Baseline fee rates are defined as the gross weekly fee that local authorities are prepared to pay independent sector nursing and residential homes for the care of individuals for whom they accept financial responsibility.
- The Department of Health is expected to publish a green paper setting out proposals for the long-term reform of adult social care funding in June 2009.
- One in three people over 65 will die with dementia
- Alzheimer's Society research shows that 700,000 people in the UK have a form of dementia, more than half have Alzheimer's disease. In less than 20 years nearly a million people will be living with dementia. This will soar to 1.7 million people by 2051.
- Alzheimer's Society champions the rights of people living with dementia and the millions of people who care for them.
- Alzheimer's Society works in England, Wales and Northern Ireland.
- Alzheimer's Society needs to raise money to help people live well with dementia today and for research to find a cure for tomorrow. You can donate now by calling 0845 306 0898 or visiting alzheimers.uk
- Alzheimer's Society provides a National Dementia Helpline, the number is 0845 300 0336 or visit alzheimers.uk
Source
Alzheimer's Society
Baseline fee rates for the 200,000 council supported elderly people in independent sector care homes across the UK have received an average uplift of 2.6% for financial year 2009/10, according to Laing & Buisson's annual survey published in the June edition of Community Care Market News. This is a slight fall compared to the 3% increase seen in last year's round of uplifts.
Alzheimer's Society comment:
'Everyday over 250, 000 people with dementia in care homes need care and support. Good care homes show us that good care can make a huge difference to people's quality of life but sadly there is a huge variation in the quality of care being delivered. Often the difference between good care and poor care is the amount of money invested in resources, training, support and staff.
'In these times of unprecedented fiscal stringency and low rises in baseline fee, councils and care homes must show extra vigilance when commissioning for quality care. The proposed green paper on Adult Funding of Social Care must also deliver a transparent, fair and sustainable system of who pays for care.'
Neil Hunt
Chief Executive
Alzheimer's Society
Notes
- Baseline fee rates are defined as the gross weekly fee that local authorities are prepared to pay independent sector nursing and residential homes for the care of individuals for whom they accept financial responsibility.
- The Department of Health is expected to publish a green paper setting out proposals for the long-term reform of adult social care funding in June 2009.
- One in three people over 65 will die with dementia
- Alzheimer's Society research shows that 700,000 people in the UK have a form of dementia, more than half have Alzheimer's disease. In less than 20 years nearly a million people will be living with dementia. This will soar to 1.7 million people by 2051.
- Alzheimer's Society champions the rights of people living with dementia and the millions of people who care for them.
- Alzheimer's Society works in England, Wales and Northern Ireland.
- Alzheimer's Society needs to raise money to help people live well with dementia today and for research to find a cure for tomorrow. You can donate now by calling 0845 306 0898 or visiting alzheimers.uk
- Alzheimer's Society provides a National Dementia Helpline, the number is 0845 300 0336 or visit alzheimers.uk
Source
Alzheimer's Society
суббота, 21 мая 2011 г.
Prana Biotechnology Raises Approximately 6 Million US Dollars To Fully Fund Its Phase IIa Clinical Trial Of PBT2 In Patients With Alzheimer's Disease
Prana
Biotechnology Limited (Nasdaq: PRAN; ASX: PBT), today announced it has
entered into agreements to raise approximately 6.0 million US Dollars (7.8
million A Dollars) from new institutional investors in Australia, existing
institutional investors in the United States and a founding member of the
Company. As a result, the Company now has 10.2 million US Dollars (13.3 million A Dollars)
in cash to immediately commence its Phase IIa trial of PBT2 in Patients
with early Alzheimer's disease, for which it has received full regulatory
approval in Sweden.
The investment involves the purchase of 21.8 million ordinary shares
(equivalent to 2.18 million ADRs) at a price of A$0.357 per ordinary share
(approximately US$2.74 per ADR). In addition, the investors receive three-
year options to purchase an additional 4.35 million ordinary shares
(equivalent to 435,000 ADRs) at an exercise price of A$0.446 per ordinary
share (approximately US$3.42 per ADR), which could raise an additional
US$1.5 million (A$1.9 million) for the Company.
"We believe these commitments from new and existing investors reinforce
the enthusiasm for PBT2 and its potential as an effective treatment for
Alzheimer's disease," said Geoffrey Kempler, chairman and CEO. "The
proceeds raised in this private offering will fully fund the upcoming Phase
IIa clinical trial of PBT2 to its conclusion. We are optimistic that this
trial will demonstrate the safety and tolerability, as well as the potency
and efficacy of PBT2 for the treatment of Alzheimer's disease. We believe
that our drug, unlike any currently available Alzheimer's drug, could offer
a disease modifying therapy for patients, which is of enormous interest to
major pharmaceutical companies."
Prana has received the regulatory and ethics approvals needed to start
the Phase IIa study of patients with early Alzheimer's disease at seven
Swedish sites. Screening of patients will commence next week. The Company
plans to announce the results of the PBT2 Phase IIa trial in the fourth
quarter of calendar 2007.
Mr. Kempler concluded, "PBT2 is one of over 300 proprietary molecules
that Prana has developed as candidates to treat a variety of
neurodegenerative disorders. We plan to use the balance of the funds raised
today for other activities over the next 12 months, designed to strengthen
the evidence in support of our MPAC ("Metal Protein Attenuating Compound")
theory and development platform for our target diseases."
The private placement will proceed in two stages: (1) shares available
for immediate issue, which represents a total of approximately A$5.6
million; and (2) the balance to be issued upon the Company receiving
shareholder approval at an Extraordinary General Meeting, which is expected
to occur on or about December 28, 2006.
Prana Biotechnology had 12.85 million ADRs (128,474,260 ordinary
shares) outstanding as of October 13, 2006; this private placement will
increase the total issued shares to 15.02 million ADRs (150,238,728
ordinary shares). Each 10 Prana ordinary shares traded on the ASX (ticker:
PBT) is equivalent to a single ADR traded on the NASDAQ Stock Market
(ticker: PRAN).
About Prana Biotechnology Limited
Prana Biotechnology was established to commercialize research into
Alzheimer's disease and other major age-related neuro-degenerative
disorders. The company was incorporated in 1997 and listed on the
Australian Stock Exchange in March 2000 and listed on NASDAQ in September
2002. Researchers at prominent international institutions including the
University of Melbourne and Massachusetts General Hospital, a teaching
hospital of Harvard Medical School, discovered Prana's technology.
For further information, please visit our web site at pranabio.
Forward-Looking Statements
This press release contains "forward-looking statements" within the
meaning of section 27A of the Securities Act of 1933 and section 21E of the
Securities Exchange Act of 1934. The Company has tried to identify such
forward-looking statements by use of such words as "expects," "intends,"
"hopes," "anticipates," "believes," "could," "may," "evidences" and
"estimates," and other similar expressions, but these words are not the
exclusive means of identifying such statements. Such statements include,
but are not limited to any statements relating to the Company's drug
development program, including, but not limited to the initiation, progress
and outcomes of clinical trials of the Company's drug development program,
including, but not limited to, PBT2, and any other statements that are not
historical facts. Such statements involve risks and uncertainties,
including, but not limited to, those risks and uncertainties relating to
the difficulties or delays in financing, development, testing, regulatory
approval, production and marketing of the Company's drug components,
including, but not limited to, PBT2, the ability of the Company to procure
additional future sources of financing, unexpected adverse side effects or
inadequate therapeutic efficacy of the Company's drug compounds, including,
but not limited to, PBT2, that could slow or prevent products coming to
market, the uncertainty of patent protection for the Company's intellectual
property or trade secrets, including, but not limited to, the intellectual
property relating to PBT2, and other risks detailed from time to time in
the filings the Company makes with Securities and Exchange Commission
including its annual reports on From 20-F and its reports on Form 6-K. Such
statements are based on management's current expectations, but actual
results may differ materially due to various factions including those risks
and uncertainties mentioned or referred to in this press release.
Accordingly, you should not rely on those forward-looking statements as a
prediction of actual future results.
Prana Biotechnology Limited
pranabio
Biotechnology Limited (Nasdaq: PRAN; ASX: PBT), today announced it has
entered into agreements to raise approximately 6.0 million US Dollars (7.8
million A Dollars) from new institutional investors in Australia, existing
institutional investors in the United States and a founding member of the
Company. As a result, the Company now has 10.2 million US Dollars (13.3 million A Dollars)
in cash to immediately commence its Phase IIa trial of PBT2 in Patients
with early Alzheimer's disease, for which it has received full regulatory
approval in Sweden.
The investment involves the purchase of 21.8 million ordinary shares
(equivalent to 2.18 million ADRs) at a price of A$0.357 per ordinary share
(approximately US$2.74 per ADR). In addition, the investors receive three-
year options to purchase an additional 4.35 million ordinary shares
(equivalent to 435,000 ADRs) at an exercise price of A$0.446 per ordinary
share (approximately US$3.42 per ADR), which could raise an additional
US$1.5 million (A$1.9 million) for the Company.
"We believe these commitments from new and existing investors reinforce
the enthusiasm for PBT2 and its potential as an effective treatment for
Alzheimer's disease," said Geoffrey Kempler, chairman and CEO. "The
proceeds raised in this private offering will fully fund the upcoming Phase
IIa clinical trial of PBT2 to its conclusion. We are optimistic that this
trial will demonstrate the safety and tolerability, as well as the potency
and efficacy of PBT2 for the treatment of Alzheimer's disease. We believe
that our drug, unlike any currently available Alzheimer's drug, could offer
a disease modifying therapy for patients, which is of enormous interest to
major pharmaceutical companies."
Prana has received the regulatory and ethics approvals needed to start
the Phase IIa study of patients with early Alzheimer's disease at seven
Swedish sites. Screening of patients will commence next week. The Company
plans to announce the results of the PBT2 Phase IIa trial in the fourth
quarter of calendar 2007.
Mr. Kempler concluded, "PBT2 is one of over 300 proprietary molecules
that Prana has developed as candidates to treat a variety of
neurodegenerative disorders. We plan to use the balance of the funds raised
today for other activities over the next 12 months, designed to strengthen
the evidence in support of our MPAC ("Metal Protein Attenuating Compound")
theory and development platform for our target diseases."
The private placement will proceed in two stages: (1) shares available
for immediate issue, which represents a total of approximately A$5.6
million; and (2) the balance to be issued upon the Company receiving
shareholder approval at an Extraordinary General Meeting, which is expected
to occur on or about December 28, 2006.
Prana Biotechnology had 12.85 million ADRs (128,474,260 ordinary
shares) outstanding as of October 13, 2006; this private placement will
increase the total issued shares to 15.02 million ADRs (150,238,728
ordinary shares). Each 10 Prana ordinary shares traded on the ASX (ticker:
PBT) is equivalent to a single ADR traded on the NASDAQ Stock Market
(ticker: PRAN).
About Prana Biotechnology Limited
Prana Biotechnology was established to commercialize research into
Alzheimer's disease and other major age-related neuro-degenerative
disorders. The company was incorporated in 1997 and listed on the
Australian Stock Exchange in March 2000 and listed on NASDAQ in September
2002. Researchers at prominent international institutions including the
University of Melbourne and Massachusetts General Hospital, a teaching
hospital of Harvard Medical School, discovered Prana's technology.
For further information, please visit our web site at pranabio.
Forward-Looking Statements
This press release contains "forward-looking statements" within the
meaning of section 27A of the Securities Act of 1933 and section 21E of the
Securities Exchange Act of 1934. The Company has tried to identify such
forward-looking statements by use of such words as "expects," "intends,"
"hopes," "anticipates," "believes," "could," "may," "evidences" and
"estimates," and other similar expressions, but these words are not the
exclusive means of identifying such statements. Such statements include,
but are not limited to any statements relating to the Company's drug
development program, including, but not limited to the initiation, progress
and outcomes of clinical trials of the Company's drug development program,
including, but not limited to, PBT2, and any other statements that are not
historical facts. Such statements involve risks and uncertainties,
including, but not limited to, those risks and uncertainties relating to
the difficulties or delays in financing, development, testing, regulatory
approval, production and marketing of the Company's drug components,
including, but not limited to, PBT2, the ability of the Company to procure
additional future sources of financing, unexpected adverse side effects or
inadequate therapeutic efficacy of the Company's drug compounds, including,
but not limited to, PBT2, that could slow or prevent products coming to
market, the uncertainty of patent protection for the Company's intellectual
property or trade secrets, including, but not limited to, the intellectual
property relating to PBT2, and other risks detailed from time to time in
the filings the Company makes with Securities and Exchange Commission
including its annual reports on From 20-F and its reports on Form 6-K. Such
statements are based on management's current expectations, but actual
results may differ materially due to various factions including those risks
and uncertainties mentioned or referred to in this press release.
Accordingly, you should not rely on those forward-looking statements as a
prediction of actual future results.
Prana Biotechnology Limited
pranabio
пятница, 20 мая 2011 г.
Blacks, Hispanics More Concerned About Alzheimer's Diseases Than Whites, Survey Finds
Blacks and Hispanics are more concerned than whites about Alzheimer's disease but less knowledgeable about means to delay its onset, according to a new survey, United Press International reports. The survey was presented recently at the Congressional Black Caucus' Spring Health Braintrust and National Minority Quality Forum leadership summit in Washington, D.C.
The findings are based on a national telephone survey conducted by Dutko Research and Polling and commissioned by pharmaceutical subsidiary Eisai and CBC. The survey included responses from 601 black adults and 602 Hispanics from March 26 to April 7. The survey found that blacks expressed higher levels of concern about Alzheimer's disease than their white counterparts, but about half of black respondents knew that there were actions that people could take to delay the onset of Alzheimer's disease.
Sharon Richardson of Eisai, who presented the findings at the summit, said in a statement, "African-Americans and Hispanics are more likely to develop Alzheimer's. In addition, they have higher rates of diabetes, hypertension, high cholesterol and cardiovascular disease -- all of which increase the risk of Alzheimer's" (United Press International, 5/4).
Reprinted with kind permission from kaisernetwork. You can view the entire Kaiser Daily Health Policy Report, search the archives, or sign up for email delivery at kaisernetwork/dailyreports/healthpolicy. The Kaiser Daily Health Policy Report is published for kaisernetwork, a free service of The Henry J. Kaiser Family Foundation.
© 2009 Advisory Board Company and Kaiser Family Foundation. All rights reserved.
The findings are based on a national telephone survey conducted by Dutko Research and Polling and commissioned by pharmaceutical subsidiary Eisai and CBC. The survey included responses from 601 black adults and 602 Hispanics from March 26 to April 7. The survey found that blacks expressed higher levels of concern about Alzheimer's disease than their white counterparts, but about half of black respondents knew that there were actions that people could take to delay the onset of Alzheimer's disease.
Sharon Richardson of Eisai, who presented the findings at the summit, said in a statement, "African-Americans and Hispanics are more likely to develop Alzheimer's. In addition, they have higher rates of diabetes, hypertension, high cholesterol and cardiovascular disease -- all of which increase the risk of Alzheimer's" (United Press International, 5/4).
Reprinted with kind permission from kaisernetwork. You can view the entire Kaiser Daily Health Policy Report, search the archives, or sign up for email delivery at kaisernetwork/dailyreports/healthpolicy. The Kaiser Daily Health Policy Report is published for kaisernetwork, a free service of The Henry J. Kaiser Family Foundation.
© 2009 Advisory Board Company and Kaiser Family Foundation. All rights reserved.
четверг, 19 мая 2011 г.
Hypertension Linked To Dementia In Older Women
Older women with hypertension are at increased risk for developing brain lesions that cause dementia later in life, according to data from the Women's Health Initiative Memory Study (WHIMS). The findings were published in the December 2009 online issue of the Journal of Clinical Hypertension.
The research was conducted as part of the Women's Health Initiative (WHI), the largest multi-site longitudinal study looking at health risks among postmenopausal women. WHIMS, which involves a subgroup of the women enrolled in WHI, looks at the influence of hormone therapy on thinking and memory. All the women in WHIMS were 65 or older.
Upon enrolling in the trial and annually during their participation in it, the women had their blood pressure measured and underwent tests to measure their cognitive ability. Some of the WHIMS participants - 1,403 of them - also underwent magnetic resonance imaging (MRI) at 14 U.S. academic centers in 2005 and 2006. All of these women were free of dementia when they enrolled. Examination of the data on these 1,403 women was led by Lewis H. Kuller, M.D., Dr.P.H., of the University of Pittsburgh, in conjunction with researchers at other WHI centers, including Dr. Sylvia Wassertheil-Smoller, Ph.D., professor of epidemiology and population health and the Dorothy and William Manealoff Foundation & Molly Rosen Chair in Social Medicine at Albert Einstein College of Medicine. Dr. Wassertheil-Smoller is also the principal investigator of Einstein's WHI and WHIMS studies.
The MRI studies revealed that women who, on entry to the WHIMS trial, had elevated blood pressure (defined as systolic blood pressure ?‰?140 mmHg, or diastolic blood pressure ?‰? 90 mmHg, or being on antihypertensive drug therapy), had significantly higher amounts of white matter lesions (WMLs) when they underwent MRIs eight years later. Normal blood pressure is defined as a systolic blood pressure of 120 or less and a diastolic pressure of 80 or less.
"Based on our findings, we would encourage women to maintain their blood pressure at normal levels, which may reduce their risk of dementia," says study co-author Dr. Wassertheil-Smoller.
The small blood vessels in the brain are especially susceptible to damage from even moderately elevated blood pressure - resulting in damage to the white matter served by those vessels. The brain's white matter is composed of whitish myelin-coated axons (nerve cell appendages) that allow nerve cells to communicate with each other and help the regions of the brain work together. Several studies have found that damage to white matter, as indicated by the presence of WMLs, seems to be an independent risk factor for dementia.
The current study reinforces earlier research showing that hypertension plays a role in causing dementia, suggesting that preventing hypertension from developing - through weight loss, exercise or other lifestyle changes - would be beneficial.
"However, we don't know whether hypertension treatment will prevent WMLs from developing, or how much blood pressure should be lowered so that these brain lesions won't occur," says Dr. Wassertheil-Smoller. "We do have suggestive evidence that the progression of WMLs can be slowed by anti-hypertensive therapy."
"Nonetheless," she adds, "it would be prudent for women to keep their blood pressure low, and the earlier in life they start doing so, the better. At present, keeping blood pressure at normal levels is probably the most effective way we know of to prevent dementia from occurring." According to baseline data on more than 98,705 women ages 50-79 who enrolled in the WHI study, 37.8% had hypertension, which is defined as systolic blood pressure ?‰?140 mm Hg and/or diastolic blood pressure ?‰?90 mm Hg or being on medication for high blood pressure; 64.3% of the hypertensive women were treated with drugs, and blood pressure was controlled in only 36.1% of the hypertensive women, with lower rates of control in the oldest group.
Dr. Wassertheil-Smoller notes that high blood pressure is also a major risk factor for stroke, "so it is certainly not good for the brain." She says that further clinical trials are needed to better establish whether anti-hypertensive therapy can prevent or slow WMLs, and, if so, to find the specific drug therapies that work best.
The study, "Relationship of Hypertension, Blood Pressure (BP) and BP Control with White Matter Abnormalities in the Women's Health Initiative Memory Study (WHIMS) MRI Study," was published in the December 16 online edition of the Journal of Clinical Hypertension. Other contributors include: Karen L. Margolis, M.D., Health Partners Research Foundation, Minneapolis, Minn.; Sarah A. Jaramillo, M.S. and Jeff Williamson, M.D., Wake Forest University School of Medicine, Winston-Salem, N.C.; Nick R. Bryan, M.D., University of Pennsylvania, Philadelphia, Penn.; Diana Kerwin, M.D., Froedtert & Medical College of Wisconsin, Milwaukee, Wis.; Marian Limacher, M.D., University of Florida, Gainesville, Fla.; and Jennifer G. Robinson, M.D., M.P.H., University of Iowa, Iowa City, Iowa.
Source
Albert Einstein College of Medicine of Yeshiva University
The research was conducted as part of the Women's Health Initiative (WHI), the largest multi-site longitudinal study looking at health risks among postmenopausal women. WHIMS, which involves a subgroup of the women enrolled in WHI, looks at the influence of hormone therapy on thinking and memory. All the women in WHIMS were 65 or older.
Upon enrolling in the trial and annually during their participation in it, the women had their blood pressure measured and underwent tests to measure their cognitive ability. Some of the WHIMS participants - 1,403 of them - also underwent magnetic resonance imaging (MRI) at 14 U.S. academic centers in 2005 and 2006. All of these women were free of dementia when they enrolled. Examination of the data on these 1,403 women was led by Lewis H. Kuller, M.D., Dr.P.H., of the University of Pittsburgh, in conjunction with researchers at other WHI centers, including Dr. Sylvia Wassertheil-Smoller, Ph.D., professor of epidemiology and population health and the Dorothy and William Manealoff Foundation & Molly Rosen Chair in Social Medicine at Albert Einstein College of Medicine. Dr. Wassertheil-Smoller is also the principal investigator of Einstein's WHI and WHIMS studies.
The MRI studies revealed that women who, on entry to the WHIMS trial, had elevated blood pressure (defined as systolic blood pressure ?‰?140 mmHg, or diastolic blood pressure ?‰? 90 mmHg, or being on antihypertensive drug therapy), had significantly higher amounts of white matter lesions (WMLs) when they underwent MRIs eight years later. Normal blood pressure is defined as a systolic blood pressure of 120 or less and a diastolic pressure of 80 or less.
"Based on our findings, we would encourage women to maintain their blood pressure at normal levels, which may reduce their risk of dementia," says study co-author Dr. Wassertheil-Smoller.
The small blood vessels in the brain are especially susceptible to damage from even moderately elevated blood pressure - resulting in damage to the white matter served by those vessels. The brain's white matter is composed of whitish myelin-coated axons (nerve cell appendages) that allow nerve cells to communicate with each other and help the regions of the brain work together. Several studies have found that damage to white matter, as indicated by the presence of WMLs, seems to be an independent risk factor for dementia.
The current study reinforces earlier research showing that hypertension plays a role in causing dementia, suggesting that preventing hypertension from developing - through weight loss, exercise or other lifestyle changes - would be beneficial.
"However, we don't know whether hypertension treatment will prevent WMLs from developing, or how much blood pressure should be lowered so that these brain lesions won't occur," says Dr. Wassertheil-Smoller. "We do have suggestive evidence that the progression of WMLs can be slowed by anti-hypertensive therapy."
"Nonetheless," she adds, "it would be prudent for women to keep their blood pressure low, and the earlier in life they start doing so, the better. At present, keeping blood pressure at normal levels is probably the most effective way we know of to prevent dementia from occurring." According to baseline data on more than 98,705 women ages 50-79 who enrolled in the WHI study, 37.8% had hypertension, which is defined as systolic blood pressure ?‰?140 mm Hg and/or diastolic blood pressure ?‰?90 mm Hg or being on medication for high blood pressure; 64.3% of the hypertensive women were treated with drugs, and blood pressure was controlled in only 36.1% of the hypertensive women, with lower rates of control in the oldest group.
Dr. Wassertheil-Smoller notes that high blood pressure is also a major risk factor for stroke, "so it is certainly not good for the brain." She says that further clinical trials are needed to better establish whether anti-hypertensive therapy can prevent or slow WMLs, and, if so, to find the specific drug therapies that work best.
The study, "Relationship of Hypertension, Blood Pressure (BP) and BP Control with White Matter Abnormalities in the Women's Health Initiative Memory Study (WHIMS) MRI Study," was published in the December 16 online edition of the Journal of Clinical Hypertension. Other contributors include: Karen L. Margolis, M.D., Health Partners Research Foundation, Minneapolis, Minn.; Sarah A. Jaramillo, M.S. and Jeff Williamson, M.D., Wake Forest University School of Medicine, Winston-Salem, N.C.; Nick R. Bryan, M.D., University of Pennsylvania, Philadelphia, Penn.; Diana Kerwin, M.D., Froedtert & Medical College of Wisconsin, Milwaukee, Wis.; Marian Limacher, M.D., University of Florida, Gainesville, Fla.; and Jennifer G. Robinson, M.D., M.P.H., University of Iowa, Iowa City, Iowa.
Source
Albert Einstein College of Medicine of Yeshiva University
среда, 18 мая 2011 г.
New Therapeutic Targets For Neurodegenerative Diseases
The focus of work in the Neurosciences Department's Neurobiology Laboratory at the University of the Basque Country's Faculty of Medicine and Odontology is the investigation of the molecular and cellular bases of neurodegenerative illnesses - those that affect the brain and the spinal cord. Some of these neurodegenerative illnesses are well known and affect a significant part of the population, such as Alzheimer's disease and multiple sclerosis.
Researchers at the University of the Basque Country (UPV-EHU) are studying the signals in the central nervous system - the brain and the spinal cord - that do not function well, in particular, those signals that cause the death of nerve cells. There are basically two types of cells in the central nervous system: neurones and the glial cells. Both types are sensitive to these functioning errors and both can die. In the case of Alzheimer's disease, it is the neurones, above all, that die. However, in the case of multiple sclerosis, it is a class of glial cells - known as oligodendrocytes - that perish.
From in vitro cells to biological samples of human origin
The researchers at the Neurobiology Laboratory are investigating cells in cultures - neurones, oligodendrocytes or other cells of the nervous system -, and are trying to reproduce in vitro circumstances that are thought to be relevant in these ailments. That is to say, they are creating the conditions that cause the death of these cells, in order to determine what molecules intervene in the process - from the moment of the lethal signal to the point where the cells collapse. In this type of experimental work a series of molecules involved in the death process are identified, the aim being to come up with pharmaceutical medicines that will improve treatment.
Apart from working with in vitro cells, they are also experimenting with animals that reproduce some of the elements involved in neurodegenerative illnesses under certain conditions, i.e. sensory symptoms, motor symptoms, etc. and that can be induced in these animals. And they are examining if these substances that have proved to be interesting with the in vitro cells are also efficacious in these experimental models of the diseases.
Moreover, over the past few years they have had the opportunity to study samples of brains of patients who have died of some neurodegenerative illness, such as, for example, multiple sclerosis. The illnesses leaves a mark in these samples and, although the brain has been at a terminal stage of the illness, they can investigate to see if there are signs of alterations to the molecules similar to those observed in the experiments, both with cells and with the animals. In this way it can be determined if the molecular targets discovered experimentally are relevant or not to the neurodegenerative processes and, if they are, develop pharmaceutical medicines that can neutralise these processes or the elements that enable them to progress, the goal being to halt the process of death.
In collaboration with neurologists they have also been able to access biological samples of patients who have given their consent and donated them to research. Biological samples such as, fundamentally, blood, given that changes in blood plasma that may indicate alterations at the brain level can be identified.
In search of biological samples
All this is a dynamic process that enables clues to be found and which are, in some cases, relevant for developing pharmaceutical drugs that can halt, or at least slow down, the course of a neurodegenerative illness. Apart from finding these molecules or targets that interact with pharmaceutical medicines, in order to stop the process of progressive deterioration, substances that favour the survival of the neurones and oligodendrocytes are also sought; substances such as, for example, antioxidants, given that, in many of the neurodegenerative illnesses the cells die because oxidative stress is produced. In recent years the Neurobiology Laboratory researchers have found a number of antioxidants that put a brake on the dying process and can act as a neuroprotector. Antioxidants of natural origin that are in our diet - fruit, vegetables, and so on - and which, in some way appear to alleviate the damage cause by these illnesses.
In short, the goal is to gain more knowledge about the molecular bases of these pathologies, define therapeutic targets (molecules of the cell that recognise a pharmaceutical drug and thus respond to it) and, in the last analysis, to come up with pharmaceutical medicines that improve treatment.
Contact: Irati Kortabitarte
Elhuyar Fundazioa
Researchers at the University of the Basque Country (UPV-EHU) are studying the signals in the central nervous system - the brain and the spinal cord - that do not function well, in particular, those signals that cause the death of nerve cells. There are basically two types of cells in the central nervous system: neurones and the glial cells. Both types are sensitive to these functioning errors and both can die. In the case of Alzheimer's disease, it is the neurones, above all, that die. However, in the case of multiple sclerosis, it is a class of glial cells - known as oligodendrocytes - that perish.
From in vitro cells to biological samples of human origin
The researchers at the Neurobiology Laboratory are investigating cells in cultures - neurones, oligodendrocytes or other cells of the nervous system -, and are trying to reproduce in vitro circumstances that are thought to be relevant in these ailments. That is to say, they are creating the conditions that cause the death of these cells, in order to determine what molecules intervene in the process - from the moment of the lethal signal to the point where the cells collapse. In this type of experimental work a series of molecules involved in the death process are identified, the aim being to come up with pharmaceutical medicines that will improve treatment.
Apart from working with in vitro cells, they are also experimenting with animals that reproduce some of the elements involved in neurodegenerative illnesses under certain conditions, i.e. sensory symptoms, motor symptoms, etc. and that can be induced in these animals. And they are examining if these substances that have proved to be interesting with the in vitro cells are also efficacious in these experimental models of the diseases.
Moreover, over the past few years they have had the opportunity to study samples of brains of patients who have died of some neurodegenerative illness, such as, for example, multiple sclerosis. The illnesses leaves a mark in these samples and, although the brain has been at a terminal stage of the illness, they can investigate to see if there are signs of alterations to the molecules similar to those observed in the experiments, both with cells and with the animals. In this way it can be determined if the molecular targets discovered experimentally are relevant or not to the neurodegenerative processes and, if they are, develop pharmaceutical medicines that can neutralise these processes or the elements that enable them to progress, the goal being to halt the process of death.
In collaboration with neurologists they have also been able to access biological samples of patients who have given their consent and donated them to research. Biological samples such as, fundamentally, blood, given that changes in blood plasma that may indicate alterations at the brain level can be identified.
In search of biological samples
All this is a dynamic process that enables clues to be found and which are, in some cases, relevant for developing pharmaceutical drugs that can halt, or at least slow down, the course of a neurodegenerative illness. Apart from finding these molecules or targets that interact with pharmaceutical medicines, in order to stop the process of progressive deterioration, substances that favour the survival of the neurones and oligodendrocytes are also sought; substances such as, for example, antioxidants, given that, in many of the neurodegenerative illnesses the cells die because oxidative stress is produced. In recent years the Neurobiology Laboratory researchers have found a number of antioxidants that put a brake on the dying process and can act as a neuroprotector. Antioxidants of natural origin that are in our diet - fruit, vegetables, and so on - and which, in some way appear to alleviate the damage cause by these illnesses.
In short, the goal is to gain more knowledge about the molecular bases of these pathologies, define therapeutic targets (molecules of the cell that recognise a pharmaceutical drug and thus respond to it) and, in the last analysis, to come up with pharmaceutical medicines that improve treatment.
Contact: Irati Kortabitarte
Elhuyar Fundazioa
вторник, 17 мая 2011 г.
NIH Grant To Study Brain Disorder Among Chinese
A new University of Central Florida study could help tens of thousands of Chinese-Americans who have difficulty speaking after they suffer from strokes or other illnesses.
Assistant Professor Anthony Kong of Communication Sciences & Disorders has been awarded a first-of-its-kind $727,000 National Institutes of Health grant to research aphasia among Chinese speakers.
Aphasia is a condition in which people have difficulty understanding and speaking, usually after a stroke or head trauma. The trauma damages the left side of the brain, which is largely responsible for language comprehension and production. A tumor, brain infection or dementia can also cause the condition.
About 1 million people in the United States have aphasia. Up to 38 percent of people who suffer a stroke develop it.
"Aphasia can have devastating effects on daily communication and conversational skills that can severely hamper qualify of life," Kong said. "The overarching goal of this study is to improve assessment methods and provide some treatment guidelines for Chinese speakers with aphasia worldwide."
Several studies have looked at how the brain processes the English language and how aphasia impacts language ability among English speakers. But no large-scale, comprehensive studies have been conducted among any Asian language speakers.
Contrary to popular belief, people do not acquire and process all languages the same. Existing research shows the brain's processing pattern for acquiring Chinese languages is quite different from Latin-based languages, which makes it essential to have the kind of information this study will produce available for assessment and treatment, Kong said.
There are very distinct ways that aphasia manifests itself among Cantonese speakers compared to English speakers, Kong said. He saw it first-hand while earning his doctorate and working in a Singapore hospital that saw hundreds of patients with aphasia who spoke English, Mandarin, Cantonese, Malay and Hindi, among other languages.
Much of Kong's work will be conducted in his native Hong Kong because the community has a homogenous Cantonese-speaking population. Data and recommendations from the study, however, will have implications for all Chinese speakers with aphasia around the world. The information also will help further research about conditions across different languages.
Beginning in June, Kong and his team will interview and conduct extensive videotaped observations of more than 360 native Cantonese speakers with and without the condition. He will then create a database of information, which will include the distinctive linguistic symptoms of Chinese aphasia, the rhythm, stress and intonation of Chinese aphasic speech, and non-verbal behaviors of Chinese speakers with aphasia as a result of stroke. He will also document the same three categories in non-aphasiac subjects to create a baseline for comparison.
The information his team will collect is not available anywhere at this time and is essential in developing proper diagnosis and treatment of the condition among Chinese speakers. There are only a few existing tools to assess the condition among Cantonese speakers, one of which Kong developed when he was a graduate student. In comparison, more than 200 assessment tools exist for English speakers.
Kong's team includes Dr. Sam Po Law of the University of Hong Kong, Dr. Alice Su Ying Lee of University College Cork in the Republic of Ireland and several students at the University of Hong Kong. Several hospitals and service agencies also are helping with the study. Pilot programs conducted the past two summers were funded by grants from UCF's College of Health and Public Affairs.
Source:
Zenaida Gonzalez Kotala
University of Central Florida
Assistant Professor Anthony Kong of Communication Sciences & Disorders has been awarded a first-of-its-kind $727,000 National Institutes of Health grant to research aphasia among Chinese speakers.
Aphasia is a condition in which people have difficulty understanding and speaking, usually after a stroke or head trauma. The trauma damages the left side of the brain, which is largely responsible for language comprehension and production. A tumor, brain infection or dementia can also cause the condition.
About 1 million people in the United States have aphasia. Up to 38 percent of people who suffer a stroke develop it.
"Aphasia can have devastating effects on daily communication and conversational skills that can severely hamper qualify of life," Kong said. "The overarching goal of this study is to improve assessment methods and provide some treatment guidelines for Chinese speakers with aphasia worldwide."
Several studies have looked at how the brain processes the English language and how aphasia impacts language ability among English speakers. But no large-scale, comprehensive studies have been conducted among any Asian language speakers.
Contrary to popular belief, people do not acquire and process all languages the same. Existing research shows the brain's processing pattern for acquiring Chinese languages is quite different from Latin-based languages, which makes it essential to have the kind of information this study will produce available for assessment and treatment, Kong said.
There are very distinct ways that aphasia manifests itself among Cantonese speakers compared to English speakers, Kong said. He saw it first-hand while earning his doctorate and working in a Singapore hospital that saw hundreds of patients with aphasia who spoke English, Mandarin, Cantonese, Malay and Hindi, among other languages.
Much of Kong's work will be conducted in his native Hong Kong because the community has a homogenous Cantonese-speaking population. Data and recommendations from the study, however, will have implications for all Chinese speakers with aphasia around the world. The information also will help further research about conditions across different languages.
Beginning in June, Kong and his team will interview and conduct extensive videotaped observations of more than 360 native Cantonese speakers with and without the condition. He will then create a database of information, which will include the distinctive linguistic symptoms of Chinese aphasia, the rhythm, stress and intonation of Chinese aphasic speech, and non-verbal behaviors of Chinese speakers with aphasia as a result of stroke. He will also document the same three categories in non-aphasiac subjects to create a baseline for comparison.
The information his team will collect is not available anywhere at this time and is essential in developing proper diagnosis and treatment of the condition among Chinese speakers. There are only a few existing tools to assess the condition among Cantonese speakers, one of which Kong developed when he was a graduate student. In comparison, more than 200 assessment tools exist for English speakers.
Kong's team includes Dr. Sam Po Law of the University of Hong Kong, Dr. Alice Su Ying Lee of University College Cork in the Republic of Ireland and several students at the University of Hong Kong. Several hospitals and service agencies also are helping with the study. Pilot programs conducted the past two summers were funded by grants from UCF's College of Health and Public Affairs.
Source:
Zenaida Gonzalez Kotala
University of Central Florida
понедельник, 16 мая 2011 г.
Testing New Fluorescent Lighting For Synchronizing Older Patients' Sleep-Wake Cycles
Change the lighting; improve your health. It's a strategy researchers from Case Western Reserve University's Frances Payne Bolton School of Nursing and the School of Medicine, the Geriatric Research Education and Clinical Center at the Louis Stokes Cleveland Veterans Affairs Medical Center (GRECC), Rensselaer Polytechnic Institute's Lighting Research Center and GE Consumer & Industrial have begun to test in a long-term care facility where daylight, which has proven health benefits, is not readily available.
The researchers removed some standard fluorescent lighting and installed new blue-white lamp prototypes developed by GE scientists at the company's Nela Park campus.
Research team members hypothesize that periods of blue light, like daylight, can help regulate the sleep-wake rhythm, which is a behavioral pattern linked to the 24-hour biochemical circadian cycle of the hormone melatonin. Depending on the level of the hormone, people are awake or sleepy.
The researchers want to regulate the sleep-wake cycle by regulating the amount of exposure to blue (wakefulness) and yellow (sleepiness) light. By increasing exposure to blue-white light during the day and yellow-white light in the evening, researchers hope to help patients regulate their sleep-wake cycles so that they are more awake during the day and more asleep at night.
Patricia Higgins, associate professor at the School of Nursing and one of the lead investigators, says the project may prove to be especially beneficial for people suffering from dementia.
In a recently conducted pilot study with five male patients, each suffering from dementia and living in a long-term care facility, researchers installed the blue-white lights in an activities room where most residents gathered for meals and daytime activities.
"We wanted to see whether lighting could affect the participants' sleep-wake rhythms," says Higgins. "While the group was small, the results show promise in raising activity levels during daytime hours and increasing sleep at nighttime."
The researchers plan a larger study with residents with dementia at two Northeast Ohio long-term care facilities. The study will include men and women to see if light impacts the genders differently. An unexpected side effect of the lighting is that once adjusted to the blue-white light, most employees reported that they liked the new lighting conditions.
For a number of decades it has been known that light affects how people feel. Those particularly sensitive to changes in light have benefited from a boost in the brightness of light sources. The new lighting used in the test changes the color without overpowering individuals with brightness, according to the researchers.
"Why waste light if you can tune it to the right color and maximize the amount of useful light," says Mariana Figueiro, assistant professor at Rensselaer and program director at Rensselaer's Lighting Research Center."Light is a good stimulus for the circadian system, which regulates your sleep-wake cycles," says Thomas Hornick, associate director at the GRECC at the Veterans Administration Hospital and associate professor at the Case Western Reserve University School of Medicine. He says it is known that certain drugs do better when given at the appropriate time in the circadian cycle.
As a safe, nonpharmacological intervention, researchers also hope to apply information from the study to changing the lighting in hospitals where patients may have a speedier recovery or improved quality of life with a good night's rest.
"We're innovators at heart," says Mark Duffy, engineering and technology systems manager, GE Consumer & Industrial. "Our goal entering this collaboration was to apply the passion and inventiveness, which we bring to every customer need or application, to a project that has implications for society at large. We're proud to be part of this effort."
If changing the lighting works to improve health, the researchers plan to take what would be a natural next step: trying to influence public policy to include new lighting standards for healthcare facilities.
Source:
Susan Griffith
Case Western Reserve University
The researchers removed some standard fluorescent lighting and installed new blue-white lamp prototypes developed by GE scientists at the company's Nela Park campus.
Research team members hypothesize that periods of blue light, like daylight, can help regulate the sleep-wake rhythm, which is a behavioral pattern linked to the 24-hour biochemical circadian cycle of the hormone melatonin. Depending on the level of the hormone, people are awake or sleepy.
The researchers want to regulate the sleep-wake cycle by regulating the amount of exposure to blue (wakefulness) and yellow (sleepiness) light. By increasing exposure to blue-white light during the day and yellow-white light in the evening, researchers hope to help patients regulate their sleep-wake cycles so that they are more awake during the day and more asleep at night.
Patricia Higgins, associate professor at the School of Nursing and one of the lead investigators, says the project may prove to be especially beneficial for people suffering from dementia.
In a recently conducted pilot study with five male patients, each suffering from dementia and living in a long-term care facility, researchers installed the blue-white lights in an activities room where most residents gathered for meals and daytime activities.
"We wanted to see whether lighting could affect the participants' sleep-wake rhythms," says Higgins. "While the group was small, the results show promise in raising activity levels during daytime hours and increasing sleep at nighttime."
The researchers plan a larger study with residents with dementia at two Northeast Ohio long-term care facilities. The study will include men and women to see if light impacts the genders differently. An unexpected side effect of the lighting is that once adjusted to the blue-white light, most employees reported that they liked the new lighting conditions.
For a number of decades it has been known that light affects how people feel. Those particularly sensitive to changes in light have benefited from a boost in the brightness of light sources. The new lighting used in the test changes the color without overpowering individuals with brightness, according to the researchers.
"Why waste light if you can tune it to the right color and maximize the amount of useful light," says Mariana Figueiro, assistant professor at Rensselaer and program director at Rensselaer's Lighting Research Center."Light is a good stimulus for the circadian system, which regulates your sleep-wake cycles," says Thomas Hornick, associate director at the GRECC at the Veterans Administration Hospital and associate professor at the Case Western Reserve University School of Medicine. He says it is known that certain drugs do better when given at the appropriate time in the circadian cycle.
As a safe, nonpharmacological intervention, researchers also hope to apply information from the study to changing the lighting in hospitals where patients may have a speedier recovery or improved quality of life with a good night's rest.
"We're innovators at heart," says Mark Duffy, engineering and technology systems manager, GE Consumer & Industrial. "Our goal entering this collaboration was to apply the passion and inventiveness, which we bring to every customer need or application, to a project that has implications for society at large. We're proud to be part of this effort."
If changing the lighting works to improve health, the researchers plan to take what would be a natural next step: trying to influence public policy to include new lighting standards for healthcare facilities.
Source:
Susan Griffith
Case Western Reserve University
воскресенье, 15 мая 2011 г.
Researchers From The University Of The Basque Country Find New Path For Novel Alzheimer's Therapies
Researchers from the University of the Basque Country (UPV/EHU) have found a new Alzheimer's-related mechanism that could give rise to the development of new therapies against this disease. The study was recently published in the Cell Calcium journal, and the authors have already applied for a European patent to protect the commercial exploitation of this new discovery.
The novelty lies in a new mechanism through which the amyloid peptide, the major pathogen in Alzheimer's disease, provokes neuronal death. The Basque researchers have found that this peptide activates some receptors that lead cells to overexcitation and subsequent death; when such receptors are blocked with specific drugs, neurons are protected from the peptide-related lethal effects. This finding is particularly relevant for the development of new therapies slowing down Alzheimer's progression.
The research work was supervised by Dr. Carlos Matute, Director of Neurotek research centre and Head of the Neurobiology Laboratory of the Neurosciences Department at the University of the Basque Country (UPV/EHU). The research team led by Dr. Matute deals with the molecular and cell fundamentals of neurodegenerative diseases such as Alzheimer's or multiple sclerosis. In particular, it focuses on the mechanism leading to cell death in the nervous system by using different tests based on cell cultures, experimental animals, human brains coming from demised people suffering these diseases and living patients' samples.
This team, which has already released many patents, also searches for markers supporting early diagnosis of these diseases.
Source: Elhuyar Fundazioa
The novelty lies in a new mechanism through which the amyloid peptide, the major pathogen in Alzheimer's disease, provokes neuronal death. The Basque researchers have found that this peptide activates some receptors that lead cells to overexcitation and subsequent death; when such receptors are blocked with specific drugs, neurons are protected from the peptide-related lethal effects. This finding is particularly relevant for the development of new therapies slowing down Alzheimer's progression.
The research work was supervised by Dr. Carlos Matute, Director of Neurotek research centre and Head of the Neurobiology Laboratory of the Neurosciences Department at the University of the Basque Country (UPV/EHU). The research team led by Dr. Matute deals with the molecular and cell fundamentals of neurodegenerative diseases such as Alzheimer's or multiple sclerosis. In particular, it focuses on the mechanism leading to cell death in the nervous system by using different tests based on cell cultures, experimental animals, human brains coming from demised people suffering these diseases and living patients' samples.
This team, which has already released many patents, also searches for markers supporting early diagnosis of these diseases.
Source: Elhuyar Fundazioa
суббота, 14 мая 2011 г.
Findings Suggest That A Biphasic Sleep Schedule Not Only Refreshes The Mind, But Can Make You Smarter
If you see a student dozing in the library or a co-worker catching 40 winks in her cubicle, don't roll your eyes. New research from the University of California, Berkeley, shows that an hour's nap can dramatically boost and restore your brain power. Indeed, the findings suggest that a biphasic sleep schedule not only refreshes the mind, but can make you smarter.
Conversely, the more hours we spend awake, the more sluggish our minds become, according to the findings. The results support previous data from the same research team that pulling an all-nighter - a common practice at college during midterms and finals - decreases the ability to cram in new facts by nearly 40 percent, due to a shutdown of brain regions during sleep deprivation.
"Sleep not only rights the wrong of prolonged wakefulness but, at a neurocognitive level, it moves you beyond where you were before you took a nap," said Matthew Walker, an assistant professor of psychology at UC Berkeley and the lead investigator of these studies.
In the recent UC Berkeley sleep study, 39 healthy young adults were divided into two groups - nap and no-nap. At noon, all the participants were subjected to a rigorous learning task intended to tax the hippocampus, a region of the brain that helps store fact-based memories. Both groups performed at comparable levels.
At 2 p.m., the nap group took a 90-minute siesta while the no-nap group stayed awake. Later that day, at 6 p.m., participants performed a new round of learning exercises. Those who remained awake throughout the day became worse at learning. In contrast, those who napped did markedly better and actually improved in their capacity to learn.
These findings reinforce the researchers' hypothesis that sleep is needed to clear the brain's short-term memory storage and make room for new information, said Walker, who presented his preliminary findings on Sunday, Feb. 21, at the annual meeting of the American Association of the Advancement of Science (AAAS) in San Diego, Calif.
Since 2007, Walker and other sleep researchers have established that fact-based memories are temporarily stored in the hippocampus before being sent to the brain's prefrontal cortex, which may have more storage space.
"It's as though the e-mail inbox in your hippocampus is full and, until you sleep and clear out those fact e-mails, you're not going to receive any more mail. It's just going to bounce until you sleep and move it into another folder," Walker said.
In the latest study, Walker and his team have broken new ground in discovering that this memory- refreshing process occurs when nappers are engaged in a specific stage of sleep. Electroencephalogram tests, which measure electrical activity in the brain, indicated that this refreshing of memory capacity is related to Stage 2 non-REM sleep, which takes place between deep sleep (non-REM) and the dream state known as Rapid Eye Movement (REM). Previously, the purpose of this stage was unclear, but the new results offer evidence as to why humans spend at least half their sleeping hours in Stage 2, non-REM, Walker said.
"I can't imagine Mother Nature would have us spend 50 percent of the night going from one sleep stage to another for no reason," Walker said. "Sleep is sophisticated. It acts locally to give us what we need."
Walker and his team will go on to investigate whether the reduction of sleep experienced by people as they get older is related to the documented decrease in our ability to learn as we age. Finding that link may be helpful in understanding such neurodegenerative conditions as Alzheimer's disease, Walker said.
In addition to Walker, co-investigators of these new findings are UC Berkeley post-doctoral fellow Bryce A. Mander and psychology undergraduate Sangeetha Santhanam.
Source:
Yasmin Anwar
University of California - Berkeley
Conversely, the more hours we spend awake, the more sluggish our minds become, according to the findings. The results support previous data from the same research team that pulling an all-nighter - a common practice at college during midterms and finals - decreases the ability to cram in new facts by nearly 40 percent, due to a shutdown of brain regions during sleep deprivation.
"Sleep not only rights the wrong of prolonged wakefulness but, at a neurocognitive level, it moves you beyond where you were before you took a nap," said Matthew Walker, an assistant professor of psychology at UC Berkeley and the lead investigator of these studies.
In the recent UC Berkeley sleep study, 39 healthy young adults were divided into two groups - nap and no-nap. At noon, all the participants were subjected to a rigorous learning task intended to tax the hippocampus, a region of the brain that helps store fact-based memories. Both groups performed at comparable levels.
At 2 p.m., the nap group took a 90-minute siesta while the no-nap group stayed awake. Later that day, at 6 p.m., participants performed a new round of learning exercises. Those who remained awake throughout the day became worse at learning. In contrast, those who napped did markedly better and actually improved in their capacity to learn.
These findings reinforce the researchers' hypothesis that sleep is needed to clear the brain's short-term memory storage and make room for new information, said Walker, who presented his preliminary findings on Sunday, Feb. 21, at the annual meeting of the American Association of the Advancement of Science (AAAS) in San Diego, Calif.
Since 2007, Walker and other sleep researchers have established that fact-based memories are temporarily stored in the hippocampus before being sent to the brain's prefrontal cortex, which may have more storage space.
"It's as though the e-mail inbox in your hippocampus is full and, until you sleep and clear out those fact e-mails, you're not going to receive any more mail. It's just going to bounce until you sleep and move it into another folder," Walker said.
In the latest study, Walker and his team have broken new ground in discovering that this memory- refreshing process occurs when nappers are engaged in a specific stage of sleep. Electroencephalogram tests, which measure electrical activity in the brain, indicated that this refreshing of memory capacity is related to Stage 2 non-REM sleep, which takes place between deep sleep (non-REM) and the dream state known as Rapid Eye Movement (REM). Previously, the purpose of this stage was unclear, but the new results offer evidence as to why humans spend at least half their sleeping hours in Stage 2, non-REM, Walker said.
"I can't imagine Mother Nature would have us spend 50 percent of the night going from one sleep stage to another for no reason," Walker said. "Sleep is sophisticated. It acts locally to give us what we need."
Walker and his team will go on to investigate whether the reduction of sleep experienced by people as they get older is related to the documented decrease in our ability to learn as we age. Finding that link may be helpful in understanding such neurodegenerative conditions as Alzheimer's disease, Walker said.
In addition to Walker, co-investigators of these new findings are UC Berkeley post-doctoral fellow Bryce A. Mander and psychology undergraduate Sangeetha Santhanam.
Source:
Yasmin Anwar
University of California - Berkeley
пятница, 13 мая 2011 г.
AHRQ News And Numbers: Approximately Five Percent Of Seniors Report One Or More Cognitive Disorders
Slightly over over 5 percent of the nearly 39 million Americans age 65 and older in 2007 reported one or more cognitive disorders, such as senility or dementia, according to the latest News and Numbers from the Agency for Healthcare Research and Quality.
Seniors age 85 and older were the most likely to have reported one or more cognitive disorders (18.4 percent), compared to seniors ages 75 to 84 (6 percent) and seniors ages 65 to 74 (1.1 percent).
AHRQ found that for elderly Americans age 65 and older in 2007:
- Seniors with less than a high school education were more likely to have reported one or more cognitive disorders than seniors that were high school graduates (8.6 percent and 4.9 percent, respectively) or seniors with more than a high school education (2.7 percent ).
- Nearly 8 percent of poor seniors reported one or more cognitive disorders compared to 4.1 percent of middle and high income seniors reporting such a condition.
- Nearly 11 percent of seniors who had both Medicare and another type of supplemental public insurance reported one or more cognitive disorders, compared to 5 percent of seniors with Medicare only and 4.1 percent of seniors with Medicare and supplemental private insurance.
- Average annual health care expense for seniors reporting one or more cognitive disorders totaled $15,549 a year, compared to $9,019 for seniors not reporting any cognitive disorders.
AHRQ, which is part of the U.S. Department of Health and Human Services, improves the quality, safety, efficiency, and effectiveness of health care for all Americans. The data in this AHRQ News and Numbers summary are taken from the Medical Expenditure Panel Survey (MEPS), a detailed source of information on the health services used by Americans, the frequency with which they are used, the cost of those services, and how they are paid. For more information, go to: Person Characteristics of the Elderly Reporting One or More Cognitive Disorders, 2007 .
Source:
AHRQ News and Numbers
Seniors age 85 and older were the most likely to have reported one or more cognitive disorders (18.4 percent), compared to seniors ages 75 to 84 (6 percent) and seniors ages 65 to 74 (1.1 percent).
AHRQ found that for elderly Americans age 65 and older in 2007:
- Seniors with less than a high school education were more likely to have reported one or more cognitive disorders than seniors that were high school graduates (8.6 percent and 4.9 percent, respectively) or seniors with more than a high school education (2.7 percent ).
- Nearly 8 percent of poor seniors reported one or more cognitive disorders compared to 4.1 percent of middle and high income seniors reporting such a condition.
- Nearly 11 percent of seniors who had both Medicare and another type of supplemental public insurance reported one or more cognitive disorders, compared to 5 percent of seniors with Medicare only and 4.1 percent of seniors with Medicare and supplemental private insurance.
- Average annual health care expense for seniors reporting one or more cognitive disorders totaled $15,549 a year, compared to $9,019 for seniors not reporting any cognitive disorders.
AHRQ, which is part of the U.S. Department of Health and Human Services, improves the quality, safety, efficiency, and effectiveness of health care for all Americans. The data in this AHRQ News and Numbers summary are taken from the Medical Expenditure Panel Survey (MEPS), a detailed source of information on the health services used by Americans, the frequency with which they are used, the cost of those services, and how they are paid. For more information, go to: Person Characteristics of the Elderly Reporting One or More Cognitive Disorders, 2007 .
Source:
AHRQ News and Numbers
среда, 11 мая 2011 г.
Alzheimer's And Parkinson's Disease Research Presented By Revalesio At National Scientific Conference
Revalesio Corporation and Rush University will present research on the use of RNS60 at the American Society of Neurochemistry (ASN) meeting in St. Louis.
Researchers at Rush University Medical Center demonstrated profound anti-inflammatory activity of RNS60, a biologically active fluid possessing charge-stabilized nanostructures (CSN), in models of Alzheimer's and Parkinson's diseases. These findings establish RNS60 as a strong candidate for further development as a novel therapeutic in neurodegenerative diseases.
The ASN's annual conference, scheduled for March 16-18, brings together molecular and cellular neuroscientists to share the latest research and advance the field of neurology.
RNS60 demonstrates "protective" effect in Alzheimer's disease and Parkinson's disease
Research conducted at Rush University revealed that RNS60 protected cultured cells against beta amyloid-induced cell death, a known driver of Alzheimer's disease. Since RNS60 is unique in its anti-inflammatory activity, these results identify a novel approach to inhibiting neuronal damage from beta amyloid and potentially a new approach for treating Alzheimer's disease. Revalesio will present further research demonstrating the prevention of tau hyperphosphorylation - another key factor in the progression of Alzheimer's disease - at the American Academy of Neurology meeting April 9-16 in Honolulu, HI.
At the ASN conference, Revalesio will also present data related to Parkinson's disease. In a neurotoxin model of the disease, RNS60 protected neurons, restored dopamine levels, and improved the motor function of Parkinson's affected mice. These results suggest a potential therapeutic benefit of RNS60 for patients suffering from Parkinson's disease.
About charge-stabilized nanostructures (CSN)
Revalesio has pioneered the novel use of charge-stabilized nanostructures to alter whole cell conductance through effects on voltage-gated ion channels and other voltage-sensing proteins, thereby modulating the expression of G protein-coupled receptors and the secretion of cytokines, chemokines and adhesion molecules. These changes to whole cell conductance reduce inflammatory signals that are linked to numerous diseases, including neurodegenerative, respiratory and cardiovascular diseases.
Source:
Revalesio Corporation
Researchers at Rush University Medical Center demonstrated profound anti-inflammatory activity of RNS60, a biologically active fluid possessing charge-stabilized nanostructures (CSN), in models of Alzheimer's and Parkinson's diseases. These findings establish RNS60 as a strong candidate for further development as a novel therapeutic in neurodegenerative diseases.
The ASN's annual conference, scheduled for March 16-18, brings together molecular and cellular neuroscientists to share the latest research and advance the field of neurology.
RNS60 demonstrates "protective" effect in Alzheimer's disease and Parkinson's disease
Research conducted at Rush University revealed that RNS60 protected cultured cells against beta amyloid-induced cell death, a known driver of Alzheimer's disease. Since RNS60 is unique in its anti-inflammatory activity, these results identify a novel approach to inhibiting neuronal damage from beta amyloid and potentially a new approach for treating Alzheimer's disease. Revalesio will present further research demonstrating the prevention of tau hyperphosphorylation - another key factor in the progression of Alzheimer's disease - at the American Academy of Neurology meeting April 9-16 in Honolulu, HI.
At the ASN conference, Revalesio will also present data related to Parkinson's disease. In a neurotoxin model of the disease, RNS60 protected neurons, restored dopamine levels, and improved the motor function of Parkinson's affected mice. These results suggest a potential therapeutic benefit of RNS60 for patients suffering from Parkinson's disease.
About charge-stabilized nanostructures (CSN)
Revalesio has pioneered the novel use of charge-stabilized nanostructures to alter whole cell conductance through effects on voltage-gated ion channels and other voltage-sensing proteins, thereby modulating the expression of G protein-coupled receptors and the secretion of cytokines, chemokines and adhesion molecules. These changes to whole cell conductance reduce inflammatory signals that are linked to numerous diseases, including neurodegenerative, respiratory and cardiovascular diseases.
Source:
Revalesio Corporation
вторник, 10 мая 2011 г.
Diabetes Drug Could Be A Potential Treatment For Alzheimer's - Alzheimer's Society Comment
New research claims that a drug commonly used in the treatment of type II diabetes can help treat Alzheimer's disease.
A paper published in the Proceedings of the National Academy of Sciences of the United States of America (PNAS) found that metformin can reduce the amount of the abnormal tau protein in the brains of mice. Healthy nerve cells produce tau but in Alzheimer's, the abnormal form is produced which does not function correctly.
Alzheimer's Society comment:
'Previous research has suggested that metformin reduces the risk of dementia in diabetic people, and this study provides some understanding of why this might be. The fact that the drug is safe for humans means it could potentially be tested more quickly than a completely new drug. However, further research is needed to fully understand the link between diabetes and Alzheimer's.'
'A million more people are set to develop dementia in the next 10 years. It is important that people maintain a healthy lifestyle in order to reduce their risk and that greater investment in dementia research is made to further our understanding of the condition.'
Dr Anne Corbett
Research Communications Manager
Research Reference: Professor Susann Schweiger, et al. 'The Biguanidemetformin acts on tauphosphorylation via mTOR/PP2vAsignalling', Proceedings of the National Academy of Sciences of the United States of America, November 2010.
Source:
Alzheimer's Society
A paper published in the Proceedings of the National Academy of Sciences of the United States of America (PNAS) found that metformin can reduce the amount of the abnormal tau protein in the brains of mice. Healthy nerve cells produce tau but in Alzheimer's, the abnormal form is produced which does not function correctly.
Alzheimer's Society comment:
'Previous research has suggested that metformin reduces the risk of dementia in diabetic people, and this study provides some understanding of why this might be. The fact that the drug is safe for humans means it could potentially be tested more quickly than a completely new drug. However, further research is needed to fully understand the link between diabetes and Alzheimer's.'
'A million more people are set to develop dementia in the next 10 years. It is important that people maintain a healthy lifestyle in order to reduce their risk and that greater investment in dementia research is made to further our understanding of the condition.'
Dr Anne Corbett
Research Communications Manager
Research Reference: Professor Susann Schweiger, et al. 'The Biguanidemetformin acts on tauphosphorylation via mTOR/PP2vAsignalling', Proceedings of the National Academy of Sciences of the United States of America, November 2010.
Source:
Alzheimer's Society
понедельник, 9 мая 2011 г.
Mediterranean Diet Lowers Alzheimer's Risk
If you follow a Mediterranean diet your chances of developing Alzheimer's disease could be 68% lower than people who don't, say researchers from Columbia University Medical Center, New York.
You can read about this study in the journal Archives of Neurology, October issue.
The researchers say that it is either the Mediterranean diet's protection from oxidative stress and/or the reduction it brings about in brain inflammation that protects, rather than any benefits on blood vessels.
The researchers looked at information on 2,000 people, of which 194 had Alzheimer's disease - their average age was 76 years. Depending on how close each person's diet had been to a Mediterranean one, they were given a score, from 0 to 9 (9 being closest).
The scientists found that the people who scored 7-9 had a 68% lower risk of developing Alzheimer's disease, when compared to the people who scored 0-3. Those scoring 4-6 had a 53% lower risk, compared to those scoring 0-3.
Lead researcher, Dr. Nikolaos Scarmeas, said "It seems that this diet is protective. Taking into account that this diet is protective for other conditions such as coronary heart disease, heart attack, high blood pressure, obesity and a series of cancers, it seems to make sense to follow this diet anyway, and the diet may also protect from Alzheimer's disease."
What is a Mediterranean Diet?
-- Olive oil is a major source of monounsaturated fat
-- Consumption of plenty of fruits, vegetables, bread, cereals, potatoes, beans, seeds and nuts
-- Consumption of moderate to low amounts of dairy products, fish, poultry
-- Consumption of small amounts of red meat
-- Consumption of small amounts of saturated fat
-- Consumption of low to moderate amounts of wine
"Mediterranean Diet, Alzheimer Disease, and Vascular Mediation"
Nikolaos Scarmeas, MD; Yaakov Stern, PhD; Richard Mayeux, MD; Jose A. Luchsinger, MD
Arch Neurol. 2006;63
doi:10.1001/archneur.63.12.noc60109
Click here to see article online
Written by:
You can read about this study in the journal Archives of Neurology, October issue.
The researchers say that it is either the Mediterranean diet's protection from oxidative stress and/or the reduction it brings about in brain inflammation that protects, rather than any benefits on blood vessels.
The researchers looked at information on 2,000 people, of which 194 had Alzheimer's disease - their average age was 76 years. Depending on how close each person's diet had been to a Mediterranean one, they were given a score, from 0 to 9 (9 being closest).
The scientists found that the people who scored 7-9 had a 68% lower risk of developing Alzheimer's disease, when compared to the people who scored 0-3. Those scoring 4-6 had a 53% lower risk, compared to those scoring 0-3.
Lead researcher, Dr. Nikolaos Scarmeas, said "It seems that this diet is protective. Taking into account that this diet is protective for other conditions such as coronary heart disease, heart attack, high blood pressure, obesity and a series of cancers, it seems to make sense to follow this diet anyway, and the diet may also protect from Alzheimer's disease."
What is a Mediterranean Diet?
-- Olive oil is a major source of monounsaturated fat
-- Consumption of plenty of fruits, vegetables, bread, cereals, potatoes, beans, seeds and nuts
-- Consumption of moderate to low amounts of dairy products, fish, poultry
-- Consumption of small amounts of red meat
-- Consumption of small amounts of saturated fat
-- Consumption of low to moderate amounts of wine
"Mediterranean Diet, Alzheimer Disease, and Vascular Mediation"
Nikolaos Scarmeas, MD; Yaakov Stern, PhD; Richard Mayeux, MD; Jose A. Luchsinger, MD
Arch Neurol. 2006;63
doi:10.1001/archneur.63.12.noc60109
Click here to see article online
Written by:
воскресенье, 8 мая 2011 г.
Single-Molecule, Real-Time Measurements Of A Key Biological Process
Biophysicists at TUM, the Technische Universitaet Muenchen, have published the results of single-molecule experiments that bring a higher-resolution tool to the study of protein folding. How proteins arrive at the three-dimensional shapes that determine their essential functions - or cause grave diseases when folding goes wrong - is considered one of the most important and least understood questions in the biological and medical sciences. Folding itself follows a path determined by its energy landscape, a complex property described in unprecedented detail by the TUM researchers. In this week's issue of the Proceedings of the National Academy of Sciences (USA), they report taking hold of a single, zipper-like protein molecule and mapping changes in its energy landscape during folding and unfolding.
Previous studies, including atomic force microscopy experiments by the same Munich laboratory, have gone a long way toward characterizing energy thresholds or barriers that stand between a protein's unfolded and folded states. Detailed observations of the quick transition from one state to the other have remained elusive. The results published this week open the door to higher-resolution, direct measurements. Better characterization of the folding process is seen as a vital link in understanding the chain of events leading from DNA coding for a protein to that protein's biological function. Another motivation for research in this field is the search for new drugs and therapies, because malfunctions in protein folding are implicated in a number of serious diseases - including diabetes, cancer, cystic fibrosis, prion diseases, and Alzheimer's.
This is the latest in a long series of single-molecule biophysical experiments carried out by Professor Matthias Rief and colleagues in the TUM Department of Physics. Co-authors Christof Gebhardt and Thomas Bornschloegl are members of Rief's lab; Gebhardt also is a member of the Munich Center for Integrated Protein Science.
As a model system for studying real-time protein folding dynamics, the TUM scientists chose a so-called leucine zipper found in yeast. It offers, as proteins go, a relatively simple "coiled coil" structure and zipper-like folding action: Picture two amino acid strings side by side, joined at the bottom, open at the top, and made essentially to zip together.
The researchers extended this structure so that they could make independent measurements at the top, bottom, and middle parts of the zipper. They took hold of the free ends at the top of the zipper with handles made of double-stranded DNA. These DNA handles in turn were attached to tiny beads that could be directly manipulated by "optical tweezers" - a tool based on the ability of laser beams with a certain kind of profile to pin down nanoscale objects. One end of the protein molecule was held fixed, and the other was held under tension but with some freedom to move, so that folding dynamics could be measured directly, in real time, as the protein zipped and unzipped. This arrangement enabled measurements with high resolution in both space and time.
"What I consider the major improvement is that the new experiments allow the observation of thousands of transitions between the folded and the unfolded state," Rief said. "This enables us to detect not only the folded and unfolded states but also, directly, the excursions of the large energy barriers separating those states. This has previously been impossible, and it now allows direct insight into the precise energy profile of this barrier."
Publication: Full distance resolved folding energy landscape of one single protein molecule, by J. Christof M. Gebhart, Thomas Bornschloegl, and Matthias Rief, PNAS Early Edition for the week of Jan. 18, 2010.
Source: Patrick Regan
Technische Universitaet Muenchen
Previous studies, including atomic force microscopy experiments by the same Munich laboratory, have gone a long way toward characterizing energy thresholds or barriers that stand between a protein's unfolded and folded states. Detailed observations of the quick transition from one state to the other have remained elusive. The results published this week open the door to higher-resolution, direct measurements. Better characterization of the folding process is seen as a vital link in understanding the chain of events leading from DNA coding for a protein to that protein's biological function. Another motivation for research in this field is the search for new drugs and therapies, because malfunctions in protein folding are implicated in a number of serious diseases - including diabetes, cancer, cystic fibrosis, prion diseases, and Alzheimer's.
This is the latest in a long series of single-molecule biophysical experiments carried out by Professor Matthias Rief and colleagues in the TUM Department of Physics. Co-authors Christof Gebhardt and Thomas Bornschloegl are members of Rief's lab; Gebhardt also is a member of the Munich Center for Integrated Protein Science.
As a model system for studying real-time protein folding dynamics, the TUM scientists chose a so-called leucine zipper found in yeast. It offers, as proteins go, a relatively simple "coiled coil" structure and zipper-like folding action: Picture two amino acid strings side by side, joined at the bottom, open at the top, and made essentially to zip together.
The researchers extended this structure so that they could make independent measurements at the top, bottom, and middle parts of the zipper. They took hold of the free ends at the top of the zipper with handles made of double-stranded DNA. These DNA handles in turn were attached to tiny beads that could be directly manipulated by "optical tweezers" - a tool based on the ability of laser beams with a certain kind of profile to pin down nanoscale objects. One end of the protein molecule was held fixed, and the other was held under tension but with some freedom to move, so that folding dynamics could be measured directly, in real time, as the protein zipped and unzipped. This arrangement enabled measurements with high resolution in both space and time.
"What I consider the major improvement is that the new experiments allow the observation of thousands of transitions between the folded and the unfolded state," Rief said. "This enables us to detect not only the folded and unfolded states but also, directly, the excursions of the large energy barriers separating those states. This has previously been impossible, and it now allows direct insight into the precise energy profile of this barrier."
Publication: Full distance resolved folding energy landscape of one single protein molecule, by J. Christof M. Gebhart, Thomas Bornschloegl, and Matthias Rief, PNAS Early Edition for the week of Jan. 18, 2010.
Source: Patrick Regan
Technische Universitaet Muenchen
суббота, 7 мая 2011 г.
Report Launched Today Reveals That The Dementia Research Agenda In Most EU Countries Remains Critically Under-Funded And Under-Valued
A report launched today by the leading Think Tank, International Longevity Centre - UK (ILC-UK) reveals that the dementia research agenda in most EU countries remains critically under-funded and under-valued.
The report, 'The European Dementia Research Agenda' finds there is widespread disparity in the diagnosis, treatment and care of people with dementia across Europe.
It argues that research needs to be afforded a greater role in tackling Alzheimer's disease and other dementias. The report suggests investment in clinical research and translational research will reap its own rewards and holds the key to improved prevention, diagnosis and treatment.
While some countries are striving forward such as Germany and France (1), the report found, many EU countries are trailing behind with no specifically targeted dementia research funding and/or national strategies.
With over seven million people in the EU living with dementia and with the numbers forecast to double in the next twenty years, the escalating economic, health, and social care costs necessitate fundamental changes to policy interventions for Member States and EU Institutions. (2)
Baroness Sally Greengross, the Chief Executive of the ILC-UK said:
"The evidence shows health and social care systems across Europe will face collapse if we do not prioritise public spending on dementia now. Research needs to be at the heart of any future government initiatives.
We know the prejudice and stigma attached to dementia has not served it well in terms of the 'public sell'. This has to change and all governments have to lead by example. In particular we need more investment in research to improve prevention, diagnosis and treatment."
The report made possible through an unrestricted grant from Pfizer, summarises the presentations, discussions and ideas which emerged from an expert working group meeting on dementia research held in the European Parliament in November 2010. It also brings together recent research on the scale, cost, national and EU responses to dementia and recent EU initiatives.
Today ILC-UK issued a Call to Action for the European Commission, the European Parliament, EU governments, and wider civil society. (3)
Among the 13 recommendations are:
For the European Commission to:
- Organise an annual conference on dementia research
- Prioritise dementia research under Framework Programme 8, given the growing burden and financial, health, social and human cost of dementia across Europe
- Develop a European Charter to increase the participation of people with dementia in clinical trials, share best practice and examine current obstacles
For the Members of the European Parliament to:
- Support the drafting and adoption of a United Nations Convention on the Human Rights of Older People
For Governments of the Member States to:
- Ensure parity in funding for dementia research in line with other chronic diseases and the disease burden
- Ensure the implementation and adequate resourcing of comprehensive national strategies to address all aspects of dementia.
- Increase the number of health care professionals trained in dementia
- Create national centres of excellence in dementia research.
For NGOs, clinicians, industry and academia to:
- Work with professional bodies that represent, regulate and are responsible for the training of GPs and other health care professionals to encourage more Continuing Professional Development in dementia and the exchange of best practice.
The author of the report Sally-Marie Bamford, ILC-UK Senior Researcher added:
"It is clear from listening to the delegates at the meeting that we have more in common with our European neighbours than we may think. Across the shores, politicians and policy-makers are all grappling with the thorny of problem of dementia.
While there are certainly some frontrunners in the dementia policy race, all countries need to recognise that investing in dementia research is essential. Officials in charge of the public purse need to stop thinking 'Can we afford to do this?', but rather 'Can we afford not to!'."(4)
Notes
1. In France, dementia research is embedded in the French national plan and includes 200 million Euros over five years through the creation of a Foundation for Scientific Cooperation on Alzheimer's disease. In the UK, The Government launched the National Dementia Strategy for England in February 2009, held a Ministerial Dementia Research Summit in July 2009 and a ministerial working group has been established to look at next steps.
2. A recent report by Standard and Poor argues that developed countries have between four to six years to address the issue of long term care and dementia care, before our economies crumble under the strain.
3. The conclusions and 'Calls to Action' outlined in the report 'The European Dementia Research Agenda' accompany this press release.
4. The spend on dementia research is ??32 million a year in the UK, which is only one eighth of what the Government spends on cancer. If scientists could develop a treatment that would reduce severe cognitive impairment in older people by just 1% per year, this would cancel out all estimated increases in the long-term care costs due to our ageing population. Source: Cognitive impairment in older people: its implications for future demand for services and costs. Adelina Comas-Herrera, Raphael Wittenberg, Linda Pickard, Martin Knapp and MRC-CFAS. PSSRU discussion paper
Source:
ILC-UK
The report, 'The European Dementia Research Agenda' finds there is widespread disparity in the diagnosis, treatment and care of people with dementia across Europe.
It argues that research needs to be afforded a greater role in tackling Alzheimer's disease and other dementias. The report suggests investment in clinical research and translational research will reap its own rewards and holds the key to improved prevention, diagnosis and treatment.
While some countries are striving forward such as Germany and France (1), the report found, many EU countries are trailing behind with no specifically targeted dementia research funding and/or national strategies.
With over seven million people in the EU living with dementia and with the numbers forecast to double in the next twenty years, the escalating economic, health, and social care costs necessitate fundamental changes to policy interventions for Member States and EU Institutions. (2)
Baroness Sally Greengross, the Chief Executive of the ILC-UK said:
"The evidence shows health and social care systems across Europe will face collapse if we do not prioritise public spending on dementia now. Research needs to be at the heart of any future government initiatives.
We know the prejudice and stigma attached to dementia has not served it well in terms of the 'public sell'. This has to change and all governments have to lead by example. In particular we need more investment in research to improve prevention, diagnosis and treatment."
The report made possible through an unrestricted grant from Pfizer, summarises the presentations, discussions and ideas which emerged from an expert working group meeting on dementia research held in the European Parliament in November 2010. It also brings together recent research on the scale, cost, national and EU responses to dementia and recent EU initiatives.
Today ILC-UK issued a Call to Action for the European Commission, the European Parliament, EU governments, and wider civil society. (3)
Among the 13 recommendations are:
For the European Commission to:
- Organise an annual conference on dementia research
- Prioritise dementia research under Framework Programme 8, given the growing burden and financial, health, social and human cost of dementia across Europe
- Develop a European Charter to increase the participation of people with dementia in clinical trials, share best practice and examine current obstacles
For the Members of the European Parliament to:
- Support the drafting and adoption of a United Nations Convention on the Human Rights of Older People
For Governments of the Member States to:
- Ensure parity in funding for dementia research in line with other chronic diseases and the disease burden
- Ensure the implementation and adequate resourcing of comprehensive national strategies to address all aspects of dementia.
- Increase the number of health care professionals trained in dementia
- Create national centres of excellence in dementia research.
For NGOs, clinicians, industry and academia to:
- Work with professional bodies that represent, regulate and are responsible for the training of GPs and other health care professionals to encourage more Continuing Professional Development in dementia and the exchange of best practice.
The author of the report Sally-Marie Bamford, ILC-UK Senior Researcher added:
"It is clear from listening to the delegates at the meeting that we have more in common with our European neighbours than we may think. Across the shores, politicians and policy-makers are all grappling with the thorny of problem of dementia.
While there are certainly some frontrunners in the dementia policy race, all countries need to recognise that investing in dementia research is essential. Officials in charge of the public purse need to stop thinking 'Can we afford to do this?', but rather 'Can we afford not to!'."(4)
Notes
1. In France, dementia research is embedded in the French national plan and includes 200 million Euros over five years through the creation of a Foundation for Scientific Cooperation on Alzheimer's disease. In the UK, The Government launched the National Dementia Strategy for England in February 2009, held a Ministerial Dementia Research Summit in July 2009 and a ministerial working group has been established to look at next steps.
2. A recent report by Standard and Poor argues that developed countries have between four to six years to address the issue of long term care and dementia care, before our economies crumble under the strain.
3. The conclusions and 'Calls to Action' outlined in the report 'The European Dementia Research Agenda' accompany this press release.
4. The spend on dementia research is ??32 million a year in the UK, which is only one eighth of what the Government spends on cancer. If scientists could develop a treatment that would reduce severe cognitive impairment in older people by just 1% per year, this would cancel out all estimated increases in the long-term care costs due to our ageing population. Source: Cognitive impairment in older people: its implications for future demand for services and costs. Adelina Comas-Herrera, Raphael Wittenberg, Linda Pickard, Martin Knapp and MRC-CFAS. PSSRU discussion paper
Source:
ILC-UK
пятница, 6 мая 2011 г.
Alzheimer Europe Welcomes Launch Of English Dementia Strategy
This week, the English Health Secretary, Alan Johnson and Care Services Minister, Phil Hope launched the first-ever National Dementia Strategy for England. In support of the Strategy, the government has pledged an extra GBP 150 million.
The 17 recommendations contained in the Strategy are based on the three key themes of (i) raising awareness and understanding, (ii) early diagnosis and support and (iii) living well with dementia Having worked closely alongside the government to develop the Strategy, the Alzheimer's Society believes that the strategy "will make an incredible difference to the lives of people with dementia and their carers".
Welcoming the launch of the Strategy, Maurice O'Connell, Chairman of Alzheimer Europe, said, "I am delighted for the 570,000 people living with dementia in England, as well as their carers, that this long-awaited Strategy will now be implemented and that England joins Norway, France and Scotland in giving dementia the priority it deserves. I hope that other national European policy-makers take heed and implement their own national dementia strategies."
Alzheimer Europe is the umbrella organisation of national Alzheimer associations and currently has 31 member organisations in 27 European countries. The mission statement of the organisation is to change perceptions, practice and policy to ensure equal access of people with dementia to a high level of care services and treatment options.
Alzheimer Europe
The 17 recommendations contained in the Strategy are based on the three key themes of (i) raising awareness and understanding, (ii) early diagnosis and support and (iii) living well with dementia Having worked closely alongside the government to develop the Strategy, the Alzheimer's Society believes that the strategy "will make an incredible difference to the lives of people with dementia and their carers".
Welcoming the launch of the Strategy, Maurice O'Connell, Chairman of Alzheimer Europe, said, "I am delighted for the 570,000 people living with dementia in England, as well as their carers, that this long-awaited Strategy will now be implemented and that England joins Norway, France and Scotland in giving dementia the priority it deserves. I hope that other national European policy-makers take heed and implement their own national dementia strategies."
Alzheimer Europe is the umbrella organisation of national Alzheimer associations and currently has 31 member organisations in 27 European countries. The mission statement of the organisation is to change perceptions, practice and policy to ensure equal access of people with dementia to a high level of care services and treatment options.
Alzheimer Europe
четверг, 5 мая 2011 г.
Lexicon Advances LX6171 For Cognitive Disorders Into Phase 1b Clinical Trial
Lexicon
Genetics Incorporated (Nasdaq: LEXG) announced today that it has initiated
a Phase 1b clinical trial of LX6171, its oral drug candidate for the
treatment of cognitive impairment associated with disorders such as
Alzheimer's disease, schizophrenia and vascular dementia. These disorders
affect millions of people worldwide, and their prevalence is increasing as
the population ages.
"LX6171 was well tolerated at all dose levels studied and obtained good
systemic exposure in its initial Phase 1 trial, a single ascending-dose
study completed last year, and we are pleased to advance the compound into
this next stage of clinical development," said Philip M. Brown, M.D., J.D.,
vice president of clinical development at Lexicon. "This second clinical
trial for LX6171, in addition to our recently commenced Phase 1 trial of
LX1031 for irritable bowl syndrome, underscores our focus on developing
Lexicon's discoveries into breakthrough treatments for human disease."
The Phase 1b trial is a randomized, double-blind, placebo-controlled,
multiple ascending-dose study to further evaluate LX6171's safety,
tolerability and pharmacokinetics. LX6171 will be studied in approximately
40 normal healthy volunteers, including a cohort of elderly subjects.
Lexicon expects results from this trial in mid-2007.
About LX6171
LX6171 is an oral drug candidate that was generated by Lexicon
medicinal chemists and is being developed to treat disorders characterized
by cognitive impairment, such as Alzheimer's disease, schizophrenia or
vascular dementia. Its target was internally identified as a selective and
potent inhibitor of a novel membrane protein that is expressed exclusively
in the central nervous system. In an initial Phase 1 trial, LX6171 was well
tolerated at all dose levels studied, with no clinically significant
changes noted. In preclinical studies, LX6171 demonstrated improved
learning and memory in healthy and aged animal models.
About Cognitive Disorders
Cognitive disorders such as delirium and dementia produce a significant
impairment of cognition and/or memory representing a marked deterioration
from a previous level of functioning. Alzheimer's disease is one of the
most well recognized disorders associated with cognitive impairment.
Alzheimer's disease is an irreversible, progressive brain disorder that
develops gradually and results in memory loss, behavior and personality
changes. Existing therapies that address cognitive impairment in
Alzheimer's patients generally have limited efficacy in early-stage
patients, and have side-effect profiles that limit their utility in some
patients.
About Lexicon
Lexicon is a biopharmaceutical company discovering and developing
breakthrough treatments for human disease. Lexicon currently has clinical
programs underway for such areas of major unmet medical need as irritable
bowel syndrome and cognitive disorders. The company has used its
proprietary gene knockout technology to discover more than 100 promising
drug targets and create an extensive pipeline of clinical and preclinical
programs in the therapeutic areas of diabetes and obesity, cardiovascular
disease, psychiatric and neurological disorders, cancer, immune system
disorders and ophthalmic disease. To advance the development and
commercialization of its programs, Lexicon is working both independently
and through collaborators which include Genentech, Inc., Bristol-Myers
Squibb Company, N.V. Organon and Takeda, Ltd. For additional information
about Lexicon and its programs, please visit
lexicon-genetics.
Safe Harbor Statement
This press release contains "forward-looking statements," including
statements relating to Lexicon's regulatory filings and clinical
development program for LX6171 and the potential therapeutic and commercial
potential of LX6171 and other potential drug candidates in Lexicon's
preclinical pipeline. This press release also contains forward-looking
statements relating to Lexicon's growth and future operating results,
discovery and development of products, strategic alliances and intellectual
property, as well as other matters that are not historical facts or
information. All forward-looking statements are based on management's
current assumptions and expectations and involve risks, uncertainties and
other important factors, specifically including those relating to Lexicon's
ability to successfully conduct clinical development of LX6171 and
preclinical development of other potential drug candidates, advance
additional candidates into preclinical and clinical development, obtain
necessary regulatory approvals, achieve its operational objectives, obtain
patent protection for its discoveries and establish strategic alliances, as
well as additional factors relating to manufacturing, intellectual property
rights, and the therapeutic or commercial value of its drug candidates,
that may cause Lexicon's actual results to be materially different from any
future results expressed or implied by such forward-looking statements.
Information identifying such important factors is contained under "Factors
Affecting Forward-Looking Statements" and "Business -- Risk Factors" in
Lexicon's annual report on Form 10-K for the year ended December 31, 2005,
as filed with the Securities and Exchange Commission. Lexicon undertakes no
obligation to update or revise any such forward-looking statements, whether
as a result of new information, future events or otherwise.
Lexicon Genetics Incorporated
lexicon-genetics
Genetics Incorporated (Nasdaq: LEXG) announced today that it has initiated
a Phase 1b clinical trial of LX6171, its oral drug candidate for the
treatment of cognitive impairment associated with disorders such as
Alzheimer's disease, schizophrenia and vascular dementia. These disorders
affect millions of people worldwide, and their prevalence is increasing as
the population ages.
"LX6171 was well tolerated at all dose levels studied and obtained good
systemic exposure in its initial Phase 1 trial, a single ascending-dose
study completed last year, and we are pleased to advance the compound into
this next stage of clinical development," said Philip M. Brown, M.D., J.D.,
vice president of clinical development at Lexicon. "This second clinical
trial for LX6171, in addition to our recently commenced Phase 1 trial of
LX1031 for irritable bowl syndrome, underscores our focus on developing
Lexicon's discoveries into breakthrough treatments for human disease."
The Phase 1b trial is a randomized, double-blind, placebo-controlled,
multiple ascending-dose study to further evaluate LX6171's safety,
tolerability and pharmacokinetics. LX6171 will be studied in approximately
40 normal healthy volunteers, including a cohort of elderly subjects.
Lexicon expects results from this trial in mid-2007.
About LX6171
LX6171 is an oral drug candidate that was generated by Lexicon
medicinal chemists and is being developed to treat disorders characterized
by cognitive impairment, such as Alzheimer's disease, schizophrenia or
vascular dementia. Its target was internally identified as a selective and
potent inhibitor of a novel membrane protein that is expressed exclusively
in the central nervous system. In an initial Phase 1 trial, LX6171 was well
tolerated at all dose levels studied, with no clinically significant
changes noted. In preclinical studies, LX6171 demonstrated improved
learning and memory in healthy and aged animal models.
About Cognitive Disorders
Cognitive disorders such as delirium and dementia produce a significant
impairment of cognition and/or memory representing a marked deterioration
from a previous level of functioning. Alzheimer's disease is one of the
most well recognized disorders associated with cognitive impairment.
Alzheimer's disease is an irreversible, progressive brain disorder that
develops gradually and results in memory loss, behavior and personality
changes. Existing therapies that address cognitive impairment in
Alzheimer's patients generally have limited efficacy in early-stage
patients, and have side-effect profiles that limit their utility in some
patients.
About Lexicon
Lexicon is a biopharmaceutical company discovering and developing
breakthrough treatments for human disease. Lexicon currently has clinical
programs underway for such areas of major unmet medical need as irritable
bowel syndrome and cognitive disorders. The company has used its
proprietary gene knockout technology to discover more than 100 promising
drug targets and create an extensive pipeline of clinical and preclinical
programs in the therapeutic areas of diabetes and obesity, cardiovascular
disease, psychiatric and neurological disorders, cancer, immune system
disorders and ophthalmic disease. To advance the development and
commercialization of its programs, Lexicon is working both independently
and through collaborators which include Genentech, Inc., Bristol-Myers
Squibb Company, N.V. Organon and Takeda, Ltd. For additional information
about Lexicon and its programs, please visit
lexicon-genetics.
Safe Harbor Statement
This press release contains "forward-looking statements," including
statements relating to Lexicon's regulatory filings and clinical
development program for LX6171 and the potential therapeutic and commercial
potential of LX6171 and other potential drug candidates in Lexicon's
preclinical pipeline. This press release also contains forward-looking
statements relating to Lexicon's growth and future operating results,
discovery and development of products, strategic alliances and intellectual
property, as well as other matters that are not historical facts or
information. All forward-looking statements are based on management's
current assumptions and expectations and involve risks, uncertainties and
other important factors, specifically including those relating to Lexicon's
ability to successfully conduct clinical development of LX6171 and
preclinical development of other potential drug candidates, advance
additional candidates into preclinical and clinical development, obtain
necessary regulatory approvals, achieve its operational objectives, obtain
patent protection for its discoveries and establish strategic alliances, as
well as additional factors relating to manufacturing, intellectual property
rights, and the therapeutic or commercial value of its drug candidates,
that may cause Lexicon's actual results to be materially different from any
future results expressed or implied by such forward-looking statements.
Information identifying such important factors is contained under "Factors
Affecting Forward-Looking Statements" and "Business -- Risk Factors" in
Lexicon's annual report on Form 10-K for the year ended December 31, 2005,
as filed with the Securities and Exchange Commission. Lexicon undertakes no
obligation to update or revise any such forward-looking statements, whether
as a result of new information, future events or otherwise.
Lexicon Genetics Incorporated
lexicon-genetics
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