Most of the cognitive tests that have been used to decide whether someone has Alzheimer's disease or vascular dementia have not been very helpful when used alone. A new report published by the American Psychological Association concluded that when older people are confused and forgetful, doctors should base their diagnoses on many different types of information, including medical history and brain imaging.
Both Alzheimer's disease and vascular dementia affect learning and memory, behavior and day-to-day function. Even so, they're caused by different problems in the brain and require different medical approaches. It's important to tell them apart accurately, stresses the study in July's Neuropsychology. Valid diagnoses can help doctors treat patients more effectively, and help patients and families better understand their situations.
Jane Mathias, PhD, and Jennifer Burke, M.Psych.(Clinical), both from the University of Adelaide, analyzed 81 previously published studies that compared the cognitive testing of people diagnosed with dementia of the Alzheimer's (4,867) and vascular type (2,263). The average age across participants was 75.
Of the 118 different tests that were used in more than one study, Mathias and Burke found that only two were able to adequately differentiate between Alzheimer's and vascular dementia.
The Emotional Recognition Task (the ability to identify facial expressions in photographs and match emotional expressions to situations, at which people with Alzheimer's were better) and Delayed Story Recall (at which people with vascular dementia were better), were the only tests that appeared to reliably tell the two groups apart.
Even so, whether due to individual variability (people start at different baselines) or possible undiagnosed mixtures of Alzheimer's and vascular disease, there was enough overlap between the two groups to signal the need for more information. Because of these muddied waters, "The combined picture is what's important, so we need to look at how we can improve diagnosis by combining different measures," said Mathias.
Of note, many commonly used tests -- such as Digit Span (repeating a set of numbers forward, backward), verbal fluency (generating words by first letter or category, such as animals), drawing tasks and more - were unable to distinguish between dementia types. "While these tests may assist in diagnosing dementia, they do not adequately discriminate between Alzheimer's disease and vascular dementia," wrote the authors. Teasing apart different types of dementia is often harder than deciding whether someone is showing cognitive decline in the first place, Mathias explained.
Although the two tests that worked best would most reliably contribute to a clinical diagnosis, "All cognitive tests should be used cautiously and only in conjunction with other information (imaging, medical history) when diagnosing patients," the authors said.
Article: "Cognitive Functioning in Alzheimer's and Vascular Dementia: A Meta-Analysis," J. L. Mathias, PhD, and J. Burke, M.Psych.(Clinical), University of Adelaide; Neuropsychology, Vol. 23, No. 4.
Source
The American Psychological Association
вторник, 30 августа 2011 г.
суббота, 27 августа 2011 г.
Alzheimer's Society Backs 'Caring With Confidence', UK
Alzheimer's Society has welcomed the launch of 'Caring with Confidence', a new learning programme that will deliver knowledge and skills to carers across England.
Seven learning sessions aimed at improving support for carers will be launched in locations across the country from yesterday. In addition, Alzheimer's Society has won a tender to provide special sessions for carers of people with dementia. These sessions will be available later in the year in Sussex, Somerset, Devon and Hampshire.
Research by Caring with Confidence highlighted that:
- More than 60% of people believe their caring role affected their health (16% a lot 46% a little)
- One in five people caring 50 plus hours a week are also juggling a full-time job, and 23% of those people asked had been caring for at least 10 years
- Support or provision should explain how to deal with the benefits and healthcare system (46% and 41% said these topics would be very or extremely useful) as well as providing practical information and advice about the condition they are dealing with (38% very or extremely useful)
Neil Hunt, chief executive, Alzheimer's Society says,
'This research confirms the difficult situation that carers face and shows us that a little help can go a long way. Hundreds of carers call the Alzheimer's Society Dementia Helpline every year telling us they need more support and advice to help them cope.
Caring with Confidence is an important step towards delivering support when people need it most. We are very excited to be part of the programme. Alzheimer's Society will shortly provide a Caring with Confidence session specifically for carers of people with dementia in four locations across England. We hope this will be the beginning of opportunities to make the programme available for carers everywhere.'
Stephen Jacobs, OBE, Caring with Confidence Project Board Chair, adds,
'The contribution made by carers is huge, but it is a role that is often taken on at short notice and without preparation, leaving carers to struggle with the vital responsibilities that they have assumed - this is where Caring with Confidence can help.'
Notes
- The research referred to in the press release was conducted by an independent market research company for Caring with Confidence during February, March and April 2008. The study saw 1084 carers contacted and six detailed group discussions were held.
- 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 those who care for them. Alzheimer's Society works in England, Wales and Northern Ireland
- The Alzheimer's Society needs to raise money to care for people today and 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
Seven learning sessions aimed at improving support for carers will be launched in locations across the country from yesterday. In addition, Alzheimer's Society has won a tender to provide special sessions for carers of people with dementia. These sessions will be available later in the year in Sussex, Somerset, Devon and Hampshire.
Research by Caring with Confidence highlighted that:
- More than 60% of people believe their caring role affected their health (16% a lot 46% a little)
- One in five people caring 50 plus hours a week are also juggling a full-time job, and 23% of those people asked had been caring for at least 10 years
- Support or provision should explain how to deal with the benefits and healthcare system (46% and 41% said these topics would be very or extremely useful) as well as providing practical information and advice about the condition they are dealing with (38% very or extremely useful)
Neil Hunt, chief executive, Alzheimer's Society says,
'This research confirms the difficult situation that carers face and shows us that a little help can go a long way. Hundreds of carers call the Alzheimer's Society Dementia Helpline every year telling us they need more support and advice to help them cope.
Caring with Confidence is an important step towards delivering support when people need it most. We are very excited to be part of the programme. Alzheimer's Society will shortly provide a Caring with Confidence session specifically for carers of people with dementia in four locations across England. We hope this will be the beginning of opportunities to make the programme available for carers everywhere.'
Stephen Jacobs, OBE, Caring with Confidence Project Board Chair, adds,
'The contribution made by carers is huge, but it is a role that is often taken on at short notice and without preparation, leaving carers to struggle with the vital responsibilities that they have assumed - this is where Caring with Confidence can help.'
Notes
- The research referred to in the press release was conducted by an independent market research company for Caring with Confidence during February, March and April 2008. The study saw 1084 carers contacted and six detailed group discussions were held.
- 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 those who care for them. Alzheimer's Society works in England, Wales and Northern Ireland
- The Alzheimer's Society needs to raise money to care for people today and 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
среда, 24 августа 2011 г.
Brain Activity, Drugs Could Affect Alzheimer's Progression
The activity of connections among brain cells significantly affects levels of the toxic protein beta-amyloid (A?) that is a major cause of Alzheimer's disease (AD), researchers have found. A? is produced by the cleavage of amyloid precursor protein (APP) within brain cells.
Findings suggest that the kind of mental activity people practice or drugs they might take for depression or anxiety could affect their AD risk or the disease progression.
In an article in the December 22, 2005, issue of Neuron, David Holtzman and colleagues detailed studies in which they determined how neuronal activity affected the level of A? in the "interstitial fluid" (ISF) between cells. The brain damage of AD is caused in considerable part by high levels of A? in the ISF, where it aggregates into the brain-clogging plaque that kills brain cells.
In studies with mice, they found that stimulating brain cells while sampling ISF revealed a significant increase in A? levels. Conversely, when they administered drugs that blocked neuronal activity, A? levels dropped.
Their studies also revealed that A? appeared to be released from the same kinds of sac-like vesicles in neurons that transport the chemical signals called neurotransmitters that one neuron uses to triggers a nerve impulse in its neighbor. Such vesicles launch their cargoes across the connections called synapses between neurons.
One important question arising from their findings, noted the researchers, is the effect of cognitive activity--such as that produced by an enriched environment--on A? levels. Both animal and human studies have suggested that such activity affects A? plaque levels.
"One hypothesis is that enrichment may increase overall synaptic activity in some brain regions and decrease it in others, depending on the environmental alteration," wrote Holtzman and his colleagues. "For example, certain memory tasks in humans simultaneously increase and decrease activity within different brain areas. Increased activity might result in increased susceptibility to A? deposition if the activated neural circuits contain high levels of human APP expression, thereby increasing A? release from those pathways. Conversely, if synaptic activity decreases in a brain area that is normally vulnerable to A? pathology, then there may be reduced A? deposition as a consequence of enrichment," they wrote.
Overall, the researchers concluded that "these findings are consistent with the possibility that physical and environmental changes resulting in altered neuronal/synaptic activity throughout life can modulate the amount of A? that accumulates in plaques in a region-dependent manner.
"That synaptic activity and A? levels are directly linked in vivo may have important treatment implications," they wrote. "Drugs used to treat neuropsychiatric disorders, such as depression or anxiety, among many others, directly influence neurotransmitters, and their receptors, thereby altering synaptic activity," they wrote. "Thus, it is likely that these drugs might influence A? levels within specified neuronal networks as well. If so, such drugs could potentially influence risk or progression of AD. Understanding the effects of drugs on ISF A? may enable the design of ways to decrease soluble A? levels, including synaptotoxic A? oligomers, in specific brain regions.
"Defining the relationship between normal brain function and the metabolism of a key protein involved in a neurodegenerative disease may provide new clues into the factors that regulate the biology of AD as well as other disorders of the nervous system," they wrote.
John R. Cirrito, Kelvin A. Yamada, Mary Beth Finn, Steven Mennerick, and David M. Holtzman of the Washington University School of Medicine in St. Louis, Missouri; Robert S. Sloviter of the University of Arizona in Tucson, Arizona; Kelly R. Bales, Patrick C. May, Darryle D. Schoepp, and Steven M. Paul of Lilly Research Laboratories in Indianapolis, Indiana. This work was supported by National Institutes of Health grants AG13956 (D.M.H.), AG11355 (D.M.H.), and DA07261 (J.R.C.); an Alzheimer's Association Zenith Award (D.M.H.); MetLife Foundation (D.M.H.); and Eli Lilly and Co. The authors have declared a conflict of interest. K.R.B., P.C.M., D.D.S., and S.M.P. are employees and shareholders of Eli Lilly and Co.
Cirrito et al.: "Synaptic Activity Regulates Interstitial Fluid Amyloid-b Levels In Vivo." Publishing in Neuron, Vol. 48, 913-922, December 22, 2005, DOI 10.1016/j.neuron.2005.10.028 neuron.
Heidi Hardman
hhardmancell
Cell Press
cellpress
Findings suggest that the kind of mental activity people practice or drugs they might take for depression or anxiety could affect their AD risk or the disease progression.
In an article in the December 22, 2005, issue of Neuron, David Holtzman and colleagues detailed studies in which they determined how neuronal activity affected the level of A? in the "interstitial fluid" (ISF) between cells. The brain damage of AD is caused in considerable part by high levels of A? in the ISF, where it aggregates into the brain-clogging plaque that kills brain cells.
In studies with mice, they found that stimulating brain cells while sampling ISF revealed a significant increase in A? levels. Conversely, when they administered drugs that blocked neuronal activity, A? levels dropped.
Their studies also revealed that A? appeared to be released from the same kinds of sac-like vesicles in neurons that transport the chemical signals called neurotransmitters that one neuron uses to triggers a nerve impulse in its neighbor. Such vesicles launch their cargoes across the connections called synapses between neurons.
One important question arising from their findings, noted the researchers, is the effect of cognitive activity--such as that produced by an enriched environment--on A? levels. Both animal and human studies have suggested that such activity affects A? plaque levels.
"One hypothesis is that enrichment may increase overall synaptic activity in some brain regions and decrease it in others, depending on the environmental alteration," wrote Holtzman and his colleagues. "For example, certain memory tasks in humans simultaneously increase and decrease activity within different brain areas. Increased activity might result in increased susceptibility to A? deposition if the activated neural circuits contain high levels of human APP expression, thereby increasing A? release from those pathways. Conversely, if synaptic activity decreases in a brain area that is normally vulnerable to A? pathology, then there may be reduced A? deposition as a consequence of enrichment," they wrote.
Overall, the researchers concluded that "these findings are consistent with the possibility that physical and environmental changes resulting in altered neuronal/synaptic activity throughout life can modulate the amount of A? that accumulates in plaques in a region-dependent manner.
"That synaptic activity and A? levels are directly linked in vivo may have important treatment implications," they wrote. "Drugs used to treat neuropsychiatric disorders, such as depression or anxiety, among many others, directly influence neurotransmitters, and their receptors, thereby altering synaptic activity," they wrote. "Thus, it is likely that these drugs might influence A? levels within specified neuronal networks as well. If so, such drugs could potentially influence risk or progression of AD. Understanding the effects of drugs on ISF A? may enable the design of ways to decrease soluble A? levels, including synaptotoxic A? oligomers, in specific brain regions.
"Defining the relationship between normal brain function and the metabolism of a key protein involved in a neurodegenerative disease may provide new clues into the factors that regulate the biology of AD as well as other disorders of the nervous system," they wrote.
John R. Cirrito, Kelvin A. Yamada, Mary Beth Finn, Steven Mennerick, and David M. Holtzman of the Washington University School of Medicine in St. Louis, Missouri; Robert S. Sloviter of the University of Arizona in Tucson, Arizona; Kelly R. Bales, Patrick C. May, Darryle D. Schoepp, and Steven M. Paul of Lilly Research Laboratories in Indianapolis, Indiana. This work was supported by National Institutes of Health grants AG13956 (D.M.H.), AG11355 (D.M.H.), and DA07261 (J.R.C.); an Alzheimer's Association Zenith Award (D.M.H.); MetLife Foundation (D.M.H.); and Eli Lilly and Co. The authors have declared a conflict of interest. K.R.B., P.C.M., D.D.S., and S.M.P. are employees and shareholders of Eli Lilly and Co.
Cirrito et al.: "Synaptic Activity Regulates Interstitial Fluid Amyloid-b Levels In Vivo." Publishing in Neuron, Vol. 48, 913-922, December 22, 2005, DOI 10.1016/j.neuron.2005.10.028 neuron.
Heidi Hardman
hhardmancell
Cell Press
cellpress
воскресенье, 21 августа 2011 г.
Age Concern And Help The Aged Comment On Dementia Research, UK
Michelle Mitchell, Charity Director for Age Concern and Help the Aged, said:
'The fact that dementia research remains so disproportionately underfunded will be deeply concerning to older people, their families and anyone who has experienced this cruel disease.
'The financial burden of this disease is already very high and this will increase further as the population ages unless we find a cure or learn how to prevent dementia.
'Dementia is not going to go away and it is therefore of paramount importance to both sufferers now and society as a whole, that we invest in research.
'This is why Age Concern and Help the Aged are a major funder of dementia research and we strongly support calls for more funding for this vital work.'
Visit our Disconnected Mind website to find out about our research into the causes of mental decline.
Notes
Age UK is the new force combining Age Concern and Help the Aged. We will be known by our new name from Spring 2010. The Age UK family includes Age Scotland, Age Cymru and Age NI.
Source
Help The Aged
'The fact that dementia research remains so disproportionately underfunded will be deeply concerning to older people, their families and anyone who has experienced this cruel disease.
'The financial burden of this disease is already very high and this will increase further as the population ages unless we find a cure or learn how to prevent dementia.
'Dementia is not going to go away and it is therefore of paramount importance to both sufferers now and society as a whole, that we invest in research.
'This is why Age Concern and Help the Aged are a major funder of dementia research and we strongly support calls for more funding for this vital work.'
Visit our Disconnected Mind website to find out about our research into the causes of mental decline.
Notes
Age UK is the new force combining Age Concern and Help the Aged. We will be known by our new name from Spring 2010. The Age UK family includes Age Scotland, Age Cymru and Age NI.
Source
Help The Aged
четверг, 18 августа 2011 г.
Number Of Older People Being Admitted To Hospital Increased By Two Thirds In A Decade, Alzheimer's Society Comment
The number of people aged 60 and over in hospitals is increasing at a faster rate than any other age range according to a report released yesterday.
According to the Hospital Episode Statistics: Admitted Patient Care - England 2009/10, the number of patients aged 75 and over has risen by two thirds (66 per cent) in the past decade. The number of 60-74 year olds being admitted also rose by 48 per cent. This compared to an average increase of 38 per cent.
Alzheimer's Society comment:
'It is important we don't accept these steep increases in the number of older people being admitted to hospital as an inevitable consequence of an ageing population. Many of these admissions could be avoided if better help and support was available at an earlier stage, preventing the need for expensive and distressing crisis care later on.
'People with dementia represent a very large proportion of these admissions. As many as one in four people on hospital wards have the condition and many stay in hospital far longer than necessary. Investing in care in the community now would enable many of these people to stay at home for longer and could help save the NHS millions of pounds.'
Ruth Sutherland
Interim Chief Executive
Source:
Alzheimer's Society
According to the Hospital Episode Statistics: Admitted Patient Care - England 2009/10, the number of patients aged 75 and over has risen by two thirds (66 per cent) in the past decade. The number of 60-74 year olds being admitted also rose by 48 per cent. This compared to an average increase of 38 per cent.
Alzheimer's Society comment:
'It is important we don't accept these steep increases in the number of older people being admitted to hospital as an inevitable consequence of an ageing population. Many of these admissions could be avoided if better help and support was available at an earlier stage, preventing the need for expensive and distressing crisis care later on.
'People with dementia represent a very large proportion of these admissions. As many as one in four people on hospital wards have the condition and many stay in hospital far longer than necessary. Investing in care in the community now would enable many of these people to stay at home for longer and could help save the NHS millions of pounds.'
Ruth Sutherland
Interim Chief Executive
Source:
Alzheimer's Society
понедельник, 15 августа 2011 г.
Four New Research Studies Describe Experimental Immunotherapies For Alzheimer's
The primary therapeutic target in Alzheimer's disease has been the beta amyloid peptide, which clusters outside cells in the brain to form sticky clumps known as plaques. Recently, more attention has been given to the tau protein, which aggregates inside the brain cells of people with Alzheimer's, forming neurofibrillary tangles. Precisely how these proteins interact in causing the disease is unclear.
Four new research studies reported today at the Alzheimer's Association International Conference on Alzheimer's Disease 2010 (AAICAD 2010) in Honolulu, HI describe experimental immunotherapies for Alzheimer's two of which target tau directly and two of which may reduce tau even though their primary target was beta amyloid.
"It is very important that we have a variety of therapeutic targets in the fight against Alzheimer's disease," said William Thies, PhD, Chief Medical and Scientific Officer at the Alzheimer's Association. "The more opportunities that we investigate to intervene and change the relentless and progressive course of Alzheimer's, the better chance that we will find something that works."
"Importantly, these studies teach us more not only about tau-targeted therapies but also about the progression of Alzheimer's disease," Thies added. "It may be that amyloid changes in the brain happen early in the disease and tau-related changes happen 'downstream' where they have a more direct effect on cognitive function. However, this is still to be determined."
"We need more basic research about what causes Alzheimer's, as well as therapy-related studies, to fill the front end of the drug pipeline and get us the better treatments and prevention strategies that we so desperately need to head off the epidemic of Alzheimer's," Thies said.
Beta Amyloid Immunotherapy with Bapineuzumab in Alzheimer's May Also Reduce Tau
Bapineuzumab (Janssen Alzheimer Immunotherapy and Pfizer) is an antibody to the beta amyloid plaques that are associated with Alzheimer's disease, and is currently in Phase 3 testing as a treatment for mild to moderate Alzheimer's. An abnormal form of the tau protein known as phospho-tau (P-tau) forms into tangles which are the other established lesions in the brain of people with Alzheimer's. The amount of P-tau in cerebrospinal fluid (CSF) is believed to be a marker of active loss of brain cells in people with Alzheimer's; prior studies have shown increases in P-tau in people with mild cognitive impairment who later develop Alzheimer's. P-tau was studied as a therapeutic biomarker in the Phase 2 clinical trials of bapineuzumab.
The pooled exploratory analysis reported at AAICAD 2010 by Kaj Blennow, MD, PhD, of the University of Gothenburg, Sweden, and colleagues included a subgroup of participants from two randomized, multicenter, double-blind, placebo-controlled, multiple-ascending-dose studies conducted in the United States (Study 201) or in the United Kingdom and Finland (Study 202). Study 201 enrolled 35 patients (20 bapineuzumab, 15 placebo) in the CSF substudy, and Study 202 enrolled 11 patients (7 bapineuzumab, 4 placebo) in the CSF substudy. CSF was collected at baseline and 2 weeks after the week 52 infusion.
The researchers found that Study 201 showed a trend (p=0.0564) towards a decrease in CSF P-tau in bapineuzumab-treated compared with placebo-treated cases. In Study 202, no significant treatment effects were seen. When they combined data from both studies, they found a statistically significant decrease (p=0.0270) in P-tau in bapineuzumab-treated compared with placebo-treated patients.
"These observations suggest that immunotherapy treatment targeting amyloid may also alter neurodegenerative processes that occur later in the disease process and that are more directly associated with loss of function," Blennow said. "However, this was a small study and these findings need to be confirmed."
Another Immunization Therapy for Alzheimer's with Beta Amyloid Also Reduces Tau
AN1792 (Elan) showed early promise as a beta amyloid immunotherapy for Alzheimer's. In 2002, a Phase 2 trial reported that about 6 percent of participants developed serious brain inflammation symptoms resembling meningoencephalitis. The trial was stopped as was further clinical development. However, participants in the first AN1792 trial continue to be observed.
Delphine Boche, PhD, of the University of Southampton's School of Medicine, UK, and colleagues studied the levels of beta amyloid and phospho-tau in six regions of cerebral grey matter that are affected by Alzheimer's pathology in the brains of 10 people with Alzheimer's who were immunized with AN1792 and compared the findings with 28 unimmunized Alzheimer cases. They had previously shown a reduction of beta amyloid in people treated with AN1792 and now looked to see if it had any effect on tau.
The researchers found statistically significant reductions in tau and beta amyloid in the immunized patients compared with untreated Alzheimer's. The reduction in tau appeared to be specifically in the dendrites, which are the branched projections of a neuron that conduct the electrochemical stimulation received from other nerve cells to the cell body. In contrast, tau in the bodies of the nerve cells, where the tangles form, seemed unaffected.
"The findings show that treatment aimed at beta amyloid may also modify tau changes in Alzheimer's," Boche said. "The lack of change in tau in the bodies of nerve cells might explain why the people in the original AN1792 trial didn't experience an improvement in cognitive functioning even though we saw amyloid clearance."
"This study demonstrates a link between these two Alzheimer's-related proteins, which has been suspected but not clearly demonstrated in the human brain. The findings give us more basic information about the interaction between beta amyloid and tau in Alzheimer's and may clarify how the disease progresses in the brain," Boche said.
Tau Antibodies Reduce Brain Tangles in Alzheimer-Model Mice
Allal Boutajangout, PhD, of the New York University School of Medicine, and colleagues previously reported that active tau immunization clears tau tangles from the brain and reduces or prevents functional impairments in two different tangle-model mice. In a study reported at AAICAD 2010, they assessed the efficacy of passive immunization for 13 weeks with the PHF1 antibody to tau in a mouse model of Alzheimer's tangles.
The researchers found that weekly injections of PHF1 in the tangle mice reduced the amount of tau aggregates in the brain and decreased functional impairment. The treated mice performed better than controls on the traverse beam task (p
Four new research studies reported today at the Alzheimer's Association International Conference on Alzheimer's Disease 2010 (AAICAD 2010) in Honolulu, HI describe experimental immunotherapies for Alzheimer's two of which target tau directly and two of which may reduce tau even though their primary target was beta amyloid.
"It is very important that we have a variety of therapeutic targets in the fight against Alzheimer's disease," said William Thies, PhD, Chief Medical and Scientific Officer at the Alzheimer's Association. "The more opportunities that we investigate to intervene and change the relentless and progressive course of Alzheimer's, the better chance that we will find something that works."
"Importantly, these studies teach us more not only about tau-targeted therapies but also about the progression of Alzheimer's disease," Thies added. "It may be that amyloid changes in the brain happen early in the disease and tau-related changes happen 'downstream' where they have a more direct effect on cognitive function. However, this is still to be determined."
"We need more basic research about what causes Alzheimer's, as well as therapy-related studies, to fill the front end of the drug pipeline and get us the better treatments and prevention strategies that we so desperately need to head off the epidemic of Alzheimer's," Thies said.
Beta Amyloid Immunotherapy with Bapineuzumab in Alzheimer's May Also Reduce Tau
Bapineuzumab (Janssen Alzheimer Immunotherapy and Pfizer) is an antibody to the beta amyloid plaques that are associated with Alzheimer's disease, and is currently in Phase 3 testing as a treatment for mild to moderate Alzheimer's. An abnormal form of the tau protein known as phospho-tau (P-tau) forms into tangles which are the other established lesions in the brain of people with Alzheimer's. The amount of P-tau in cerebrospinal fluid (CSF) is believed to be a marker of active loss of brain cells in people with Alzheimer's; prior studies have shown increases in P-tau in people with mild cognitive impairment who later develop Alzheimer's. P-tau was studied as a therapeutic biomarker in the Phase 2 clinical trials of bapineuzumab.
The pooled exploratory analysis reported at AAICAD 2010 by Kaj Blennow, MD, PhD, of the University of Gothenburg, Sweden, and colleagues included a subgroup of participants from two randomized, multicenter, double-blind, placebo-controlled, multiple-ascending-dose studies conducted in the United States (Study 201) or in the United Kingdom and Finland (Study 202). Study 201 enrolled 35 patients (20 bapineuzumab, 15 placebo) in the CSF substudy, and Study 202 enrolled 11 patients (7 bapineuzumab, 4 placebo) in the CSF substudy. CSF was collected at baseline and 2 weeks after the week 52 infusion.
The researchers found that Study 201 showed a trend (p=0.0564) towards a decrease in CSF P-tau in bapineuzumab-treated compared with placebo-treated cases. In Study 202, no significant treatment effects were seen. When they combined data from both studies, they found a statistically significant decrease (p=0.0270) in P-tau in bapineuzumab-treated compared with placebo-treated patients.
"These observations suggest that immunotherapy treatment targeting amyloid may also alter neurodegenerative processes that occur later in the disease process and that are more directly associated with loss of function," Blennow said. "However, this was a small study and these findings need to be confirmed."
Another Immunization Therapy for Alzheimer's with Beta Amyloid Also Reduces Tau
AN1792 (Elan) showed early promise as a beta amyloid immunotherapy for Alzheimer's. In 2002, a Phase 2 trial reported that about 6 percent of participants developed serious brain inflammation symptoms resembling meningoencephalitis. The trial was stopped as was further clinical development. However, participants in the first AN1792 trial continue to be observed.
Delphine Boche, PhD, of the University of Southampton's School of Medicine, UK, and colleagues studied the levels of beta amyloid and phospho-tau in six regions of cerebral grey matter that are affected by Alzheimer's pathology in the brains of 10 people with Alzheimer's who were immunized with AN1792 and compared the findings with 28 unimmunized Alzheimer cases. They had previously shown a reduction of beta amyloid in people treated with AN1792 and now looked to see if it had any effect on tau.
The researchers found statistically significant reductions in tau and beta amyloid in the immunized patients compared with untreated Alzheimer's. The reduction in tau appeared to be specifically in the dendrites, which are the branched projections of a neuron that conduct the electrochemical stimulation received from other nerve cells to the cell body. In contrast, tau in the bodies of the nerve cells, where the tangles form, seemed unaffected.
"The findings show that treatment aimed at beta amyloid may also modify tau changes in Alzheimer's," Boche said. "The lack of change in tau in the bodies of nerve cells might explain why the people in the original AN1792 trial didn't experience an improvement in cognitive functioning even though we saw amyloid clearance."
"This study demonstrates a link between these two Alzheimer's-related proteins, which has been suspected but not clearly demonstrated in the human brain. The findings give us more basic information about the interaction between beta amyloid and tau in Alzheimer's and may clarify how the disease progresses in the brain," Boche said.
Tau Antibodies Reduce Brain Tangles in Alzheimer-Model Mice
Allal Boutajangout, PhD, of the New York University School of Medicine, and colleagues previously reported that active tau immunization clears tau tangles from the brain and reduces or prevents functional impairments in two different tangle-model mice. In a study reported at AAICAD 2010, they assessed the efficacy of passive immunization for 13 weeks with the PHF1 antibody to tau in a mouse model of Alzheimer's tangles.
The researchers found that weekly injections of PHF1 in the tangle mice reduced the amount of tau aggregates in the brain and decreased functional impairment. The treated mice performed better than controls on the traverse beam task (p
пятница, 12 августа 2011 г.
Alzheimer's Disease: Modulating Enkephalin May Reduce Cognitive Deficits
Alzheimer's disease (AD) is an incurable disease that is increasing in prevalence and will increase even more rapidly as the Baby Boom generation enters the age of highest risk. The available AD drugs are only partially effective in some patients. New strategies are urgently needed.
In a new study, published in the Journal of Neuroscience, researchers in the laboratory of Lennart Mucke, MD, director of the Gladstone Institute of Neurological Disease (GIND), have determined in mouse models that modulating the activity of enkephalin peptides in the brain might reduce the cognitive deficits seen in Alzheimer's disease.
Enkephalins are part of the endogenous opioid system, which modulates learning and memory and other brain functions. They are produced by several different cell types in the brain, particularly in areas affected by AD. Enkephalins are derived by enzymatic cleavage from a precursor protein, preproenkephalin, and stored in vesicles. Upon stimulation, enkephalins are released with neurotransmitters, such as glutamate.
"The enkephalin pathway is an intriguing candidate for us because it is involved in many functions that are affected by Alzheimer's and other neurodegenerative diseases," said Dr. Mucke. "We were not sure, though, whether it contributed causally to the disease or acts as a compensatory mechanism."
To better understand the activities of the enkephalins in AD, the Mucke team examined their functions in a transgenic mouse model of AD. These mice express two proteins associated with AD - human amyloid precursor protein (hAPP) and its cleavage product, A??? peptides - in neurons and exhibit several characteristics of AD.
The team found increased levels of preproenkephalin mRNA and of enkephalin in brain regions important for memory that are affected in early stages of AD.
When they genetically manipulated the mice to make them more or less susceptible to neuronal damage, the scientists found that the enkephalin levels were also affected. Furthermore, as levels of the enkephalins increased, the ability of mice to complete behavioral tests declined. Compounds that blocked opioid receptors, through which enkaphalins exert their effects, reduced cognitive deficits. AD patients also showed increased levels of enkephalins in brain regions affected by the disease.
"Our results indicate that the high levels of enkephalins may contribute to cognitive impairments in hAPP mice and maybe also in AD patients," said Dr. Mucke. "Although these are early results, they are encouraging and may lead the way to a new AD therapy based on limiting enkephalin production or signaling."
William J. Meilandt , Gui-Qiu Yy, Jeannie Chin, Erik D. Roberson, Jorge. J. Palop, Tiffany Wu, and Kimberly Scearce-Levie also contributed to the study. The research was supported by the National Institutes of Health and the Gladstone Institutes.
About the Gladstone Institutes:
The J. David Gladstone Institutes, affiliated with the University of California, San Francisco (UCSF), is dedicated to the health and welfare of humankind through research into the causes and prevention of some of the world's most devastating diseases. Gladstone is comprised of the Gladstone Institute of Cardiovascular Disease, the Gladstone Institute of Virology and Immunology, and the Gladstone Institute of Neurological Disease. More information can be found at gladstone.ucsf/
Source: Valerie Tucker
Gladstone Institutes
In a new study, published in the Journal of Neuroscience, researchers in the laboratory of Lennart Mucke, MD, director of the Gladstone Institute of Neurological Disease (GIND), have determined in mouse models that modulating the activity of enkephalin peptides in the brain might reduce the cognitive deficits seen in Alzheimer's disease.
Enkephalins are part of the endogenous opioid system, which modulates learning and memory and other brain functions. They are produced by several different cell types in the brain, particularly in areas affected by AD. Enkephalins are derived by enzymatic cleavage from a precursor protein, preproenkephalin, and stored in vesicles. Upon stimulation, enkephalins are released with neurotransmitters, such as glutamate.
"The enkephalin pathway is an intriguing candidate for us because it is involved in many functions that are affected by Alzheimer's and other neurodegenerative diseases," said Dr. Mucke. "We were not sure, though, whether it contributed causally to the disease or acts as a compensatory mechanism."
To better understand the activities of the enkephalins in AD, the Mucke team examined their functions in a transgenic mouse model of AD. These mice express two proteins associated with AD - human amyloid precursor protein (hAPP) and its cleavage product, A??? peptides - in neurons and exhibit several characteristics of AD.
The team found increased levels of preproenkephalin mRNA and of enkephalin in brain regions important for memory that are affected in early stages of AD.
When they genetically manipulated the mice to make them more or less susceptible to neuronal damage, the scientists found that the enkephalin levels were also affected. Furthermore, as levels of the enkephalins increased, the ability of mice to complete behavioral tests declined. Compounds that blocked opioid receptors, through which enkaphalins exert their effects, reduced cognitive deficits. AD patients also showed increased levels of enkephalins in brain regions affected by the disease.
"Our results indicate that the high levels of enkephalins may contribute to cognitive impairments in hAPP mice and maybe also in AD patients," said Dr. Mucke. "Although these are early results, they are encouraging and may lead the way to a new AD therapy based on limiting enkephalin production or signaling."
William J. Meilandt , Gui-Qiu Yy, Jeannie Chin, Erik D. Roberson, Jorge. J. Palop, Tiffany Wu, and Kimberly Scearce-Levie also contributed to the study. The research was supported by the National Institutes of Health and the Gladstone Institutes.
About the Gladstone Institutes:
The J. David Gladstone Institutes, affiliated with the University of California, San Francisco (UCSF), is dedicated to the health and welfare of humankind through research into the causes and prevention of some of the world's most devastating diseases. Gladstone is comprised of the Gladstone Institute of Cardiovascular Disease, the Gladstone Institute of Virology and Immunology, and the Gladstone Institute of Neurological Disease. More information can be found at gladstone.ucsf/
Source: Valerie Tucker
Gladstone Institutes
вторник, 9 августа 2011 г.
Depression Increases Risk Of Alzheimer's Disease
People who have had depression are more likely to develop Alzheimer's disease than people who have never had depression, according to a study published in the April 8, 2008, issue of Neurology®, the medical journal of the American Academy of Neurology.
The study involved 486 people age 60 to 90 who had no dementia. Of those, 134 people had experienced at least one episode of depression that prompted them to seek medical advice.
The participants were followed for an average of six years. During that time 33 people developed Alzheimer's disease. People who had experienced depression were 2.5 times more likely to develop Alzheimer's disease than people who had never had depression. The risk was even higher for those whose depression occurred before the age of 60; they were nearly four times more likely to develop Alzheimer's than those with no depression.
"We don't know yet whether depression contributes to the development of Alzheimer's disease or whether another unknown factor causes both depression and dementia," said study author Monique M.B. Breteler, MD, PhD, with the Erasmus University Medical Center in Rotterdam, the Netherlands. "We'll need to do more studies to understand the relationship between depression and dementia."
One theory was that depression leads to loss of cells in two areas of the brain, the hippocampus and the amygdala, which then contributes to Alzheimer's disease. But this study found no difference in the size of these two brain areas between people with depression and people who had never had depression.
The study also assessed whether the participants had symptoms of depression at the start of the study. But those with depressive symptoms at the start of the study were not more likely to develop Alzheimer's than those with no depression at the start of the study.
The study was supported by the Netherlands Organization for Scientific Research and the Health Research and Development Council.
The American Academy of Neurology, an association of more than 21,000 neurologists and neuroscience professionals, is dedicated to improving patient care through education and research. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as stroke, Alzheimer's disease, epilepsy, Parkinson's disease, and multiple sclerosis.
For more information about the American Academy of Neurology, visit aan.
American Academy of Neurology (AAN)
1080 Montreal Ave.
St. Paul, MN 55116
United States
neurology
The study involved 486 people age 60 to 90 who had no dementia. Of those, 134 people had experienced at least one episode of depression that prompted them to seek medical advice.
The participants were followed for an average of six years. During that time 33 people developed Alzheimer's disease. People who had experienced depression were 2.5 times more likely to develop Alzheimer's disease than people who had never had depression. The risk was even higher for those whose depression occurred before the age of 60; they were nearly four times more likely to develop Alzheimer's than those with no depression.
"We don't know yet whether depression contributes to the development of Alzheimer's disease or whether another unknown factor causes both depression and dementia," said study author Monique M.B. Breteler, MD, PhD, with the Erasmus University Medical Center in Rotterdam, the Netherlands. "We'll need to do more studies to understand the relationship between depression and dementia."
One theory was that depression leads to loss of cells in two areas of the brain, the hippocampus and the amygdala, which then contributes to Alzheimer's disease. But this study found no difference in the size of these two brain areas between people with depression and people who had never had depression.
The study also assessed whether the participants had symptoms of depression at the start of the study. But those with depressive symptoms at the start of the study were not more likely to develop Alzheimer's than those with no depression at the start of the study.
The study was supported by the Netherlands Organization for Scientific Research and the Health Research and Development Council.
The American Academy of Neurology, an association of more than 21,000 neurologists and neuroscience professionals, is dedicated to improving patient care through education and research. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as stroke, Alzheimer's disease, epilepsy, Parkinson's disease, and multiple sclerosis.
For more information about the American Academy of Neurology, visit aan.
American Academy of Neurology (AAN)
1080 Montreal Ave.
St. Paul, MN 55116
United States
neurology
суббота, 6 августа 2011 г.
Two New Studies Show Dementia Care Fails People With Sight Loss
The sight loss charity, Thomas Pocklington Trust (1), calls for a fresh approach to dementia care after new research confirms a lack of attention to sight loss. A sensory model of care practice should be developed, says the charity after two new studies revealed a widespread failing to acknowledge the importance of sight loss.
The first study, "People with dementia and sight loss: a scoping study of models of care," (2) exposes pressing and persistent problems in the care of those with dementia and sight loss. It finds that both the most widely used model of care, and the leading best-practice literature display "a fundamental lack of sensitivity about sight loss."
The second study, "Visual Hallucinations in Sight Loss and Dementia", (3) describes people with joint dementia and sight loss as a forgotten group, and finds that many cases are missed or misdiagnosed because of failures to assess for both conditions.
Says Dr. Angela McCullagh, Research and Development Director, Thomas Pocklington Trust, "Sight loss plays a major role in people's experience of dementia, yet it is almost entirely excluded from current models of care. A change in policy and practice is needed, where sight loss is made visible in dementia care."
The first study (Models of Care) looked at major texts, interviewed practitioners and audited care homes. It found that while front-line care workers try to respond to the problems of dementia and sight loss, neither official policy nor guidance provides the means to fully address the issue.
Eight leading models of practice were assessed. One specifically gives importance to visual cues. Of the rest, only two explicitly mention visual impairment. The most common model used in the UK (4), which is embedded in dementia policy, fails to take sight loss into account.
Dementia policy, says the study:
- Pays too little attention to the physical environment to be sensitive to joint dementia and sight loss.
- Overlooks sensory solutions that help groups of people such as good lighting, contrasting and tactile signage and positive sounds.
A new model of care - a sensory model - is needed, say the researchers (5).
In dementia care literature it is generally assumed that people can see:
- Issues related to joint dementia and sight loss are not highlighted or debated.
- Key words that might be expected - visual impairment, lighting, optometrists, eye care/health - are not even indexed in "best practice" texts.
- Opportunities to highlight issues of sight loss are overlooked. Eg: Multi-sensory methods such as aromatherapy and music therapy are discussed with no mention of their potential value to those with sight loss.
In dementia care practice:
- Sensitivity to and awareness of sight loss issues varies amongst practitioners.
- In care homes, inspectors often rely on notice boards to provide information.
- The importance of wearing spectacles, having eye examinations and taking up free NHS tests can be overlooked. One care home had not had an optometrist visit for over a year and managers were sceptical about the value of eye tests for people with dementia.
Interest in developing effective models of care is clear: the researchers quickly brought together over 30 organisations and staff looking for better ways to support people who have sight loss and dementia.
The second study (Hallucinations), carried out by researchers at the Institute of Psychiatry, King's College, London, reviewed existing literature on hallucinations in sight loss and dementia and found the three conditions occur together more frequently than previously recognised.
From their study the researchers predict that 30% of those with combined sight loss and dementia will have hallucinations - around 35,000 people in the UK. However, the study also led them to question whether previous research has overlooked the fact that sight loss and dementia may act together to cause hallucinations. In this case, some 118,000 people could be affected - 100% of those with joint dementia and sight loss. Despite this the study could find no evidence of initiatives, guidelines or co-ordinated working between professionals in the two fields. Many cases of combined sight loss and dementia are missed, says the study, as routine assessments for both conditions are rare. This means that someone with sight loss may be wrongly diagnosed with dementia or a diagnosis of dementia may be missed in someone with sight loss.
"Once again, people who have joint sight loss and dementia are missing out on a combined approach to care," says Dr. McCullagh. "The research shows a clear need for greater coordination amongst professionals. Now more research is needed both to widen our knowledge of this forgotten group and to develop professional practices that address their particular experiences."
Source
Thomas Pocklington Trust
The first study, "People with dementia and sight loss: a scoping study of models of care," (2) exposes pressing and persistent problems in the care of those with dementia and sight loss. It finds that both the most widely used model of care, and the leading best-practice literature display "a fundamental lack of sensitivity about sight loss."
The second study, "Visual Hallucinations in Sight Loss and Dementia", (3) describes people with joint dementia and sight loss as a forgotten group, and finds that many cases are missed or misdiagnosed because of failures to assess for both conditions.
Says Dr. Angela McCullagh, Research and Development Director, Thomas Pocklington Trust, "Sight loss plays a major role in people's experience of dementia, yet it is almost entirely excluded from current models of care. A change in policy and practice is needed, where sight loss is made visible in dementia care."
The first study (Models of Care) looked at major texts, interviewed practitioners and audited care homes. It found that while front-line care workers try to respond to the problems of dementia and sight loss, neither official policy nor guidance provides the means to fully address the issue.
Eight leading models of practice were assessed. One specifically gives importance to visual cues. Of the rest, only two explicitly mention visual impairment. The most common model used in the UK (4), which is embedded in dementia policy, fails to take sight loss into account.
Dementia policy, says the study:
- Pays too little attention to the physical environment to be sensitive to joint dementia and sight loss.
- Overlooks sensory solutions that help groups of people such as good lighting, contrasting and tactile signage and positive sounds.
A new model of care - a sensory model - is needed, say the researchers (5).
In dementia care literature it is generally assumed that people can see:
- Issues related to joint dementia and sight loss are not highlighted or debated.
- Key words that might be expected - visual impairment, lighting, optometrists, eye care/health - are not even indexed in "best practice" texts.
- Opportunities to highlight issues of sight loss are overlooked. Eg: Multi-sensory methods such as aromatherapy and music therapy are discussed with no mention of their potential value to those with sight loss.
In dementia care practice:
- Sensitivity to and awareness of sight loss issues varies amongst practitioners.
- In care homes, inspectors often rely on notice boards to provide information.
- The importance of wearing spectacles, having eye examinations and taking up free NHS tests can be overlooked. One care home had not had an optometrist visit for over a year and managers were sceptical about the value of eye tests for people with dementia.
Interest in developing effective models of care is clear: the researchers quickly brought together over 30 organisations and staff looking for better ways to support people who have sight loss and dementia.
The second study (Hallucinations), carried out by researchers at the Institute of Psychiatry, King's College, London, reviewed existing literature on hallucinations in sight loss and dementia and found the three conditions occur together more frequently than previously recognised.
From their study the researchers predict that 30% of those with combined sight loss and dementia will have hallucinations - around 35,000 people in the UK. However, the study also led them to question whether previous research has overlooked the fact that sight loss and dementia may act together to cause hallucinations. In this case, some 118,000 people could be affected - 100% of those with joint dementia and sight loss. Despite this the study could find no evidence of initiatives, guidelines or co-ordinated working between professionals in the two fields. Many cases of combined sight loss and dementia are missed, says the study, as routine assessments for both conditions are rare. This means that someone with sight loss may be wrongly diagnosed with dementia or a diagnosis of dementia may be missed in someone with sight loss.
"Once again, people who have joint sight loss and dementia are missing out on a combined approach to care," says Dr. McCullagh. "The research shows a clear need for greater coordination amongst professionals. Now more research is needed both to widen our knowledge of this forgotten group and to develop professional practices that address their particular experiences."
Source
Thomas Pocklington Trust
среда, 3 августа 2011 г.
'Growing' New Approach In Training To Improve Dementia Care
Growing, the last book in Alzheimer's Society's Feelings Matter Most series, will be launched at the third national Dementia Congress in Bournemouth.
The series challenges current practises and urges dementia care trainers to give dementia care the time it needs. Growing highlights the need to grow training from simple awareness raising to developing evidence-based learning.
Author David Sheard sets clear guidelines for organisations to develop a person-centred learning and development training strategy. In Growing, David offers health professionals a unique ten point workshop programme designed for practical delivery by accomplished trainers in the dementia care environment.
Neil Hunt, Alzheimer's Society Chief Executive said,
Dementia is not a natural part of ageing; it is caused by diseases of the brain and robs people of their lives. This series takes a fresh look at how we can best support people with dementia and confronts preconceived ideas about how to ensure the best quality care for the 700,000 people living with the condition in the UK.
The publication is part of a series of books being produced by Alzheimer's Society. To order a copy of any Alzheimer's Society publications please telephone 01736 336995 or visit alzheimers.uk
Notes
- Pictures of the publication available on request
- 1 in 3 older people will end their lives with a form of 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 champions the rights of people living with dementia and those who care for them. Alzheimer's Society works in England, Wales and Northern Ireland
- As a charity, Alzheimer's Society depends on the generosity of the public to help it care, research and campaign for people with dementia. You can donate now by calling 0845 306 0898 or visiting alzheimers.uk
Alzheimer's Society
The series challenges current practises and urges dementia care trainers to give dementia care the time it needs. Growing highlights the need to grow training from simple awareness raising to developing evidence-based learning.
Author David Sheard sets clear guidelines for organisations to develop a person-centred learning and development training strategy. In Growing, David offers health professionals a unique ten point workshop programme designed for practical delivery by accomplished trainers in the dementia care environment.
Neil Hunt, Alzheimer's Society Chief Executive said,
Dementia is not a natural part of ageing; it is caused by diseases of the brain and robs people of their lives. This series takes a fresh look at how we can best support people with dementia and confronts preconceived ideas about how to ensure the best quality care for the 700,000 people living with the condition in the UK.
The publication is part of a series of books being produced by Alzheimer's Society. To order a copy of any Alzheimer's Society publications please telephone 01736 336995 or visit alzheimers.uk
Notes
- Pictures of the publication available on request
- 1 in 3 older people will end their lives with a form of 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 champions the rights of people living with dementia and those who care for them. Alzheimer's Society works in England, Wales and Northern Ireland
- As a charity, Alzheimer's Society depends on the generosity of the public to help it care, research and campaign for people with dementia. You can donate now by calling 0845 306 0898 or visiting alzheimers.uk
Alzheimer's Society
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