The American Federation for Aging Research (AFAR), The National Institute on Aging (NIA), The Atlantic Philanthropies, The John A. Hartford Foundation, The Starr Foundation and other program partners are pleased to announce the 2009 recipients of the Paul B. Beeson Career Development Awards in Aging Research Program. This new cohort brings the total to 157 scholars who have been selected for this highly competitive and prestigious award, which seeks to create a cadre of clinically trained faculty who are committed to academic careers in aging research, teaching and practice.
Since the program's inception in 1995, Beeson Scholars have received more than $86 million in research grant support and have made their mark with innovative research-from the effects of depression in elderly health outcomes, to the connection between a certain type of cataract and Alzheimer's disease, to the development of new animal models to study the genetic basis of aging, to improving end-of-life care for under-served aging populations.
The Beeson program has become a model of cooperation between foundations and government entities. To that end, the National Institute of Mental Health (NIMH) announced that it would join as a program partner beginning in 2010. The John A. Hartford Foundation has renewed its support through 2012.
"It is crucial to encourage and support researchers who are proficient in clinical aspects of aging," said NIA Director Richard J. Hodes, MD. "The Beeson Awards provide protected research time and mentoring in a strong research environment, helping these young scientists establish their careers. Since the program began, we have seen increasing numbers of Beeson Scholars compete successfully for grant funding both from the NIA and other NIH Institutes and Centers."
The Beeson Award is granted to scholars who are laying clinically relevant groundwork in many areas related to aging, including the biology of aging and age-related diseases, as well as health outcomes, health services and clinical management issues, with the goal of enhancing the health and quality of life of older adults. Scholars receive $600,000 to $800,000 for a three-to five-year period, allowing them flexible and protected time for innovative research.
This year's scholars will study a broad array of topics such as the benefits and burdens of mammography screening for very old women, the challenges of access to kidney transplantation for elderly patients and determining the role of oxidative damage in the onset and progression of muscle loss and wasting, a common age-related condition.
"Research on aging encompasses many areas of investigation and care: from the very basic biology of aging processes to the clinical and social care needs," said Corinne Rieder, EdD, executive director of The John A. Hartford Foundation. "The Beeson program clearly addresses these needs by creating an outstanding network of the top scientists in the country who are helping to tackle the many research and clinical challenges of geriatric medicine - challenges that will only become more urgent in the future. We are pleased to renew our support for the Beeson program and welcome our new partner, the National Institute of Mental Health."
"NIMH strives to nurture talented physician scientists and to enhance the impact of their research on the enormous public health burden that mental illnesses have across the lifespan," said NIMH Director Thomas R. Insel, MD. "We hope to underwrite such support targeted at our increasingly aging population through the Beeson Scholars program."
"One of the goals of the Beeson program is to cultivate future leaders in aging research and mentor other scientists who follow, ultimately creating a network of the best talent in the field of aging," said Stephanie Lederman, executive director of AFAR. "Our Beeson Scholars have proven that we have succeeded. Critical to the success of the Beeson program, however, are the partners, who enable the program to grow and thrive. We thank the NIMH for joining us and The John A. Hartford Foundation for renewing their long-standing commitment to the program."
2009 Beeson Scholars
Cynthia M. Boyd, MD, MPH, Assistant Professor, Johns Hopkins University School of Medicine: Treatment Burden in Older Adults with Diabetes and Multimorbidity
Dena B. Dubal, MD, PhD, Assistant Adjunct Professor, University of California, San Francisco: Collagen VI: Novel Mechanisms and Functions in Alzheimer's Disease
Christiane Reitz, MD, PhD, Postdoctoral Research Scientist, Columbia University College of Physicians and Surgeons: Mapping Causative Factors in the Sortilin-related Pathway in Alzheimer's Disease
Mara Schonberg, MD, Instructor of Medicine, Harvard Medical School/Beth Israel Deaconess Medical Center: Benefits and Burdens of Screening Oldest-old Women: The Case of Mammography
Dorry Segev, MD, Assistant Professor, Johns Hopkins University School of Medicine: Access to Kidney Transplantation in Elderly Patients
Edmond Teng, MD, PhD, Clinical Instructor, University of California, Los Angeles: Assessment of Biomarkers and Behavior in a Transgenic Rat Model of Alzheimer's Disease
Heidi L. Wald, MD, MSPH, Assistant Professor of Medicine, University of Colorado Denver: Reducing Urinary Tract Infections in the Hospitalized Older Patient
Jonathan Wanagat, MD, PhD, Acting Instructor, University of Washington: Mitochondrial Genetics in Skeletal Muscle Aging
In 2007, supported by The Atlantic Philanthropies, the Beeson program expanded to the Republic of Ireland and Northern Ireland with the goal of helping to train physicians in geriatrics, build Ireland's capacity to provide high-quality care for older adults and advance knowledge of geriatric care. Five physician-scientists have been named Beeson Ireland Scholars thus far, including two this year, who received $450,000 each:
Chie Wei (Mimi) Fan, MD, RCPI, Clinical Director of Technology Research for Independent Living, St. James's Hospital: Age-related Autonomic Dysfunction and its Impact on Cognition, Gait and Falls
Ronan R. Mullan, PhD, Specialist Registrar in Rheumatology and Internal Medicine, University College Dublin: Acute Phase Serum Amyloid-A (A-SAA) in Ageing, Arthritis and Obesity - Potential Common Mechanism for Cardiovascular Disease
The Paul B. Beeson Career Development Awards in Aging Research Program is sponsored by the NIA, The Atlantic Philanthropies, The John A. Hartford Foundation, The National Institute of Mental Health, The Starr Foundation and an anonymous donor, and is administered by the NIA and AFAR. The program is named in honor of the late Paul B. Beeson, MD, who was professor emeritus of medicine at the University of Washington, and whose vision was to increase the number of physicians with a combined clinical, academic, and scientific expertise to care for a growing older population.
Source:
Stacey Harris
American Federation for Aging Research
пятница, 13 мая 2011 г.
среда, 11 мая 2011 г.
Alzheimer's is a consequence of inflammation
A group of scientists at The Scripps Research Institute has proposed a new theory about the cause of Alzheimer's disease, the progressive neurodegenerative disorder that currently afflicts some 4.5 million Americans.
According to the hypothesis, the disease arises as a consequence of inflammation, which creates abnormal metabolites out of normal brain molecules.
These abnormal metabolites then modify "amyloid beta" proteins in the brain and cause them to misfold. Misfolded amyloid beta proteins are thought to be a major player in Alzheimer's disease, because they can accumulate into the fibrils and plaques that autopsies reveal in the brains of patients with the disease. These fibrils and plaques and their precursors are implicated in neuronal loss.
The inflammation process that creates these metabolites can be triggered by numerous stimuli, including infections that precede the onset of Alzheimer's disease by a significant amount of time-perhaps years.
"If a certain inflammatory metabolite or family of metabolites confers risk later in life, then we need to know this, and we need to attack the problem," says Scripps Research Professor Jeffery W. Kelly, who is the Lita Annenberg Hazen Professor of Chemistry in The Skaggs Institute for Chemical Biology and vice president of academic affairs at Scripps Research.
Kelly and his Scripps Research colleagues present their new theory in an article that will be published in an upcoming issue of the journal Proceedings of the National Academy of Sciences.
A Progressive, Incurable Disease
Alzheimer's is a progressive neurodegenerative disease marked by memory loss, loss of language ability, loss of the ability to mentally manipulate visual information, poor judgment, confusion, restlessness, and mood swings. According to the Alzheimer's Disease Education and Referral Center, a service of the National Institute on Aging, Alzheimer's disease is now believed to inflict some 4.5 million people and is the most common form of dementia among older people in the United States. Currently, there is no cure for Alzheimer's and no way to slow the progression of the disease.
German doctor Alois Alzheimer discovered the disease in 1906, when he examined a post-mortem patient who had died with an unusual mental illness. Alzheimer found unusual clumps of protein or plaques in her brain. These plaques-made up of aggregated proteins called amyloid beta-are a clear sign of the disease, and the aggregation of amyloid beta protein is an accepted primary pathological marker for Alzheimer's.
But scientists have not been sure whether these fibrils are causing the disease or are simply a marker of it. By analogy, a tidal wave may cause massive destruction to a coastal area, but the tidal wave itself may have been caused by a distant earthquake undetected in that coastal area.
Kelly and his colleagues have studied the basic biology of Alzheimer's and related diseases for many years, looking for new treatment approaches. Now, they think they may have taken a significant step along this path by identifying the distant earthquake that causes Alzheimer's.
Basic Science Brings it All Together
Amyloid diseases are caused by the misfolding of proteins into structures that lead them to cluster together, forming microscopic fibril or plaques, which deposit in internal organs and interfere with normal function, sometimes lethally. In the case of Alzheimer's, these fibrils kill nerve cells in areas of the brain that are crucial for memory.
These diseases include Alzheimer's, Parkinson's, and a peripheral nervous system disease called familial amyloid polyneuropathy (FAP)-a collection of more than 80 rare amyloid diseases caused by the misfolding of the protein transthyretin (TTR), which the liver secretes into the bloodstream to carry thyroid hormone and vitamin A.
In the FAP diseases, mutations in the TTR protein are known to play a direct role in causing the disease. Basically, these mutations change the amino acid sequence of TTR, and these changes alter protein folding in such a way as to predispose the proteins to misfold and accumulate into microscopic fibrils, which can then grow into the protein plaques characteristic of FAP and other amyloid diseases.
However, in Alzheimer's disease, the cause of misfolding is not so obvious. A number of mutations are associated with rare forms of familial Alzheimer's, but not with most common cases (about 95 percent of the cases). This suggests there must be a more common cause of Alzheimer's disease, and Kelly has combined efforts with several of his colleagues at Scripps Research to find it.
A few years ago, Kelly started to think about traumatic head injuries, which are a major risk factor for later developing Alzheimer's disease. The body responds to such injuries with inflammatory reactions that cause the release of components of lipid membranes, such as cholesterol.
Kelly began to discuss this with his colleagues in The Skaggs Institute for Chemical Biology, Scripps Research President Richard A. Lerner, M.D., and Scripps Research Associate Professor Paul Wentworth, Jr., Ph.D. Lerner and Wentworth had recently discovered how inflammation can lead to the production of reactive oxygen species such as ozone, which can trigger pathological changes in other molecules in the body, like cholesterol.
In a paper last year, Lerner, Wentworth, and several colleagues described how ozone reacts with normal metabolites to produce toxic compounds during inflammatory processes taking place in the body. The scientists describe two such compounds, which they call the "atheronals." The scientists suggest these newly identified products are critical to the pathogenesis of the disease atherosclerosis because these atheronals were found in atherosclerotic plaques that were surgically removed from patients with atherosclerosis. (Atherosclerosis is a common vascular disease that increases the risk of heart attacks and strokes and is characterized by a hardening of the arteries over time due to deposits of fibrous tissue, calcium, fat, cholesterol, proteins, cells, and other materials on the inner "endothelial" walls of an artery).
This discovery made Kelly sit up straight when he first heard it because inflammation is increasingly seen as playing a role in neurodegenerative diseases. Also, there are a fair number of risk factors in common between the two diseases, including hypercholesterolemia and inflammation.
In their new study, Kelly and his colleagues suggest that inflammation in the brain could create a perfect storm in which cholesterol and lipids react with ozone and other inflammatory chemicals to produce abnormal reactive metabolites, which, in turn, modify the folding of normal amyloid beta protein. These modified amyloid beta proteins can catalyze misfolding in other unmodified amyloid beta proteins, starting an avalanche of misfolding that results-perhaps years or decades later-in Alzheimer's disease.
A New Way of Thinking About Disease in General
To examine the hypothesis that these metabolites may be the root cause of Alzheimer's, Kelly and his colleagues examined the post-mortem brains of Alzheimer's patients and compared these to age-matched controls.
They found evidence of atheronals in the brains of both the Alzheimer's patients and the control subjects. The levels of atheronals in the brains of the Alzheimer's patients were not significantly elevated, but this is not necessarily surprising. According to the new theory, the propagation of misfolding and the buildup of fibrils inside the brain does not depend upon continuous exposure to metabolite-modified proteins, but to exposure during a precipitating event that may occur a decade or more earlier. The creation of these metabolite-linked misfolding proteins is only the initiator of the fibril plaques.
Kelly and colleagues also performed experiments in the test tube and found that atheronals and lipid oxidation products have the ability to dramatically accelerate the misfolding of amyloid beta and to reduce the concentration of the protein needed for misfolding to take place to concentrations found in the brain.
This is an entirely new way of thinking about not only Alzheimer's disease, but disease in general. Historically, science has regarded disease as based on the up or down regulation of gene expression or protein function. But this theory suggests a new sort of pathology-the creation of a reactive metabolite by inflammatory stress, leading to the modification of a protein, the aggregation of that protein over time, and the degeneration of function in the brain or whichever internal organ hosts the aggregation.
The inflammatory metabolite theory of Alzheimer's will be difficult to prove, admits Kelly, because the presence of these abnormal metabolites are hard to detect years after they initiated the aggregation. There is, so far, no smoking gun.
"Is [this theory] right? Time will tell," says Kelly. "That's how science works."
The article, "Metabolite-initiated protein misfolding may trigger Alzheimer's disease" was authored by Qinghai Zhang, Evan T. Powers, Jorge Nieva, Mary E. Huff, Maria A. Dendle, Jan Bieschke, Charles G. Glabe, Albert Eschenmoser, Paul Wentworth, Jr., Richard A. Lerner, and Jeffery W. Kelly and appears in the online edition of the journal Proceedings of the National Academy of Sciences the week of March 15-19, 2004. The article will appear in print later this year. See:
dx.doi/10.1073/pnas.0400924101
This work was supported by The Skaggs Institute for Chemical Biology and the Lita Annenberg Hazen Foundation.
Send comments to: jasonbscripps
According to the hypothesis, the disease arises as a consequence of inflammation, which creates abnormal metabolites out of normal brain molecules.
These abnormal metabolites then modify "amyloid beta" proteins in the brain and cause them to misfold. Misfolded amyloid beta proteins are thought to be a major player in Alzheimer's disease, because they can accumulate into the fibrils and plaques that autopsies reveal in the brains of patients with the disease. These fibrils and plaques and their precursors are implicated in neuronal loss.
The inflammation process that creates these metabolites can be triggered by numerous stimuli, including infections that precede the onset of Alzheimer's disease by a significant amount of time-perhaps years.
"If a certain inflammatory metabolite or family of metabolites confers risk later in life, then we need to know this, and we need to attack the problem," says Scripps Research Professor Jeffery W. Kelly, who is the Lita Annenberg Hazen Professor of Chemistry in The Skaggs Institute for Chemical Biology and vice president of academic affairs at Scripps Research.
Kelly and his Scripps Research colleagues present their new theory in an article that will be published in an upcoming issue of the journal Proceedings of the National Academy of Sciences.
A Progressive, Incurable Disease
Alzheimer's is a progressive neurodegenerative disease marked by memory loss, loss of language ability, loss of the ability to mentally manipulate visual information, poor judgment, confusion, restlessness, and mood swings. According to the Alzheimer's Disease Education and Referral Center, a service of the National Institute on Aging, Alzheimer's disease is now believed to inflict some 4.5 million people and is the most common form of dementia among older people in the United States. Currently, there is no cure for Alzheimer's and no way to slow the progression of the disease.
German doctor Alois Alzheimer discovered the disease in 1906, when he examined a post-mortem patient who had died with an unusual mental illness. Alzheimer found unusual clumps of protein or plaques in her brain. These plaques-made up of aggregated proteins called amyloid beta-are a clear sign of the disease, and the aggregation of amyloid beta protein is an accepted primary pathological marker for Alzheimer's.
But scientists have not been sure whether these fibrils are causing the disease or are simply a marker of it. By analogy, a tidal wave may cause massive destruction to a coastal area, but the tidal wave itself may have been caused by a distant earthquake undetected in that coastal area.
Kelly and his colleagues have studied the basic biology of Alzheimer's and related diseases for many years, looking for new treatment approaches. Now, they think they may have taken a significant step along this path by identifying the distant earthquake that causes Alzheimer's.
Basic Science Brings it All Together
Amyloid diseases are caused by the misfolding of proteins into structures that lead them to cluster together, forming microscopic fibril or plaques, which deposit in internal organs and interfere with normal function, sometimes lethally. In the case of Alzheimer's, these fibrils kill nerve cells in areas of the brain that are crucial for memory.
These diseases include Alzheimer's, Parkinson's, and a peripheral nervous system disease called familial amyloid polyneuropathy (FAP)-a collection of more than 80 rare amyloid diseases caused by the misfolding of the protein transthyretin (TTR), which the liver secretes into the bloodstream to carry thyroid hormone and vitamin A.
In the FAP diseases, mutations in the TTR protein are known to play a direct role in causing the disease. Basically, these mutations change the amino acid sequence of TTR, and these changes alter protein folding in such a way as to predispose the proteins to misfold and accumulate into microscopic fibrils, which can then grow into the protein plaques characteristic of FAP and other amyloid diseases.
However, in Alzheimer's disease, the cause of misfolding is not so obvious. A number of mutations are associated with rare forms of familial Alzheimer's, but not with most common cases (about 95 percent of the cases). This suggests there must be a more common cause of Alzheimer's disease, and Kelly has combined efforts with several of his colleagues at Scripps Research to find it.
A few years ago, Kelly started to think about traumatic head injuries, which are a major risk factor for later developing Alzheimer's disease. The body responds to such injuries with inflammatory reactions that cause the release of components of lipid membranes, such as cholesterol.
Kelly began to discuss this with his colleagues in The Skaggs Institute for Chemical Biology, Scripps Research President Richard A. Lerner, M.D., and Scripps Research Associate Professor Paul Wentworth, Jr., Ph.D. Lerner and Wentworth had recently discovered how inflammation can lead to the production of reactive oxygen species such as ozone, which can trigger pathological changes in other molecules in the body, like cholesterol.
In a paper last year, Lerner, Wentworth, and several colleagues described how ozone reacts with normal metabolites to produce toxic compounds during inflammatory processes taking place in the body. The scientists describe two such compounds, which they call the "atheronals." The scientists suggest these newly identified products are critical to the pathogenesis of the disease atherosclerosis because these atheronals were found in atherosclerotic plaques that were surgically removed from patients with atherosclerosis. (Atherosclerosis is a common vascular disease that increases the risk of heart attacks and strokes and is characterized by a hardening of the arteries over time due to deposits of fibrous tissue, calcium, fat, cholesterol, proteins, cells, and other materials on the inner "endothelial" walls of an artery).
This discovery made Kelly sit up straight when he first heard it because inflammation is increasingly seen as playing a role in neurodegenerative diseases. Also, there are a fair number of risk factors in common between the two diseases, including hypercholesterolemia and inflammation.
In their new study, Kelly and his colleagues suggest that inflammation in the brain could create a perfect storm in which cholesterol and lipids react with ozone and other inflammatory chemicals to produce abnormal reactive metabolites, which, in turn, modify the folding of normal amyloid beta protein. These modified amyloid beta proteins can catalyze misfolding in other unmodified amyloid beta proteins, starting an avalanche of misfolding that results-perhaps years or decades later-in Alzheimer's disease.
A New Way of Thinking About Disease in General
To examine the hypothesis that these metabolites may be the root cause of Alzheimer's, Kelly and his colleagues examined the post-mortem brains of Alzheimer's patients and compared these to age-matched controls.
They found evidence of atheronals in the brains of both the Alzheimer's patients and the control subjects. The levels of atheronals in the brains of the Alzheimer's patients were not significantly elevated, but this is not necessarily surprising. According to the new theory, the propagation of misfolding and the buildup of fibrils inside the brain does not depend upon continuous exposure to metabolite-modified proteins, but to exposure during a precipitating event that may occur a decade or more earlier. The creation of these metabolite-linked misfolding proteins is only the initiator of the fibril plaques.
Kelly and colleagues also performed experiments in the test tube and found that atheronals and lipid oxidation products have the ability to dramatically accelerate the misfolding of amyloid beta and to reduce the concentration of the protein needed for misfolding to take place to concentrations found in the brain.
This is an entirely new way of thinking about not only Alzheimer's disease, but disease in general. Historically, science has regarded disease as based on the up or down regulation of gene expression or protein function. But this theory suggests a new sort of pathology-the creation of a reactive metabolite by inflammatory stress, leading to the modification of a protein, the aggregation of that protein over time, and the degeneration of function in the brain or whichever internal organ hosts the aggregation.
The inflammatory metabolite theory of Alzheimer's will be difficult to prove, admits Kelly, because the presence of these abnormal metabolites are hard to detect years after they initiated the aggregation. There is, so far, no smoking gun.
"Is [this theory] right? Time will tell," says Kelly. "That's how science works."
The article, "Metabolite-initiated protein misfolding may trigger Alzheimer's disease" was authored by Qinghai Zhang, Evan T. Powers, Jorge Nieva, Mary E. Huff, Maria A. Dendle, Jan Bieschke, Charles G. Glabe, Albert Eschenmoser, Paul Wentworth, Jr., Richard A. Lerner, and Jeffery W. Kelly and appears in the online edition of the journal Proceedings of the National Academy of Sciences the week of March 15-19, 2004. The article will appear in print later this year. See:
dx.doi/10.1073/pnas.0400924101
This work was supported by The Skaggs Institute for Chemical Biology and the Lita Annenberg Hazen Foundation.
Send comments to: jasonbscripps
вторник, 10 мая 2011 г.
Political Debate On Social Care Fails To Reassure The Public, UK
Almost two thirds (59%) of people are worried about the standard of care they could receive in old age while nearly a third (30%) feel none of the three main political parties are addressing the issue successfully.
The new Alzheimer's Society commissioned YouGov poll suggests the pre-election debate on social care has so far failed to convince voters that the current situation is likely to be improved. Not only does the survey of more than 2,000 people show a concern for the standard of care, it also demonstrates mixed opinions on how the care should be funded.
Social care, including help with dressing, washing and eating, is currently means tested and can cost people - including people with dementia - tens of thousands of pounds. However only one in 10 people say putting money aside to pay for a care is currently a priority.
A number of alternative funding methods have been outlined by political parties including insurance models and inheritance tax. Only eight per cent of people say they would rather risk selling their home to pay for care than take out insurance to protect themselves. However, less than a quarter (23%) would rather the government introduce a ??20,000 inheritance tax to fund the social care system than risk having to sell their home to pay for their own care.
Alzheimer's Society is now calling on all political parties to come together to tackle this issue head on and to address the concerns of their voters.
Ruth Sutherland, Acting Chief Executive of Alzheimer's Society, said:
'These results demonstrate that care for older people is a real worry for people ahead of the general election. In the context of the current broken system which burdens older people with huge bills for often substandard care this comes as little surprise.
'People with dementia are often the hardest hit and can pay up to ??40,000 a year, sometimes being forced to sell their homes, to pay for their care. Politicians now have a golden opportunity to change this picture and people with dementia could be some of the biggest winners. With the election looming we need to move away from soundbites and start hearing detailed plans for how the parties will create a care service that guarantees high quality care at a fair price.'
Notes
All figures, unless otherwise stated, are from YouGov Plc. Total sample size was 2282 adults. Fieldwork was undertaken between 5th - 8th March 2010. The survey was carried out online. The figures have been weighted and are representative of all GB adults (aged 18+).
Source
Alzheimer's Society
The new Alzheimer's Society commissioned YouGov poll suggests the pre-election debate on social care has so far failed to convince voters that the current situation is likely to be improved. Not only does the survey of more than 2,000 people show a concern for the standard of care, it also demonstrates mixed opinions on how the care should be funded.
Social care, including help with dressing, washing and eating, is currently means tested and can cost people - including people with dementia - tens of thousands of pounds. However only one in 10 people say putting money aside to pay for a care is currently a priority.
A number of alternative funding methods have been outlined by political parties including insurance models and inheritance tax. Only eight per cent of people say they would rather risk selling their home to pay for care than take out insurance to protect themselves. However, less than a quarter (23%) would rather the government introduce a ??20,000 inheritance tax to fund the social care system than risk having to sell their home to pay for their own care.
Alzheimer's Society is now calling on all political parties to come together to tackle this issue head on and to address the concerns of their voters.
Ruth Sutherland, Acting Chief Executive of Alzheimer's Society, said:
'These results demonstrate that care for older people is a real worry for people ahead of the general election. In the context of the current broken system which burdens older people with huge bills for often substandard care this comes as little surprise.
'People with dementia are often the hardest hit and can pay up to ??40,000 a year, sometimes being forced to sell their homes, to pay for their care. Politicians now have a golden opportunity to change this picture and people with dementia could be some of the biggest winners. With the election looming we need to move away from soundbites and start hearing detailed plans for how the parties will create a care service that guarantees high quality care at a fair price.'
Notes
All figures, unless otherwise stated, are from YouGov Plc. Total sample size was 2282 adults. Fieldwork was undertaken between 5th - 8th March 2010. The survey was carried out online. The figures have been weighted and are representative of all GB adults (aged 18+).
Source
Alzheimer's Society
понедельник, 9 мая 2011 г.
Study Points To Cocktail Therapy For Alzheimer's - Beverage Supplement Improves Memory, Learning In Gerbils
A dietary cocktail that includes a type of omega-3 fatty acid can improve memory and learning in gerbils, according to the latest study from MIT researchers that points to a possible beverage-based treatment for Alzheimer's and other brain diseases.
The combination of supplements, which contains three compounds normally found in the bloodstream, is now being tested in Alzheimer's patients. The cocktail has previously been shown to promote growth of new brain connections in rodents.
"It may be possible to use this treatment to partially restore brain function in people with diseases that decrease the number of brain neurons, including, for example, Alzheimer's disease, Parkinson's, strokes and brain injuries. Of course, such speculations have to be tested in double-blind, placebo-controlled clinical trials," said Richard Wurtman, Cecil H. Green Distinguished Professor of Neuropharmacology and senior author of a paper on the new work.
Such trials are now underway in Europe. A paper describing preliminary results has been submitted to the Alzheimer's Association International Conference on Alzheimer's Disease, to be held in Chicago July 26-31.
The new findings in gerbils appeared in the July 7 online edition of the Journal of FASEB (Federation of American Societies of Experimental Biology).
The researchers found that normal gerbils treated with the mixture-a combination of DHA (a type of omega-3 fatty acid), uridine and choline-performed significantly better on learning and memory tests than untreated gerbils.
Wurtman developed the treatment as a new approach to tackling Alzheimer's-restoring the synapses, or connections between brain cells, that leads to cognitive decline in Alzheimer's patients.
Synapses, where information is passed between neurons, play a critical role in learning and memory. Wurtman's laboratory has previously shown that the cocktail treatment improves those functions in rats with cognitive impairments.
The three dietary supplements under investigation are precursors to the fatty molecules that make up cell membranes, including the membranes of brain cells, which form synapses.
In the FASEB study, Wurtman and his colleagues found that gerbils that received all three supplements had up to 70 percent more phosphatides (a type of molecule that forms cell membranes) than control mice, suggesting that new synapses are forming.
"The improvements in cognition observed in normal gerbils in this study and in rats with impaired cognition, in a previous study, correlate perfectly with the evidence of increased brain synapses, as shown biochemically and anatomically," said Wurtman. "This suggests that treating the animals with the experimental mixture affects behavior by increasing the number of synapses in important brain regions.
Some of the gerbils in the studies received all three compounds and some received only two. The improvements in apparent synapse growth and cognitive ability were greatest in the rats given all three.
Omega-3 fatty acids are not produced in the body but are found in a variety of sources, including fish, eggs, flaxseed and meat from grass-fed animals. Choline can be synthesized in the body and obtained through the diet; it is found in meats, nuts and eggs. Uridine cannot be obtained from food sources, but is a component of human breast milk and can be produced in the body.
Lead author of the FASEB paper is Sarah Holguin, a recent MIT PhD recipient. Other authors are MIT undergraduates Joseph Martinez and Camille Chow.
The research was funded by the National Institutes of Health and the CBSMCT.
mit
The combination of supplements, which contains three compounds normally found in the bloodstream, is now being tested in Alzheimer's patients. The cocktail has previously been shown to promote growth of new brain connections in rodents.
"It may be possible to use this treatment to partially restore brain function in people with diseases that decrease the number of brain neurons, including, for example, Alzheimer's disease, Parkinson's, strokes and brain injuries. Of course, such speculations have to be tested in double-blind, placebo-controlled clinical trials," said Richard Wurtman, Cecil H. Green Distinguished Professor of Neuropharmacology and senior author of a paper on the new work.
Such trials are now underway in Europe. A paper describing preliminary results has been submitted to the Alzheimer's Association International Conference on Alzheimer's Disease, to be held in Chicago July 26-31.
The new findings in gerbils appeared in the July 7 online edition of the Journal of FASEB (Federation of American Societies of Experimental Biology).
The researchers found that normal gerbils treated with the mixture-a combination of DHA (a type of omega-3 fatty acid), uridine and choline-performed significantly better on learning and memory tests than untreated gerbils.
Wurtman developed the treatment as a new approach to tackling Alzheimer's-restoring the synapses, or connections between brain cells, that leads to cognitive decline in Alzheimer's patients.
Synapses, where information is passed between neurons, play a critical role in learning and memory. Wurtman's laboratory has previously shown that the cocktail treatment improves those functions in rats with cognitive impairments.
The three dietary supplements under investigation are precursors to the fatty molecules that make up cell membranes, including the membranes of brain cells, which form synapses.
In the FASEB study, Wurtman and his colleagues found that gerbils that received all three supplements had up to 70 percent more phosphatides (a type of molecule that forms cell membranes) than control mice, suggesting that new synapses are forming.
"The improvements in cognition observed in normal gerbils in this study and in rats with impaired cognition, in a previous study, correlate perfectly with the evidence of increased brain synapses, as shown biochemically and anatomically," said Wurtman. "This suggests that treating the animals with the experimental mixture affects behavior by increasing the number of synapses in important brain regions.
Some of the gerbils in the studies received all three compounds and some received only two. The improvements in apparent synapse growth and cognitive ability were greatest in the rats given all three.
Omega-3 fatty acids are not produced in the body but are found in a variety of sources, including fish, eggs, flaxseed and meat from grass-fed animals. Choline can be synthesized in the body and obtained through the diet; it is found in meats, nuts and eggs. Uridine cannot be obtained from food sources, but is a component of human breast milk and can be produced in the body.
Lead author of the FASEB paper is Sarah Holguin, a recent MIT PhD recipient. Other authors are MIT undergraduates Joseph Martinez and Camille Chow.
The research was funded by the National Institutes of Health and the CBSMCT.
mit
воскресенье, 8 мая 2011 г.
Victory For People With Alzheimer's, UK
People at all stages of Alzheimer's will now be able to access drugs on the NHS that can slow the progression of the disease.
The development comes following final guidance published by The National Institute for Health and Clinical Excellence (NICE). Alzheimer's Society services are holding celebrations around the country all week to mark the occasion.
The decision is a reversal of NICE's previous position - in place since 2007 - limiting access to only those in the moderate stages of the disease.
Andrew Chidgey, Head of Policy and Public Affairs at Alzheimer's Society, says,
'This is a victory for people with Alzheimer's and their carers, many of whom have been campaigning for this day for years. These drugs don't work for everyone, but for some people they can radically improve their quality of life. We now need more people to be diagnosed early and for them to receive the treatment, support and advice that they desperately need.'
There are currently 465,000 people living with Alzheimer's in the UK and a further 62,000 people are developing Alzheimer's each year. The drugs - Aricept, Exelon and Reminyl - will now be available on prescription for people in the early and moderate stages of Alzheimer's disease. These treatments have up to now been restricted to people in the moderate stages. A fourth drug, called Ebixa, will also be made available to people in the moderate to late stages.
Heather Roberts, 56, from Derby has Alzheimer's disease and has been heavily involved in the campaign since 2007. She says,
'It's absolutely fantastic that NICE has changed its guidelines on Alzheimer's drugs, but it's not before time. NICE should be ashamed of itself for restricting access to these essential drugs in the first place. Within six months of taking Aricept my memory had improved to how it had been two years previously. That is a measure of the difference it has made to me. I am still very independent - I've got my driving licence, regularly play tennis and enjoy going on holiday. Thank heavens NICE has finally seen sense.'
Notes
- The final decision by NICE comes following the publication in October 2010 of draft guidance and is part of a review cycle of Alzheimer's drug treatments.
- For more information on the background of Alzheimer's Society's campaigning work around NICE guidance on Alzheimer's drugs, visit here.
- If people are worried about their memory they should visit their GP. For information on drug treatments, an Alzheimer's Society factsheet is available.
Source:
Alzheimer's Society
View drug information on ARICEPT; Exelon; Reminyl.
The development comes following final guidance published by The National Institute for Health and Clinical Excellence (NICE). Alzheimer's Society services are holding celebrations around the country all week to mark the occasion.
The decision is a reversal of NICE's previous position - in place since 2007 - limiting access to only those in the moderate stages of the disease.
Andrew Chidgey, Head of Policy and Public Affairs at Alzheimer's Society, says,
'This is a victory for people with Alzheimer's and their carers, many of whom have been campaigning for this day for years. These drugs don't work for everyone, but for some people they can radically improve their quality of life. We now need more people to be diagnosed early and for them to receive the treatment, support and advice that they desperately need.'
There are currently 465,000 people living with Alzheimer's in the UK and a further 62,000 people are developing Alzheimer's each year. The drugs - Aricept, Exelon and Reminyl - will now be available on prescription for people in the early and moderate stages of Alzheimer's disease. These treatments have up to now been restricted to people in the moderate stages. A fourth drug, called Ebixa, will also be made available to people in the moderate to late stages.
Heather Roberts, 56, from Derby has Alzheimer's disease and has been heavily involved in the campaign since 2007. She says,
'It's absolutely fantastic that NICE has changed its guidelines on Alzheimer's drugs, but it's not before time. NICE should be ashamed of itself for restricting access to these essential drugs in the first place. Within six months of taking Aricept my memory had improved to how it had been two years previously. That is a measure of the difference it has made to me. I am still very independent - I've got my driving licence, regularly play tennis and enjoy going on holiday. Thank heavens NICE has finally seen sense.'
Notes
- The final decision by NICE comes following the publication in October 2010 of draft guidance and is part of a review cycle of Alzheimer's drug treatments.
- For more information on the background of Alzheimer's Society's campaigning work around NICE guidance on Alzheimer's drugs, visit here.
- If people are worried about their memory they should visit their GP. For information on drug treatments, an Alzheimer's Society factsheet is available.
Source:
Alzheimer's Society
View drug information on ARICEPT; Exelon; Reminyl.
суббота, 7 мая 2011 г.
Hispanics Have More Risk Factors For Developing Alzheimer's Disease Than Other Groups, Research Suggests
The New York Times on Tuesday examined research that found "many Hispanics may have more risk factors for developing dementia than other groups" and that a "significant number appear to be getting Alzheimer's earlier" than most U.S. residents, who commonly develop the disease in their 70s or 80s. According to the Alzheimer's Association, about 200,000 Hispanics in the U.S. have the condition but the number could increase to 1.3 million by 2050. "This is the tip of the iceberg of a huge public health challenge," Yanira Cruz, president of the National Hispanic Council on Aging, said, adding, "We really need to do more research in this population to really understand why it is that we're developing these conditions much earlier."
Overall, the number of U.S. residents with Alzheimer's is expected to increase from five million in 2008 to 16 million in 2050. According to experts, Hispanics are not more genetically predisposed to Alzheimer's but factors related to low income or cultural dislocation -- such as higher rates of diabetes, obesity, cardiovascular disease, stroke and high blood pressure -- may put them at a higher risk for dementia. Cruz said the immigration experience, along with the changes in diet and social network that it entails, could play a role in increased the risk of Alzheimer's. She said, "As you acculturate, you lose those protective factors linked to nutrition, physical activity [and a] social support system that come with you when you first arrive here."
According to the Times, less education also could make this group more vulnerable to risk factors and to dementia because, scientists say, education may increase the plasticity of the brain and its ability to compensate for symptoms. Some research also cites stress related to financial troubles or cultural adjustment as risk factors for dementia. In addition, Hispanics, who are less likely to see doctors because of financial and language barriers, often mistake the symptoms of dementia as a result of aging, according to the Times. "There's some taboos," Liany Arroyo, director of the Institute for Hispanic Health at the National Council of La Raza, said, adding that surveys his group completed indicated that some Hispanics "do not necessarily understand" what Alzheimer's is.
Alzheimer's and Hispanic groups have responded to such findings by setting up health fairs and support groups, the Times reports. Some Alzheimer's centers have opened offices in Hispanic neighborhoods, according to the Times (Belluck, New York Times, 10/21).
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.
© 2008 Advisory Board Company and Kaiser Family Foundation. All rights reserved.
Overall, the number of U.S. residents with Alzheimer's is expected to increase from five million in 2008 to 16 million in 2050. According to experts, Hispanics are not more genetically predisposed to Alzheimer's but factors related to low income or cultural dislocation -- such as higher rates of diabetes, obesity, cardiovascular disease, stroke and high blood pressure -- may put them at a higher risk for dementia. Cruz said the immigration experience, along with the changes in diet and social network that it entails, could play a role in increased the risk of Alzheimer's. She said, "As you acculturate, you lose those protective factors linked to nutrition, physical activity [and a] social support system that come with you when you first arrive here."
According to the Times, less education also could make this group more vulnerable to risk factors and to dementia because, scientists say, education may increase the plasticity of the brain and its ability to compensate for symptoms. Some research also cites stress related to financial troubles or cultural adjustment as risk factors for dementia. In addition, Hispanics, who are less likely to see doctors because of financial and language barriers, often mistake the symptoms of dementia as a result of aging, according to the Times. "There's some taboos," Liany Arroyo, director of the Institute for Hispanic Health at the National Council of La Raza, said, adding that surveys his group completed indicated that some Hispanics "do not necessarily understand" what Alzheimer's is.
Alzheimer's and Hispanic groups have responded to such findings by setting up health fairs and support groups, the Times reports. Some Alzheimer's centers have opened offices in Hispanic neighborhoods, according to the Times (Belluck, New York Times, 10/21).
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.
© 2008 Advisory Board Company and Kaiser Family Foundation. All rights reserved.
пятница, 6 мая 2011 г.
Recovery Funds Advance Alzheimer's Disease Research
American Recovery and Reinvestment Funds are being used to promote the national research efforts to better understand, diagnose and treat Alzheimer's disease. The National Institute on Aging (NIA), part of the National Institutes of Health, has targeted promising areas of research in granting the awards, such as new and ongoing studies to identify additional risk factor genes associated with Alzheimer's, improve diagnostic tools, find biomarkers, develop therapies, conduct clinical trials and explore preventive measures.
"We are delighted to announce the award of Recovery Act funds to many dedicated, hardworking scientists committed to advancing scientific discovery into Alzheimer's disease and cognitive impairment," said NIA Director Richard J. Hodes, M.D. "Over the next two years, the recipients will use this unprecedented boost in research funds to help reach our ultimate goal of understanding age-related cognitive decline and reducing the individual and societal burden of this devastating disease."
More than 100 Alzheimer's or Alzheimer's-related research grants were awarded under the Recovery Act. The full list of NIH grants can be found at grants.nih/recovery/. The grants featured here highlight how these funds will expand research. Some of the funding will advance the work of existing NIA initiatives that benefit from large-scale collaborative, interdisciplinary research:
The Neuroimaging Initiative - Identifying brain changes before symptoms appear
The Alzheimer's Disease Neuroimaging Initiative (ADNI) will receive $24 million in stimulus funds - half from the NIA and half contributed by the NIH Office of the Director - to further groundbreaking research to establish neuroimaging and biomarker measures. These funds will enable researchers - and ultimately practicing physicians - to track changes in the living brain as older people transition from normal cognitive aging to amnestic mild cognitive impairment (MCI), in which individuals have a memory deficit but generally retain other cognitive abilities, and from MCI to Alzheimer's disease. ADNI, a research partnership supported primarily by the NIA with private sector support through the Foundation for NIH, seeks to find neuroimaging and other biological markers that can be used to detect Alzheimer's disease progression and measure the effectiveness of potential therapies.
The original ADNI involved the study of 800 people who ranged from normal to those with late-stage MCI or overt Alzheimer's disease. This new grant expands the scope of ongoing research under ADNI by allowing for the enrollment of participants at an earlier stage of MCI, when symptoms are milder. Furthermore, the funding for this new grant will allow ADNI investigators to extend the length of the original study to better assess changes in individuals over time. All of the participants will have neuroimaging scans and blood and cerebrospinal fluid analyses to look for changes in the brain.
The overall impact of the added funding will be increased knowledge of the sequence and timing of events leading to MCI and Alzheimer's disease and development of better clinical and imaging/fluid biomarker methods for early detection and for monitoring the progression of these conditions. This will facilitate clinical trials of treatments to slow disease progression and will ultimately contribute to the prevention of Alzheimer's disease. Just this year, ADNI made a significant step forward in developing a test to help diagnose the beginning stages of Alzheimer's disease sooner and more accurately by measuring levels of two biomarkers - tau and beta-amyloid proteins - in cerebrospinal fluid.
"Researchers and clinicians need imaging and biomarker tools to detect and understand the very earliest signs of pathology that cause changes in the brain some 10 to 20 years before any clinical symptoms of cognitive impairment or Alzheimer's may appear,"said ADNI Principal Investigator Michael Weiner, M.D., of the San Francisco Department of Veterans Affairs Medical Center and the University of California, San Francisco. "This grant will help us in our goal of establishing a panel of biomarkers that predict those at risk of developing the disease and also reveal which therapies may be effective in treating the disease or preventing its progression."
The grant was awarded to the Northern California Institute for Research and Education, a nonprofit research foundation affiliated with the San Francisco VA Medical Center. ADNI is the largest public-private partnership on brain research under way at the NIH. In addition to the NIA, the federal ADNI partners are the National Institute of Biomedical Imaging and Bioengineering, also part of NIH, and the U.S. Food and Drug Administration, another agency of the U.S. Department of Health and Human Services.
The AD Genetics Consortium and more " Identifying genes affecting risk for late-onset Alzheimer's
A grant of more than $5.4 million will add 3,800 Alzheimer's patients and an equal number of people free of the disease to a previously funded study by the Alzheimer' Disease Genetics Consortium (ADGC). Gerard Schellenberg, Ph.D., University of Pennsylvania School of Medicine, Philadelphia, leads the consortium, which aims to identify the additional risk factor genes for late-onset Alzheimer's disease. All of these study participants are currently enrolled in the NIA-funded national network of 29 Alzheimer's Disease Centers. When added to the samples from other sources, this will make available one of the largest collections of samples to perform genome-wide association studies (GWAS) in an effort to identify the susceptibility and protective genes influencing the onset and progression of late-onset disease. The large number of DNA samples brought together in this study may enable the researchers to detect genes whose individual effects in the disorder may be small but may still play a role.
The ADGC will use research infrastructures previously established by NIA to store and make available to qualified researchers DNA samples, datasets containing a wealth of information about participants, and genetic analysis data. The combined resources will allow scientists also to search for genes associated with a number of traits associated with Alzheimer's, as well as for genes related to cognitive decline.
"This funding will bring us closer to identifying the elusive genetic variations that contribute to overall risk and development of late-onset Alzheimer's disease," said Marcelle Morrison-Bogorad, Ph.D., director of the NIA Division of Neuroscience. "With this large sample size and the rapid DNA sample and data sharing, there are tremendous opportunities for defining new disease pathways that could lead to the development of new therapies."
Additionally, $4.7 million in Recovery Act funds will be used for another important study - a GWAS project examining cognitive decline in older African-Americans. Denis Evans, M.D., of Rush University Medical Center in Chicago, will collect and analyze the DNA of 4,140 elderly African-Americans enrolled in NIA-funded aging studies already taking place in Chicago and Indianapolis. Data from this analysis will also be shared with the ADGC to help identify risk factor genes for cognitive decline and late-onset Alzheimer's. The study will assess the associations of over 900,000 genetic markers with other co-morbidities, including stroke and high blood pressure.
Another $820,000 in Recovery Act funds will advance Alzheimer's genetics research by developing methods for identifying combinations of genes that might influence age-related risk of AD. The role of different forms of translocase of outer mitochondrial membrane (TOMM40), a gene that makes a protein thought to play a role in disease onset, will be studied by Allen Roses, M.D., of the Duke University School of Medicine in Durham, N.C.; Roses discovered the link between the apolipoprotein E (APOE)-epsilon 4 gene and increased risk for late-onset Alzheimer's disease. This new study will investigate whether particular variants of TOMM40 that tend to co-occur with the APOE3 gene also interact with that gene, and if this interaction plays a role in the age of disease onset.
Additional Recovery Act research opportunities
Other studies made possible by the Recovery Act range from clinical trials to epigenomic studies to translational research:
Drug, exercise clinical trials - A clinical trial exploring whether low doses of an anti-epileptic seizure drug, levetiracetam, can improve memory and affect brain function in people with MCI will be conducted with $1.2 million in support. Michela Gallagher, Ph.D., of Johns Hopkins University, Baltimore, will use functional MRI to visualize activity in the hippocampus - a brain area that becomes overactive in MCI patients - while the clinical trial participants receiving either the drug or a placebo engage in memory tasks. In another trial, researchers will examine how exercise training, cognitive training, or a combination of both, might impact immune and inflammatory biomarkers and cognitive health in older adults with MCI. The randomized trial, under a $1 million grant to David Lowenstein, Ph.D., of the University of Miami, will examine a broad array of outcomes and will include Hispanic and non-Hispanic volunteers.
Epigenetics/translational research - A $1 million grant will support a study exploring whether changes in histone acetylation (an epigenetic, or non-genetic factor that causes genes to behave differently) are one way in which a variety of life experiences may influence the risk of developing age-related cognitive decline and dementia. David Bennett, M.D., of Rush University Medical Center, Chicago, will use brain tissues from the NIA-funded Memory and Aging Project and the Religious Orders Study to examine this question. Another epigenomics grant of $819,000 will be used in translational research to test whether overexpressing histone deacetylase (HDAC1) with small molecule probes in the brain may demonstrate therapeutic potential for Alzheimer's and stroke patients. Li-Huei Tsai, Ph.D., of Massachusetts Institute of Technology, Boston, will lead the study, which seeks to find out whether abnormal regulation of the protein may play a role in neurological disorders.
The NIA leads the federal effort supporting and conducting research on aging and the medical, social and behavioral issues of older people. For more information on research and aging, go to nia.nih.The NIA provides information on age-related cognitive change and neurodegenerative disease specifically at its Alzheimer's Disease Education and Referral (ADEAR) Center site at nia.nih/Alzheimers. To sign up for e-mail alerts about new findings or publications, please visit either website.
Source
National Institutes of Health (NIH)
"We are delighted to announce the award of Recovery Act funds to many dedicated, hardworking scientists committed to advancing scientific discovery into Alzheimer's disease and cognitive impairment," said NIA Director Richard J. Hodes, M.D. "Over the next two years, the recipients will use this unprecedented boost in research funds to help reach our ultimate goal of understanding age-related cognitive decline and reducing the individual and societal burden of this devastating disease."
More than 100 Alzheimer's or Alzheimer's-related research grants were awarded under the Recovery Act. The full list of NIH grants can be found at grants.nih/recovery/. The grants featured here highlight how these funds will expand research. Some of the funding will advance the work of existing NIA initiatives that benefit from large-scale collaborative, interdisciplinary research:
The Neuroimaging Initiative - Identifying brain changes before symptoms appear
The Alzheimer's Disease Neuroimaging Initiative (ADNI) will receive $24 million in stimulus funds - half from the NIA and half contributed by the NIH Office of the Director - to further groundbreaking research to establish neuroimaging and biomarker measures. These funds will enable researchers - and ultimately practicing physicians - to track changes in the living brain as older people transition from normal cognitive aging to amnestic mild cognitive impairment (MCI), in which individuals have a memory deficit but generally retain other cognitive abilities, and from MCI to Alzheimer's disease. ADNI, a research partnership supported primarily by the NIA with private sector support through the Foundation for NIH, seeks to find neuroimaging and other biological markers that can be used to detect Alzheimer's disease progression and measure the effectiveness of potential therapies.
The original ADNI involved the study of 800 people who ranged from normal to those with late-stage MCI or overt Alzheimer's disease. This new grant expands the scope of ongoing research under ADNI by allowing for the enrollment of participants at an earlier stage of MCI, when symptoms are milder. Furthermore, the funding for this new grant will allow ADNI investigators to extend the length of the original study to better assess changes in individuals over time. All of the participants will have neuroimaging scans and blood and cerebrospinal fluid analyses to look for changes in the brain.
The overall impact of the added funding will be increased knowledge of the sequence and timing of events leading to MCI and Alzheimer's disease and development of better clinical and imaging/fluid biomarker methods for early detection and for monitoring the progression of these conditions. This will facilitate clinical trials of treatments to slow disease progression and will ultimately contribute to the prevention of Alzheimer's disease. Just this year, ADNI made a significant step forward in developing a test to help diagnose the beginning stages of Alzheimer's disease sooner and more accurately by measuring levels of two biomarkers - tau and beta-amyloid proteins - in cerebrospinal fluid.
"Researchers and clinicians need imaging and biomarker tools to detect and understand the very earliest signs of pathology that cause changes in the brain some 10 to 20 years before any clinical symptoms of cognitive impairment or Alzheimer's may appear,"said ADNI Principal Investigator Michael Weiner, M.D., of the San Francisco Department of Veterans Affairs Medical Center and the University of California, San Francisco. "This grant will help us in our goal of establishing a panel of biomarkers that predict those at risk of developing the disease and also reveal which therapies may be effective in treating the disease or preventing its progression."
The grant was awarded to the Northern California Institute for Research and Education, a nonprofit research foundation affiliated with the San Francisco VA Medical Center. ADNI is the largest public-private partnership on brain research under way at the NIH. In addition to the NIA, the federal ADNI partners are the National Institute of Biomedical Imaging and Bioengineering, also part of NIH, and the U.S. Food and Drug Administration, another agency of the U.S. Department of Health and Human Services.
The AD Genetics Consortium and more " Identifying genes affecting risk for late-onset Alzheimer's
A grant of more than $5.4 million will add 3,800 Alzheimer's patients and an equal number of people free of the disease to a previously funded study by the Alzheimer' Disease Genetics Consortium (ADGC). Gerard Schellenberg, Ph.D., University of Pennsylvania School of Medicine, Philadelphia, leads the consortium, which aims to identify the additional risk factor genes for late-onset Alzheimer's disease. All of these study participants are currently enrolled in the NIA-funded national network of 29 Alzheimer's Disease Centers. When added to the samples from other sources, this will make available one of the largest collections of samples to perform genome-wide association studies (GWAS) in an effort to identify the susceptibility and protective genes influencing the onset and progression of late-onset disease. The large number of DNA samples brought together in this study may enable the researchers to detect genes whose individual effects in the disorder may be small but may still play a role.
The ADGC will use research infrastructures previously established by NIA to store and make available to qualified researchers DNA samples, datasets containing a wealth of information about participants, and genetic analysis data. The combined resources will allow scientists also to search for genes associated with a number of traits associated with Alzheimer's, as well as for genes related to cognitive decline.
"This funding will bring us closer to identifying the elusive genetic variations that contribute to overall risk and development of late-onset Alzheimer's disease," said Marcelle Morrison-Bogorad, Ph.D., director of the NIA Division of Neuroscience. "With this large sample size and the rapid DNA sample and data sharing, there are tremendous opportunities for defining new disease pathways that could lead to the development of new therapies."
Additionally, $4.7 million in Recovery Act funds will be used for another important study - a GWAS project examining cognitive decline in older African-Americans. Denis Evans, M.D., of Rush University Medical Center in Chicago, will collect and analyze the DNA of 4,140 elderly African-Americans enrolled in NIA-funded aging studies already taking place in Chicago and Indianapolis. Data from this analysis will also be shared with the ADGC to help identify risk factor genes for cognitive decline and late-onset Alzheimer's. The study will assess the associations of over 900,000 genetic markers with other co-morbidities, including stroke and high blood pressure.
Another $820,000 in Recovery Act funds will advance Alzheimer's genetics research by developing methods for identifying combinations of genes that might influence age-related risk of AD. The role of different forms of translocase of outer mitochondrial membrane (TOMM40), a gene that makes a protein thought to play a role in disease onset, will be studied by Allen Roses, M.D., of the Duke University School of Medicine in Durham, N.C.; Roses discovered the link between the apolipoprotein E (APOE)-epsilon 4 gene and increased risk for late-onset Alzheimer's disease. This new study will investigate whether particular variants of TOMM40 that tend to co-occur with the APOE3 gene also interact with that gene, and if this interaction plays a role in the age of disease onset.
Additional Recovery Act research opportunities
Other studies made possible by the Recovery Act range from clinical trials to epigenomic studies to translational research:
Drug, exercise clinical trials - A clinical trial exploring whether low doses of an anti-epileptic seizure drug, levetiracetam, can improve memory and affect brain function in people with MCI will be conducted with $1.2 million in support. Michela Gallagher, Ph.D., of Johns Hopkins University, Baltimore, will use functional MRI to visualize activity in the hippocampus - a brain area that becomes overactive in MCI patients - while the clinical trial participants receiving either the drug or a placebo engage in memory tasks. In another trial, researchers will examine how exercise training, cognitive training, or a combination of both, might impact immune and inflammatory biomarkers and cognitive health in older adults with MCI. The randomized trial, under a $1 million grant to David Lowenstein, Ph.D., of the University of Miami, will examine a broad array of outcomes and will include Hispanic and non-Hispanic volunteers.
Epigenetics/translational research - A $1 million grant will support a study exploring whether changes in histone acetylation (an epigenetic, or non-genetic factor that causes genes to behave differently) are one way in which a variety of life experiences may influence the risk of developing age-related cognitive decline and dementia. David Bennett, M.D., of Rush University Medical Center, Chicago, will use brain tissues from the NIA-funded Memory and Aging Project and the Religious Orders Study to examine this question. Another epigenomics grant of $819,000 will be used in translational research to test whether overexpressing histone deacetylase (HDAC1) with small molecule probes in the brain may demonstrate therapeutic potential for Alzheimer's and stroke patients. Li-Huei Tsai, Ph.D., of Massachusetts Institute of Technology, Boston, will lead the study, which seeks to find out whether abnormal regulation of the protein may play a role in neurological disorders.
The NIA leads the federal effort supporting and conducting research on aging and the medical, social and behavioral issues of older people. For more information on research and aging, go to nia.nih.The NIA provides information on age-related cognitive change and neurodegenerative disease specifically at its Alzheimer's Disease Education and Referral (ADEAR) Center site at nia.nih/Alzheimers. To sign up for e-mail alerts about new findings or publications, please visit either website.
Source
National Institutes of Health (NIH)
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