Admiral Nurses - Still Waiting For The Promised DH Urgent Review Of Anti-Psychotics 'The Drug Of Last Resort' For People With Dementia, UK

The charity for dementia and Admiral Nurses strongly supported the call for a change in practice when, in June 2008, the Department of Health (DH) announced it was to undertake an urgent review of the prescribing of anti-psychotic drugs for people with dementia. The DH stated that the review would assess the scale of inappropriate prescribing, and the reasons behind misuse of this type of medication. Anti-psychotic drugs have significant risk factors for people with dementia a particularly vulnerable group, many of whom are resident in care homes where specialist knowledge of drug treatments is often lacking.


"More than one year on we are still waiting for this review into this important issue on which both carers and professionals alike need clear guidance," says Ian Weatherhead, Lead Admiral Nurse for Admiral Nursing DIRECT - a national helpline operated exclusively by Admiral Nurses, who are specialists in dementia care.


Ian adds: "In very specific circumstances, anti-psychotic drugs have an important role to play when prescribed and used appropriately but they must always be considered as a last resort. This means a detailed assessment must be carried out so that other potential causes of behaviour change - often called 'challenging behaviour' - have been discounted, such as changes in environment, infection, constipation, anxiety and depression.



"Anti-psychotic drugs, with their known side effects, must always and only ever be used for the benefit of the person with dementia and not for the benefit of care staff."


Admiral Nursing DIRECT takes a large volume of calls every week from carers of people with dementia, people with dementia themselves, and professional staff. Many people contact the helpline with questions and concerns about medication, including anti-psychotics.


Hilary Woodhead, who leads on the development of training and learning partnerships for the charity for dementia, states: "It is vital that training and education for staff caring for people with dementia becomes a reality for all those working in front-line roles, in the community and in residential care and hospital settings. This is a cross-cutting theme in the National Dementia Strategy. Training programmes must encompass information about the appropriate use of anti-psychotic drugs to help ensure that the person with dementia remains the central focus of care."


Further advice from Admiral Nurses and Admiral Nursing DIRECT on the use of anti-psychotic drugs states:
In some cases where distressing symptoms such as hallucinations and/or severe agitation are clearly evident as a result of the dementia, and not caused by other factors, then anti-psychotics may be of help but these need to be used carefully at appropriate doses and be reviewed regularly.

Family members of people with dementia should be fully involved in any decisions taken about treatment and care wherever possible so that important information about the person and their history form an integral part of the assessment. Carers should be involved and kept informed regarding reviews of and recommended changes in medication.

If anyone is concerned about any medication that is being prescribed for someone with dementia then they should request an immediate review of the medication by the responsible medical officer before any action is taken.

Caring for people with dementia is different from caring for people who are older and frail. Specialist help is required together with focused training to ensure appropriate decisions are made concerning care and medication. Skills and knowledge concerning use of medications such as anti-psychotics must be made available to those working in care home and primary care settings. Admiral Nurses are well placed to work in partnership to provide that specialist help and training.
Source
Admiral Nurses

Music Aids Alzheimer's Patients In Remembering New Information

Researchers from Boston University School of Medicine (BUSM) have shown that patients with Alzheimer's disease (AD) are better able to remember new verbal information when it is provided in the context of music even when compared to healthy, older adults. The findings, which currently appear on-line in Neuropsychologia, offer possible applications in treating and caring for patients with AD.



AD, the most common form of dementia, is characterized by a general, progressive decline in cognitive function that typically presents first as impaired episodic memory. The onset and rate of this decline tends to vary across cognitive domains, and some functions may be preferentially spared in patients with AD.



To determine whether music can enhance new learning of information, AD patients and healthy controls were presented with either the words spoken, or the lyrics sung with full musical accompaniment along with the printed lyrics on a computer screen. The participants were presented visually with the lyrics to 40 songs. Twenty of the song lyrics were accompanied by their corresponding sung recording and 20 were accompanied by their spoken recording.



After each presentation, participants were asked to indicate whether or not they were previously familiar with the song they had just heard. The BUSM researchers found accuracy was greater in the sung condition than in the spoken condition for AD patients but not for healthy older controls.



"Our results confirmed our hypothesis that patients with AD performed better on a task of recognition memory for the lyrics of songs when those lyrics were accompanied by a sung recording than when they were accompanied by a spoken recording," said senior author Brandon Ally, PhD, an assistant professor of neurology and director of Neuropsychology Research at the BUSM Center for Translational Cognitive Neuroscience. "However, contrary to our hypothesis, healthy older adults showed no such benefit of music, he added.



These results suggest a fundamental difference in the encoding and retrieval processes for musical versus nonmusical stimuli between patients with AD and healthy older adults. "Music processing encompasses a complex neural network that recruits from all areas of the brain, that are affected at a slower rate in AD compared to the areas of the brain typically associated with memory. Thus, stimuli accompanied by music and a sung recording may create a more robust association at encoding than do stimuli accompanied by only a spoken recording in patients with AD," explained Ally.



According to the researchers understanding the nature of musical processing and memory in patients with AD may allow the development of effective and comprehensive therapies for this increasingly prevalent disease.



This research was supported by National Institute on Aging



Source:

Boston University Medical Center

Gene Link Marks Major Breakthrough In Dementia Research

Two new genes associated with Alzheimer's disease have been discovered in a British scientist led genome study.


In a separate study French researchers revealed links between a third gene and the disease.


The British study, led by Professor Julie Williams, is the largest ever Alzheimer's genome-wide association study and involved 16,000 individuals. Using a two stage process it identified strong links between the genes CLU and PICALM and Alzheimer's. The French study of more than 7,000 individuals found a further link to the gene CR1. Both studies are being published in Nature Genetics this week.


Alzheimer's Society comment:


'These studies mark a really exciting breakthrough in the ongoing efforts to identify a cause and find a cure for this devastating disease. It is the first time a new gene link has been established in 16 years and the role of British scientists shows the high standards being set by this country's researchers.


'These discoveries will enable scientists to follow new avenues of investigation as they piece together the causes of Alzheimer's disease - likely to be a mixture of genes; life style and life events. Most importantly it could also lead to new drug treatments.



'In the next 10 years one million people will develop dementia but the government currently spends eight times less on dementia research than cancer research. This investment now needs to be drastically increased so we do not miss out on the incredible opportunity to build on these findings and ultimately win the battle against dementia.'


Dr Susanne Sorensen

Head of Research

Alzheimer's Society


Notes


'Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease' by Williams et al is published in Nature Genetics on 6th September 2009.


'Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer's disease' by Amouyel is published in the same edition of Nature Genetics.

Source
Alzheimer's Society

Hope for Alzheimer's blossoms

A substance found in the Welsh national flower, which could offer hope for sufferers of Alzheimer's disease, is being supported for large scale manufacture by Cardiff University's Manufacturing Engineering Centre (MEC).


Alzheimer's disease is the most common form of dementia, making up 55 per cent of all cases of dementia. Dementia affects one person in 20 over the age of 65 and one person in five over the age of 80.


Certain species of daffodil, which thrive in the Black Mountains of South Powys, produce galanthamine, a leading drug in the alleviation of memory loss symptoms.


The University's Manufacturing Engineering Centre is now helping a company Alzeim Ltd (supported by Glasu, the EU funded LEADER+ Programme in Powys) to develop the agricultural potential of the daffodil as a medicinal plant along with the Institute of Grassland and Environmental Research at the University of Wales, Aberystwyth.


The Centre is providing support from harvesting in the field to marketing the pharmaceutical product. This includes assisting with the science of developing crops more than once a year and helping growers to assess when the best time to harvest the crop.


Frank Marsh, Marketing Director, The Manufacturing Engineering Centre said: "Galanthamine has major investment potential. Furthermore, the potential for Welsh hill farms is huge. The benefits are extensive, not only to Welsh bioscience and the pharmaceutical industry, but also to the ageing population."


Frank Marsh

manufacturingcf.ac.uk

44-292-087-0019

Cardiff University

cardiff.ac.uk

Powerful New Evidence Shows Statin Drugs Reduce Risk Of Alzheimer's Disease

Pharmaceutical Corporation (NASDAQ:NYMX) holds U.S. and global patent rights for the use of statin drugs for the prevention and treatment of Alzheimer's disease (AD). The newly published results of a major long-term study (J Neurol NeuroSurg Psychiatry Oct. 17, 2008) now provides powerful new evidence that taking statins substantially reduces the risk of AD.


In this comprehensive study, researchers in The Netherlands found that older men and women who took statin drugs during the multi-year study had a 43% lower risk of AD. No such reduction in AD risk was found for non-statin cholesterol lowering medication.


The study was part of the Rotterdam Study, a highly respected long term prospective study of factors that determine the occurrence of common diseases of the elderly, such as heart disease and Alzheimer's disease. Researchers followed 6,992 men and women recruited at age 55 years or older from baseline (1990-1993) until January 2005 for incident AD. During this period, participants were screened periodically for signs of dementia and those with suspected cognitive decline were referred for exhaustive in-depth evaluation for dementia and AD diagnosis. They were also continuously monitored for incident dementia through access to medical records databases. The researchers had complete access to the participants' prescription medication records, including statins, thus eliminating a potential source of error compared to earlier studies that relied on self-reported drug use.


The 47% reduction in AD risk for people taking statins was similar in size to the positive effect for statins found in some earlier large scale observational or prospective studies: 67% reduction in the risk of AD (Current Alzheimer Research 2008; 5: 416-421); 48% reduction in risk of dementia or cognitive impairment for statin users (Neurology 2008; 71; 344-350); 74% unadjusted lower risk of AD for statin users (Arch Neurol 2002; 59: 223-227); 69.6% lower prevalence of AD for statin users (Arch Neurol 2000; 57: 1439-1443); 71% lower relative risk of AD for statin users (Lancet 2000; 356:1627-1631).


Statins are widely used cholesterol-lowering drugs with a well-established track record of safety. They have an estimated global market over $25 billion and represent a potential new way of treating or preventing AD. AD is the leading cause of dementia in the elderly, afflicting an estimated 4.5 million people in the U.S.


This press release contains certain "forward-looking statements" as defined in the United States Private Securities Litigation Reform Act of 1995 that involve a number of risks and uncertainties. There can be no assurance that such statements will prove to be accurate and the actual results and future events could differ materially from management's current expectations. The conduct of clinical trials and the development of drug products involve substantial risks and uncertainties and actual results may differ materially from expectations. Promising early results do not ensure that later stage or larger scale clinical trials will be successful or will proceed as expected. Such factors are detailed from time to time in Nymox's filings with the United States Securities and Exchange Commission and other regulatory authorities.
Source

Roy Wolvin

Nymox Pharmaceutical Corporation

Scientists See Brain Aging Before Symptoms Appear

UCLA scientists have used innovative brain-scan technology developed at UCLA, along with patient-specific information on Alzheimer's disease risk, to help diagnose brain aging, often before symptoms appear. Published in the January issue of Archives of General Psychiatry, their study may offer a more accurate method for tracking brain aging.



Researchers used positron emission tomography (PET), which allows "a window into the brain" of living people and specifically reveals plaques and tangles, the hallmarks of neurodegeneration. The PET scans were complemented by information on patients' age and congnitive status and a genetic profile.



"Combining key patient information with a brain scan may give us better predictive power in targeting those who may benefit from early interventions, as well as help test how well treatments are working," said study author Dr. Gary Small, who holds UCLA's Parlow-Solomon Chair on Aging and is a professor at the Semel Institute for Neuroscience and Human Behavior at UCLA.



Scientists took PET brain scans of 76 non-demented volunteers after they had been intravenously injected with a new chemical marker called FDDNP, which binds to plaque and tangle deposits in the brain. Researchers were then able to pinpoint where these abnormal protein deposits were accumulating.



They reported that older age correlated with higher concentrations of FDDNP in the medial and lateral temporal regions of the brain, areas involved with memory, where plaques and tangles usually collect. The average age of study volunteers was 67.



Thirty-four of the 76 volunteers carried the APOE-4 gene allele, which heightens the risk for developing Alzheimer's disease. This group demonstrated higher FDDNP levels in the frontal region of the brain, also involved in memory, than study participants without allele.



"We found that for many volunteers, the imaging scans reflected subtle brain changes, which take place before symptoms manifest," said Small, who is also director of the UCLA Center on Aging.



Small noted that the brain will try to compensate for any problems, which is why cognitive symptoms may not become apparent until much later.



"This type of scan offers an opportunity to see what is really going on in the brain," he said.



Another subset of the volunteers had mild cognitive impairment (MCI), a condition that increases the risk of developing Alzheimer's disease. These 36 volunteers had higher measures of FDDNP in the medial temporal brain regions than normal volunteers. Those who had both MCI and the APOE-4 gene had higher concentrations of FDDNP in the medial temporal brain regions than volunteers who had MCI but not APOE-4.



"We could see more advancing disease in those with mild cognitive impairment, who are already demonstrating some minimal symptoms," Small said. "Eventually, this imaging method, together with patient information like age, cognitive status and genetics, may help us better manage brain aging."
















According to Small, in the future, brain aging may be controlled similarly to high cholesterol or high blood pressure. Patients would receive a brain scan and perhaps a genetic test to predict their risk. Medications and other interventions could be prescribed, if necessary, to prevent or delay future neurodegeneration, allowing doctors to protect a healthy brain before extensive damage occurs. The brain scans may also prove helpful in tracking the effectiveness of treatments.



PET, combined with the FDDNP probe, is the only imaging technology that offers a full profile of neurodegeneration that includes measures of both plaques and tangles - the physical evidence of Alzheimer's disease in the brain.



"The fact that we can see tau tangles as well as amyloid plaques is critically important in early detection of brain aging, since the tangles are the first abnormal proteins that appear in the brain, long before dementia is clinically obvious to the physician," said Dr. Jorge R. Barrio, a study author and professor of molecular and medical pharmacology at the David Geffen School of Medicine at UCLA.



Such subtleties allow more insight into how the plaques and tangles spread and ultimately how Alzheimer's disease may develop.



Currently, the new FDDNP-PET scans are used in a research setting, but clinical trials are in development to bring the technology to wider patient use.







The study was funded by both government and nonprofit agencies, including the National Institutes of Health, the U.S. Department of Energy, the Ahmanson Foundation, the Larry L. Hillblom Foundation and the Tamkin Foundation.



Additional UCLA authors include Prabha Siddarth, Ph.D.; Alison C. Burggren, Ph.D.; Linda M. Ercoli, Ph.D.; Karen J. Miller, Ph.D.; Dr. Helen Lavretsky; and Susan Y. Bookheimer, Ph.D, all from the UCLA Department of Psychiatry and Biobehavioral Sciences and the Semel Institute for Neuroscience and Human Behavior at UCLA; Vladimir Kepe, Ph.D.; S.C. Huang, Ph.D.; and Michael E. Phelps, Ph.D. from the UCLA Department of Molecular and Medical Pharmacology; and Paul M. Thompson, Ph.D., and Greg M. Cole, Ph.D., from the UCLA Department of Neurology.



Source: Rachel Champeau


University of California - Los Angeles

Dementia Care: Communication Problems Cause Physical Strain

Excessive physical strain in dementia care is not so much related to equipment or the resident's body weight as it is due to communication problems and misunderstandings. This is shown in a new study from the Sahlgrenska Academy at the University of Gothenburg, Sweden.



Dementia not only affects the memory and other cognitive functions, but also motor skills such as the ability to walk.



'The symptoms of dementia are very individual and can vary from one day to the next, and sometimes even from one moment to the next. This makes person transfers in dementia care very demanding for the personnel', says physiotherapist Cristina W??ngblad, one of the researchers behind the study recently published in the scientific journal Scandinavian Journal of Caring Sciences.



The study investigates how nurses' aides at three dementia care facilities in western Sweden feel about person transfers in the workplace and what they do to reduce the physical strain. While the residents' body weight seems to be less relevant for how straining the personnel perceive their work to be, W??ngblad found misunderstandings and communication problems to be much more important.



'A resident who is unable to read signals from the surroundings or who forgets what he or she is supposed to do reacts with anxiety, confusion and resistance. The personnel can avoid communication problems by explaining things with different words and by using body language, and thereby make person transfers much easier', says Synneve Dahlin Ivanoff, Professor of Occupational Therapy at the Sahlgrenska Academy.



Individual-specific knowledge about the residents also seems useful. For example, the personnel can make person transfers easier by giving appropriate instructions, using the right vocal pitch, assisting a resident in the way he or she prefers, and by knowing whether it is possible to ask a resident to move faster.



'The physiotherapists who train and educate dementia care personnel must be aware of the complexity of person transfers. The instructions on how residents should be moved ought to be tailored to each individual's needs and to each situation', says W??ngblad.



Source:
Cristina W??ngblad


University of Gothenburg

Alzheimer Scotland Welcomes Mental Health Report: Urgent Need For Action On Older People's Mental Health

A mental health pandemic and an inadequate response mean that over 315,000 older people in Scotland who experience mental health problems do not have satisfactory services and support, according to the final report from the UK Inquiry into Mental Health and Well-Being in Later Life (mhilli) - a major enquiry supported by Age Concern.


Alzheimer Scotland welcomed the report, which places dementia and depression at the centre of the unmet mental health needs of older people. With the rising number of older people, the situation is set to get worse. In its recent report, The Dementia Epidemic, Alzheimer Scotland highlighted that the number of people with dementia will rise by 75% to 102,000 by 2031.


Jim Jackson, Chief Executive of Alzheimer Scotland, said, 'We must ensure that mental health services for older people are given the priority they require; they must not be neglected because of the pressures to improve adult, children's and adolescent mental health services. Older people's mental health services need to be improved. The recommendations made by the Inquiry are as applicable to Scotland as the rest of the UK.


'In Scotland we need to build on the work which has been done in the Scottish Executive's 'Mental Health Delivery Plan' and the 'All our Futures' strategy for older people. There must be a concerted effort across departmental boundaries which reaches into all of Scotland's communities.'


The Inquiry report calls for action:


-- To eliminate age discrimination in mental health

-- To challenge stigma, ageism and defeatism

-- Work on preventing mental health problems and the promotion of well-being

-- Support for older people and their carers to help themselves and each other

-- Improvements in housing, health and social care services

-- An end to under-funding in older people's mental health services.


Further information from the Alzheimer Scotland report, The Dementia Epidemic: where Scotland is now and the challenge ahead, can be found at alzscot/pages/policy/dementiaepidemic.htm.


Alzheimer Scotland


Dementia affects between 58,000 and 65,000 people in Scotland in 2007. Alzheimer's disease is the main form of dementia. The second most common is vascular dementia. As yet there is no cure.


Alzheimer Scotland is Scotland's foremost voluntary organisation working for people with dementia and their carers. It:


-- speaks out for the rights and concerns of people with dementia and their carers;

-- operates services on over 60 sites throughout Scotland providing practical services such as day, evening and weekend centres, home care and befriending and carers' support services;

-- provides the 24 hour national freephone Dementia Helpline (0808 808 3000);

-- has a research programme.


Alzheimer Scotland - Action on Dementia is a company limited by guarantee, registered in Scotland 149069. Registered Office: 22 Drumsheugh Gardens, Edinburgh EH3 7RN. It is recognised as a charity by the Office of the Scottish Charity Regulator, no. SC022315.


alzscot

EPIX Pharmaceuticals Initiates Phase 2b Program In Alzheimer's Disease

EPIX Pharmaceuticals, Inc. (NASDAQ:EPIX), a biopharmaceutical company focused on discovering and developing novel therapeutics through the use of its proprietary and highly efficient in silico drug discovery platform, today announced that it has begun its Phase 2b program in Alzheimer's disease through the initiation of a clinical trial of PRX-03140, its novel 5-HT4 agonist, in combination with donepezil (Aricept®).


Under the company's collaboration agreement with GlaxoSmithKline (GSK), EPIX is entitled to receive a $7.5 million milestone payment from GSK related to the start of the Phase 2b program for PRX-03140 in Alzheimer's disease. The Phase 2b proof-of-concept program consists of two clinical trials - a six month trial evaluating PRX-03140 in combination with donepezil and a three month trial studying PRX-03140 as monotherapy; the monotherapy trial is expected to begin later in the second quarter.


"This Phase 2b program follows the encouraging results seen in our Phase 2a trial, in which monotherapy treatment with PRX-03140 resulted in a statistically significant change from baseline as well as from placebo on the ADAS-Cog score," said Michael G. Kauffman, M.D., Ph.D., chief executive officer of EPIX. "While our previous two-week trial was primarily designed to address safety, we were excited by the measurable impact on memory and cognition PRX-03140 had on many of the participating patients. Our data indicate that PRX-03140 stimulates acetylcholine release and production in the brain without the peripheral, dose-limiting side effects commonly seen with cholinesterase inhibitors. There remains a significant unmet need for Alzheimer's disease drug therapies that will improve symptoms with minimal side effects."


"We are encouraged by the PRX-03140 data we've seen to date, and based upon this, we are pleased to see EPIX begin the Phase 2b program with PRX-03140 in Alzheimer's disease," said Hugh Cowley, M.D., head of GSK's Center of Excellence for External Drug Discovery (CEEDD). "We believe that patients with Alzheimer's disease may ultimately be treated with combination therapy to manage the progression of the disease and to manage effectively the symptoms of Alzheimer's disease. As a result, we are evaluating PRX-03140 in a combination trial in concert with donepezil as well as in a monotherapy setting."


Trial Design


This randomized, double-blind, placebo-controlled trial is designed to evaluate the efficacy of PRX-03140 on cognitive function as measured by the change from baseline in the cognitive component of the Alzheimer's Disease Assessment Scale (ADAS-Cog) score. The ADAS-Cog endpoint is the current standard for evaluating drug efficacy for cognition in Alzheimer's disease and is an established and accepted regulatory endpoint. Patients will be randomized to one of three trial arms: placebo, 50 mg/daily of PRX-03140, or 150 mg/daily of PRX-03140. All patients in the trial must be treated with 10 mg of donepezil for at least four months prior to enrollment. The six month trial is expected to enroll approximately 400 adult patients with Alzheimer's disease. Changes in the Clinician and Caregiver-based Impressions of Change (CIBIC+), measures of behavior and Activities of Daily Living (ADLs) and Neuropsychological Test Battery (NTB) will also be measured. PRX-03140 has been studied in more than 180 subjects to date and previous clinical trials have shown the drug to be well-tolerated.















About PRX-03140


PRX-03140 is a novel, oral investigational drug candidate for Alzheimer's disease. It is selective for the 5-HT4 receptor in the brain and is believed to stimulate both acetylcholine production and release - which enables symptomatic improvement in Alzheimer's patients - and the alpha-secretase pathway - which may slow Alzheimer's disease progression. Recent Phase 2a results indicated that patients receiving daily oral 150 mg doses of PRX-03140 as monotherapy for two weeks achieved a mean 3.6 point improvement on the Alzheimer's Disease Assessment Scale cognitive subscale (ADAS-cog) versus a 0.9 point worsening in patients on placebo (p= 0.021).


In three Phase 1 trials and the Phase 2a trial, with more than 180 patients and healthy subjects, PRX-03140 has been well-tolerated. In a 14-day Phase 1b clinical trial, treatment with PRX-03140 resulted in changes in brain wave activity in Alzheimer's patients that are consistent with those seen in clinical trials with currently approved drugs for Alzheimer's disease. In preclinical studies, PRX-03140 has shown to improve cognitive function through increasing levels of acetylcholine, and has led to increased levels of soluble amyloid precursor protein (sAPP) and brain-derived neurotrophic factor (BDNF) in regions of the brain known to be important for memory.


About Alzheimer's Disease


Alzheimer's disease is a debilitating neurodegenerative disorder characterized by progressive loss of memory and cognitive function, affecting more than 5 million Americans according to the Alzheimer's Association, and more than 9 million worldwide according to the Alzheimer's Disease International Association. The U.S. National Institute of Aging estimates that about 5 percent of the population aged 65-74 and as many as 50 percent of those over age 85 have the disease. Although treatment options are limited, the global market for Alzheimer's disease drugs is growing, from $4 billion in 2006 to over $5 billion expected in 2010, as estimated by Thomson-Pharma.


About the GSK CEEDD


GlaxoSmithKline is enhancing the way it discovers and develops drugs by creating a small dedicated team who will feed the GSK pipeline through the efforts of its external collaborations. In essence, the CEEDD (Center of Excellence for External Drug Discovery) will 'virtualize' a portion of the GSK pipeline; namely, from Target to Clinical PoC, by forming multiple risk-sharing/reward-sharing alliances.


About EPIX


EPIX Pharmaceuticals is a biopharmaceutical company focused on discovering and developing novel therapeutics through the use of its proprietary and highly efficient in silico drug discovery platform. The company has a pipeline of internally-discovered drug candidates currently in clinical development to treat diseases of the central nervous system and lung conditions. EPIX also has collaborations with leading organizations, including GlaxoSmithKline, Amgen, Cystic Fibrosis Foundation Therapeutics and Bayer Schering Pharma. For more information, please visit the company's website at epixpharma.


This news release contains express or implied forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 that are based on current expectations of management. These statements relate to, among other things, our expectations regarding our drug discovery efforts, including the timing of our Phase 2b program with PRX-03140 in Alzheimer's disease, and the benefits of our collaboration with GlaxoSmithKline. These statements are neither promises nor guarantees, but are subject to a variety of risks and uncertainties, many of which are beyond our control, and which could cause actual results to differ materially from those contemplated in these forward-looking statements. In particular, the risks and uncertainties include, among other things: risks that product candidates may fail in the clinic or may not be successfully marketed or manufactured; risks relating to our ability to advance the development of product candidates currently in the pipeline or in clinical trials; failure to obtain the financial resources to complete development of product candidates; our inability to further identify, develop and achieve commercial success for new products and technologies; our inability to achieve commercial success for our products and technologies; our failure to comply with regulations relating to our products and product candidates, including FDA requirements; the risk that the FDA may interpret the results of our studies differently than we have; and risks of new, changing and competitive technologies and regulations in the U.S. and internationally. Existing and prospective investors are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof. We undertake no obligation to update or revise the information contained in this press release, whether as a result of new information, future events or circumstances or otherwise. For additional information regarding these and other risks that we face, see the disclosure contained in our filings with the Securities and Exchange Commission, including our most recent Annual Report on Form 10-K.

EPIX Pharmaceuticals


View drug information on ARICEPT.

Myriad Genetics' Alzheimer's Disease Drug Mechanism Of Action Detailed In Nature Article

Myriad Genetics, Inc. (NASDAQ: MYGN) announced that the mechanism of action of Flurizan® (tarenflurbil) -- its drug candidate for the treatment of Alzheimer's disease, is elucidated in the scientific journal Nature. The article, "Substrate-targeting Gamma-secretase Modulators," will be published in the June 12, 2008 issue of Nature.


Previous studies, in vitro, in animal models and in humans, have demonstrated that Flurizan selectively lowers toxic amyloid beta 42, and is the first member of a new class of drugs known as selective amyloid lowering agents (SALAs). Further, Flurizan has been shown to modify the processing of the amyloid precursor protein (APP) by the gamma secretase enzyme. The specific way in which Flurizan accomplishes this reduction in the toxic amyloid beta 42 had remained a mystery until now.


The Nature paper confirms the SALA properties of Flurizan and establishes the mechanism by which Flurizan modulates the APP-gamma secretase interaction. The authors demonstrate that the molecular target of Flurizan is the amyloid precursor protein itself -- the substrate of gamma secretase. Flurizan modifies the conformation of the APP molecule as it is bound to the gamma secretase complex. This change in the shape and/or position of APP in the complex results in cleavage by gamma secretase that produces shorter length, non-toxic amyloid beta fragments, such as amyloid beta 38 and amyloid beta 40. This exciting finding is novel in that most drugs target enzymes, blocking their function directly, but the substrate of an enzyme has not generally been seen as a drug target. These new findings are consistent with previous studies that show that Flurizan selectively lowers amyloid beta 42 by shifting the conformation of the APP/gamma secretase complex through allosteric binding.


"The article in Nature adds to the understanding of the mechanism of action of Flurizan, providing a molecular basis for its ability to slow the progression of Alzheimer's disease, as was demonstrated in previous human clinical studies," said Adrian Hobden, Ph.D., President of Myriad Pharmaceuticals, Inc. "The findings help explain why compounds like Flurizan can have a dramatic effect on lowering amyloid beta 42, the initiator of plaque formation in the human brain, and offer hope for the treatment of patients who suffer from Alzheimer's disease."


Flurizan U.S. Phase 3 Clinical Trial


Flurizan has recently completed a Phase 3 clinical trial in the U.S. of 1684 patients from 131 investigator sites. Topline data from the trial is scheduled for reporting in June 2008, and a full analysis of the data will be presented at the Alzheimer's Association's International Conference on Alzheimer's Disease in Chicago on July 29, 2008.


Flurizan is a registered trademark of Myriad Genetics, Inc. in the United States and other countries.















Myriad Genetics, Inc. is a biopharmaceutical company focused on the development of novel healthcare products. The Company develops and markets predictive medicine products, and is developing and intends to market therapeutic products. Myriad's news and other information are available on the Company's Web site at myriad.


This press release contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995, including statements relating to the publication of the article, "Substrate-targeting Gamma-secretase Modulators" in the scientific journal Nature; the ability of Flurizan to selectively lower toxic amyloid beta 42 and to modify the processing of the amyloid precursor protein (APP) by the gamma secretase enzyme; the mechanism by which Flurizan modulates the APP-gamma secretase interaction; the ability of Flurizan to have a dramatic effect on lowering amyloid beta 42, the initiator of plaque formation in the human brain, and offer hope for the treatment of patients who suffer from Alzheimer's disease; the reporting of topline data from the Phase 3 US trial in June 2008, and the presentation of a full analysis of the data at the Alzheimer's Association's International Conference on Alzheimer's Disease in Chicago on June 29, 2008. These risks and uncertainties include, but are not limited to, our inability to further identify, develop and achieve commercial success for new products and technologies; our ability to discover drugs that are safer and more efficacious than our competitors; our ability to develop molecular diagnostic products that help assess which patients are subject to greater risk of developing diseases and who would therefore benefit from new preventive therapies; the possibility of delays in the research and development necessary to select drug development candidates and delays in clinical trials; the risk that clinical trials may not result in marketable products; the risk that we may be unable to successfully finance and secure regulatory approval of and market our drug candidates, or that clinical trials will not be completed on the timelines we have estimated; uncertainties about our ability to obtain new corporate collaborations and acquire new technologies on satisfactory terms, if at all; the development of competing products and services; our ability to protect our proprietary technologies; patent-infringement claims; risks of new, changing and competitive technologies and regulations in the United States and internationally; and other factors discussed under the heading "Risk Factors" contained in Item 1A in our Annual Report on Form 10-K for the year ended June 30, 2007, which has been filed with the Securities and Exchange Commission, as well as any updates to those risk factors filed from time to time in our Quarterly Reports on Form 10-Q or Current Reports on Form 8-K. All information in this press release is as of the date of the release, and Myriad undertakes no duty to update this information unless required by law.

myriad

Summit To Shape Future Dementia Research

An initiative from the Government's National Dementia Strategy, the summit will examine research into cause, cure and care, highlighting gaps in knowledge and new opportunities for the future. A report will then be produced to help shape the future dementia research agenda.


Attendees will look at ways of building on existing investments in this area including the Dementias and Neurodegenerative Diseases Research Network (DeNDRoN) funded by the National Institute of Health Research and the recent ??30M MRC and Wellcome Trust Joint Call for research proposals in Neurodegenerative Diseases.


Phil Hope MP, Minister of State for Care Services, said:

"One million people will develop dementia in the next ten years. Our National Dementia Strategy will help people live well with dementia by improving diagnosis, care and support, but research is the key to developing new treatments, transforming care and ultimately finding a cure for this devastating condition.


Today is a vital step towards a more co-ordinated approach to dementia research. The Government is already investing strongly in research. We now all need to work together to improve the quality of dementia proposals and improve access to this investment. I look forward to receiving the report from today's important event.'"


MRC Chief Executive Sir Leszek Borysiewicz said:


"Following on from the MRC Strategic Review of Neurodegeneration, this is an opportunity to bring together experts from the whole spectrum of dementia research and key stakeholders to help the funders set priorities for the future research agenda. Recent MRC initiatives in this area will provide the necessary platform for future research, by bringing together new research consortia and support for brain banking and imaging. MRC has also been playing a leading role in developing the new EU initiative in neurodegeneration and dementia."


Dame Professor Sally Davies, Director General of DH Research and Development Directorate, said:


"The DH is very pleased to be jointly hosting this important event with the MRC. We have made significant investment in research for dementia and related conditions over the years and the Summit will help to ensure that the research we commission continues to improve the quality of care provided for people with dementia and their families".


The Dementia Research Summit will coincide with a report that will address European collaboration on dementia research. On 22 July the European Commission will confirm EU participation in a joint research programme on neurodegeneration and in particular Alzheimer's. This is the first joint initiative of this type and the UK Government and Medical Research Council are committed to playing an active role in the programme.


Key Stats


- 700,000 people have dementia in the UK and this number will rise to ??¦ in

- One in three people of 65 will die with a form of dementia

- There are 15,000 people under the age of 65 with dementia

- Dementia costs the economy ??17 billion a year

- Delaying the onset of dementia by five years would halve the number of deaths from the condition, saving 30,000 lives a year















The Dementia Strategy can be found at dh.uk/dementia.


Dementia is one of the main causes of disability in later life, ahead of some cancers, cardiovascular disease and stroke.


Department of Health


The first ever National Dementia Strategy is a landmark document that will transform the quality of dementia care. It sets out initiatives designed to make the lives of people with dementia, their carers and families better and more fulfilled.


Published on 3 February 2009, the National Dementia Strategy is backed by ??150 million over the first two years. It will increase awareness of dementia, ensure early diagnosis and intervention and radically improve the quality of care that people with the condition receive. Proposals include the introduction of a dementia specialist into every general hospital and care home and for mental health teams to assess people with dementia.


The NHS support for degenerative neurological disorder research and the National Institute for Health Research (NIHR) spend on dementia research amounted to over ??22m in 2007/8. In addition, ??20m has been invested in the national research network on dementia and neurodegenerative disease (DeNDRoN). This will increase recruitment to trials, improve the speed and quality of research, strengthen research collaboration between the NHS and industry and ensure the better integration of research and patient care.


More recently, a further ??6m has been awarded for dementia related research under the NIHR Programme Grants scheme. These prestigious awards will support major studies of interventions to enhance life with dementia in home and residential settings. Two of the five proposals supported under a targeted call by the NIHR's Health Technology Assessment Programme this year are also focused on dementia. These include studies of interventions to promote the mental health of carers of people living with dementia and the use of the Acetylcholinesterase Inhibitor Donepezil for people with Parkinson's Disease. The DH's Policy Research Programme has also recently confirmed funding of a major evaluation to underpin the implementation of the National Dementia Strategy (NDS). This will examine the impact of pilot schemes for the peer support networks and dementia advisor service announced in the NDS.


EU Joint Programming Initiative


The MRC is a leading partner in the development of Joint Programming, a European strategy aimed at co-ordinating national efforts in neurodegenerative research across the biomedical and social spectrum. The strategy will be formulated during the latter half of 2009 and will aim to:


- Speed up developments in neurodegenerative disease research and drive best practice


- Develop a Strategic Research Agenda, establishing medium to long-term research needs and objectives in the area of neurodegenerative diseases.

- Improve data sharing between research centres across the EU

- Increase the pool of people available for epidemiological and clinical studies

- Compare and improve care delivery systems across EU member states.


MRC Strategic Review of Neurodegeneration


In February 2008, the MRC convened a small review group to undertake a strategic review of neurodegeneration. The aim of the review was to formulate strategic advice to the MRC Neurosciences and Mental Health Board on the changes in health need, new scientific opportunities and the most important research and training questions that the MRC/UK could address. The review concluded that the highest priority should be to deliver innovative mechanistic and pathological research across the broad spectrum of neurodegenerative disorders over the next five years, as a basis for a substantial increase in translational research in the longer term, addressing both early diagnosis and intervention. The report made three central recommendations:


- To strengthen biological research into disease origins and mechanisms

- To improve training and critical mass

- To provide support for a strategic co-coordinated network that would address the key barriers to progress in this field


MRC-Wellcome Trust Joint Call in Neurodegeneration


At the beginning of October 2008, MRC and Wellcome Trust launched a ??30M joint call for collaborative and innovative interdisciplinary proposals in neurodegeneration. The focus of the call is on advancing understanding of biological processes underpinning neurodegenerative diseases.


The aims of call are to:


- Create consortia comprising leading UK groups - can include international researchers and pharma.

- Facilitate use of interdisciplinary approaches to address key gaps in our knowledge of the biological basis of neurodegenerative diseases.

- Catalyse development of new approaches for effective diagnosis and therapeutic interventions.


Source

Medical Research Council

California Leaders Confront Alarming Rise In Alzheimer's Cases

Anticipating a catastrophic increase in Alzheimer's disease and related dementias, California leaders have completed the much-anticipated California State Plan for Alzheimer's disease, a disease estimated to double among Californians by the year 2030. The plan is a 10-year course of action with guiding principles, goals and recommendations to prepare California for this growing health crisis.



Alzheimer's will soon soar to epidemic proportions in California, according to Alzheimer's Association research, which indicates that by 2030, the number of Californians age 55 and older living with Alzheimer's disease will double to 1.1 million. Due to a rapidly aging population, the increase will be even more dramatic among California's Asians and Latinos, who will see a tripling in those affected by 2030.



"As the author of the legislation calling for the State Plan, I wanted to bring together the best minds in California to develop new ways to address the epidemic that is Alzheimer's disease," said Senator Elaine Alquist (D-San Jose). "If we don't act now before the epicenter of the crisis hits us in 10 years, the economic and human costs will be insurmountable. Procrastination is simply not an option. I am absolutely confident that our State Plan will be a model for the nation."



The State Plan is intended to streamline government functions, reduce costs and increase efficiency through effective use of existing resources. Its goals and recommendations include a commitment to research and system changes that minimize societal stigma and improve detection, diagnosis, treatment and care for individuals and families impacted by the disease. It also addresses the challenges and opportunities to finance the recommendations. These include restoring and enhancing California's home and community-based care system, as well as support for family caregivers and the training of professionals. Proper training and support for families can help forestall the demand for services in publicly funded, high-cost settings such as hospitals, emergency rooms and nursing homes.



"Unless we invest in home and community-based care, including the family caregiver, we are simply cost shifting to nursing homes, emergency rooms and hospitals, which places an even greater burden on the state," said Joshua Chodosh, M.D., MSHS, University of California, Los Angeles and VA Greater Los Angeles Healthcare System, co-chair of the State Plan Task Force. "The cost of medical and social supports for Alzheimer's just in California is expected to jump from $16 billion to $31.3 billion by 2030. These and other statistics underscore the need for the State Plan."



Next steps include advocacy for implementation of the Plan's recommendations for long-term care policy changes. In the months ahead, a series of policy briefings will communicate the Plan's findings to the new governor, the Legislature and other policymakers and leaders. This will better prepare them to address the escalation of Alzheimer's among California's population.
















"The stakes are high. It's not just individuals diagnosed with Alzheimer's who are of concern - in fact, virtually every Californian could be affected by the disease, including family caregivers, employers and taxpayers," said Mary Sundsmo, MBA, UC San Diego Shiley-Marcos Alzheimer's Disease Research, president of the Alzheimer's Association California Council. "The impact of Alzheimer's disease is already being felt across all sectors of society, but the sheer number of aging baby boomers means the worst is yet to come. We are proud that California is addressing this growing health crisis and joining 18 other states in developing its own Alzheimer's Disease State Plan."



The State Plan was created in response to SB 491 by Sen. Elaine Alquist in 2008. Under the leadership of the Alzheimer's Association, State Health and Human Services Agency, and Alzheimer's Disease and Related Disorders Advisory Committee, a broad-based task force was appointed. The task force engaged more than 2,500 individuals in plan development, including people living with the disease, under-served communities, representatives from the health care and provider community, researchers, academicians, family caregivers, local and state government staff, and elder law experts.



The plan was funded through a unique public-private partnership, including support from The SCAN Foundation, The California Endowment, The Rosalinde and Arthur Gilbert Foundation, and Archstone Foundation.



"When properly implemented, this plan can and will benefit the entire state and every California resident. We will see a difference in how prepared California is in the face of an unavoidable and alarming rise in Alzheimer's cases," said Sundsmo.


Source:

Alzheimer's Association

Experts Predict Significant Rise In Numbers Of People With Dementia In Northern Ireland

Dementia is set to soar in Northern Ireland with experts forecasting a 27% rise over the next ten years. New research launched today by the Alzheimer's Society states that more than 20,500 people in Northern Ireland will be living with dementia by 2017.


The London School of Economics and King's College London research, commissioned by the Alzheimer's Society, reports that dementia currently affects 16,000 people in Northern Ireland.


Claire Keatinge, Northern Ireland director of the Alzheimer's Society says:


'This report gives us a clear picture of the scale of dementia here and now. We know that the number of people with dementia is set to increase by nearly a third over the next decade. We need dementia to be treated as an health and social care priority by the newly elected NI Assembly, to ensure that people with dementia and their carers throughout NI, have services and support that meet their needs.'


Together with Scotland, Northern Ireland has the highest proportion of people over 65 living in care homes in the UK with fewer people receiving day care or domiciliary services.


-- The Northern Ireland research supplements the Dementia UK report published by the Alzheimer's Society in February 2007. The independent research provides authoritative estimates for the number of people with dementia and future projections.


-- Dementia costs the UK ??17 billion per year, or ??539 per second.


-- 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 5 people over 80 have dementia.


-- The Alzheimer's Society champions the rights of people living with dementia and those who care for them. The Alzheimer's Society works in England, Wales and Northern Ireland.


-- As a charity, the 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 (UK)0845 306 0898 or visiting alzheimers.uk.

Trial Of New Drug For Alzheimer's Disease

A new drug has been shown to improve the brain function of people with early stage Alzheimer's disease and reduce a key protein associated with the disease in the spinal fluid, in a small study published in the journal Lancet Neurology and presented at the 2008 Alzheimer's Association International Conference on Alzheimer's Disease.



The drug, known as PBT2, counteracts the production and build-up of a protein called amyloid-beta that occurs in Alzheimer's disease. This protein, which can build up into a 'plaque', is believed to be toxic to brain cells and to prevent them from functioning properly.



Seventy-eight participants with early stage Alzheimer's disease took either 50mg or 250mg doses of the drug PBT2, or a placebo, over the course of 12 weeks in a randomised, double-blind clinical trial, led by a researcher from Imperial College London working with colleagues in Australia and Sweden. Both doses of PBT2 capsules were observed to be safe and well tolerated during the course of the study.



Participants undertook a number of tests to assess their cognitive function, prior to beginning treatment and at the end of the 12-week period. In two of these tests of executive function, which involves the ability to organise information, sequence events and plan, those on a 250mg dose of PBT2 showed a significant improvement over the placebo group.



The researchers also measured how the levels of amyloid-beta in spinal fluid changed during the course of the trial. They found that levels of amyloid-beta 42 in the cerebrospinal fluid of those on the 250mg dose of PBT2 were reduced by approximately 13 percent compared to placebo at the end of the 12-week period.



Amyloid-beta needs the metals zinc and copper in order to accumulate in the brain and these two metals become abnormally distributed in the brains of people with Alzheimer's disease. PBT2 works by interrupting the interaction between the metal ions and amyloid-beta, and returns levels of zinc and copper in the brain to normal levels.



In the cognitive tests, those on a 250mg dose of PBT2 were able to complete the task in a test known as Trail Making Part B an average of 42 seconds faster than they had at the beginning of the trial. The placebo group was an average of 6 seconds slower.



In the Category Fluency Test, which looks at a person's ability to come up with as many relevant words as possible in relation to a specified category, those in the 250mg group were able to produce an average of 2.4 more words than at the beginning of the trial. This compared with a decrease of 0.3 words in the placebo group.



Although memory loss is the problem most often associated with Alzheimer's disease, the executive cognitive functions assessed by these two tests typically begin to deteriorate in the early stages of the disease, though are sometimes less obvious than memory symptoms.
















There were no significant differences in participants' scores on tests assessing their memory function in the new study, but the researchers believe this may be because the memory function deteriorates at a slower rate than the executive functions at this stage of illness, making changes harder to detect in a short study.



Dr Craig Ritchie, from the Division of Neurosciences and Mental Health at Imperial College London, who led the study, said: "Alzheimer's disease is a devastating condition and it affects hundreds of thousands of people in the UK. The results of our trial are very encouraging, although it was a relatively small study, which took place over a short period of time. Our findings certainly engender much optimism that this drug may have a significant effect on the underlying pathology of Alzheimer's, with a tangible clinical benefit for patients.



"We now need further research to see how PBT2 performs in larger, longer-term trials. Our hope is that we might be able to see treatments that can substantially improve the lives of people with early Alzheimer's disease within the next five or so years," added Dr Ritchie, who has been assisting the Australian company Prana Biotechnology with the clinical development of its new drugs for ten years.



The next step for the research is to move forward with PBT2 in further trials with a view to gaining a license for the drug.



These study results follow on from a recently published study of mice which showed that PBT2, in the space of a few days, cleared amyloid-beta, improved cognition and reduced the damage to brain cells. The parent compound to PBT2, clioquinol, was shown in a small study of 36 patients in 2003 to slow the progression of Alzheimer's disease. PBT2 was developed to be even more effective than clioquinol at attacking the core pathology of the disease.







Source: Laura Gallagher


Imperial College London

One gene links newborn neurons with those that die in diseases such as Alzheimer's

In certain parts of the brain, cells called neurons go through a cycle of death and replenishment. New research from
Rockefeller University's Fernando Nottebohm, Ph.D., shows that these replaceable neurons share something in common with the
neurons that die in people with diseases such as Alzheimer's and Parkinson's: both have unusually low levels of a protein
called UCHL1.


"It would be ironic if the shortfall in a same gene brokered the path to brain disease or rejuvenation," says Nottebohm, who
is Dorothea Leonhardt Professor and head of the Laboratory of Animal Behavior. "But naturally replaced neurons may hold the
key to understanding processes of neurodegeneration."


The results appear in the May 23 Early Edition issue of Proceedings of the National Academy of Sciences.


The potential medical implications of the study came as a surprise to the researchers. They set out to answer fundamental
questions about the small number of brain neurons that can be replaced when they die: Are these cells similar to other
neurons that are not replaced in adult life? Or, in terms of which genes are "turned on," are they marked as transient?



Nottebohm's laboratory has pioneered the study of the brain pathways controlling how songbirds learn to sing. A discrete
region of the brains of songbirds, known as the high vocal center, controls their singing behavior. It was in this brain
region that, more than 20 years ago, Nottebohm discovered new neurons being born in adult birds, overturning the conventional
wisdom that all neurons in vertebrates are created by birth or soon after.


In the new study, the researchers looked at cells in the high vocal center region of the brains of 19 zebra finches, a kind
of songbird native to Australia that has long been used in studies of birdsong. Since replaceable neurons sit side-by-side
with neurons that are not replaced, the first step was to label the two kinds of cells in order to tell them apart.


The replaceable neurons send projections to another part of the brain a few millimeters away from the high vocal center to
form part of the brain pathway that controls muscle movements related to singing. The neurons that are not replaced send
their projections to a different brain region, one that controls the song learning pathway. In order to label the two cell
types, the scientists injected dyes of different colors, one green and one red, into the brain regions where the neurons
project. The dyes then traveled back to the bodies of the cells in the high vocal center. As a result, replaceable and
nonreplaceable neurons could easily be distinguished under the microscope.


Then, looking at very thin slices of brain tissue, the researchers used a technique called laser capture microdissection to
collect cells of each type. From these they purified RNA, the quantity of which corresponds to the activity of the particular
gene producing it. The microdissection technique uses a low-power laser to melt a small circle of film into the tissue. When
the film is lifted, the cell body - including its RNA - comes with it, as if removed by a hole punch.















After collecting, purifying, and amplifying the RNA from 3,500 cells for each bird, the researchers used a microarray created
in the lab to find out which of the genes in the cells were turned on. This technique allowed them to identify which genes
were active, or expressed, by comparing them with 800 known genes from the zebra finch.


They expected to find a few overactive genes in the replaceable neurons. But instead, one gene turned up in consistently low
levels.


The gene was UCHL1.


"We expected UCHL1 would be high in all kinds of neurons," says first author Anthony Lombardino, Ph.D., a postdoctoral fellow
in Nottebohm's laboratory. The gene is known to be highly expressed throughout the brain, and in fact, the UCHL1 protein is
thought to make up as much as 2 percent of total soluble brain protein. But in the zebra finch brains, nonreplaceable neurons
produced, on average, about two and a half times the amount of UCHL1 as replaceable neurons.


In addition, studies from other laboratories have pointed to deficiencies in UCHL1 in degenerative diseases such as
Alzheimer's and Parkinson's.


Experiments in mice confirmed the finding that low levels of UCHL1 correlate to the ability of neurons to be replaced. The
researchers used similar techniques to assess UCHL1 in hippocampus and olfactory bulb neurons in mouse brains, areas where
neurons are known to undergo spontaneous replacement. They found markedly low levels of UCHL1 in the replaceable neurons of
both these regions.


"Low levels of UCHL1 appear to be a feature of replaceable neurons wherever they occur," says Lombardino.


The scientists also knew that, in songbirds, most neurons born during adulthood die, but a bird's active singing increases
the survival rate of new neurons. They reasoned that, if UCHL1 levels are related to the death or survival of neurons, these
levels should increase when birds are singing and when more new neurons thus have a chance of surviving. In another
experiment the scientists allowed male finches to sing to a female before analyzing the birds' brain neurons. As predicted,
the expression of UCHL1 in replaceable neurons, but not in nonreplaceable ones, increased in birds that were singing.



"These findings suggest that rising levels of UCHL1 may be associated with a reduced risk of neuronal death," says Nottebohm.
"This study draws attention to the replaceable neurons of adult brain as a wonderful model system in which to study changes
in genomic expression related to learning, aging and neurodegeneration, in addition to those that are related to the
choreography of replacement itself."


"In addition, because we study birds that learn their songs, the story relates to a fascinating, learned behavior, so it
offers the opportunity to show how integration at different levels of biology can be made to pay," Nottebohm says. "It allows
us to think about the brain in ways that no single level of analysis would allow."


Contact: Kristine Kelly

kkellyrockefeller

212-327-7146

Rockefeller University

rockefeller

New Method To Stimulate The Immune System May Be Highly Effective At Reducing Amyloid Burden In Alzheimer's Disease

Researchers at NYU Langone Medical Center have discovered a novel way to stimulate the innate immune system of mice with Alzheimer's disease (AD) - leading to reduced amyloid deposits and the prevention of Alzheimer's disease related pathology - without causing toxic side effects. The study entitled "Induction of Toll-like Receptor 9 Signaling as a Method for Ameliorating Alzheimer's Disease Related Pathology" was published in The Journal of Neuroscience.


NYU Langone researchers stimulated the innate immune system via the Toll-like 9 receptor (TLR9) via treatment with cytosine-guanosine containing DNA oligodeoxynucleotides (CpG ODNs) in Tg2576 AD model transgenic mice. This treatment produced a 66% and 80% reduction in the cortical and vascular amyloid burden, when compared with non-treated AD mice. Also, vaccinated Tg2576 mice performed similarly to non-treated mice on a radial arm maze used in the study, showing improvements in behavior and reduced amyloid burden.


"Our results indicate that stimulation of the innate immune system through TLR9 with CpG ODNs is an effective and apparently non-toxic method to reduce the amyloid burden in the brain," said Thomas Wisniewski, MD, professor of neurology, pathology and psychiatry at NYU Langone Medical Center. "Furthermore we found that amyloid reduction was associated with significant cognitive benefits in an AD mouse model. This approach has significant implications for future human immunomodulatory approaches to prevent AD in humans."


The deposition of amyloid ?? (A??) in the central nervous system in the form of amyloid plaques is a hallmark of Alzheimer's disease. A?? accumulation destroys neurons in the brain, leading to deficits in cognitive abilities. Immunomodulation or vaccination for AD is emerging as an effective means of shifting the equilibrium from A?? accumulation to clearance; however, excessive cell mediated inflammation and cerebral microhemorrhages - two forms of toxicity- were shown to occur in previous vaccination studies targeting the adaptive immune system.


"This innate immune approach did not have any of the problems previously reported with immunomodulation targeting the adaptive immune system, such as encephalitis, hemorrhages or lack of an effect on vascular amyloid, suggesting that this method has significant advantages," said Dr. Wisniewski "The treatment with CpG ODNs has already been tested in normal human volunteers and found to be safe- in studies where CpG ODNs was to be used to treat chronic infections; hence this AD treatment has the potential to be brought to clinical trial relatively quickly."


With injection of CpG ODNs used as a treatment to stimulate the innate immune system in Tg2576 AD model mice, the animals were closely monitored for signs of toxicity during behavioral testing and later for any signs of pathology through dissection. No toxicity was evident in the CpG ODN treated group. During behavioral testing in a maze the mice differed significantly between Tg2576 AD group and the CgP ODN treated group that better navigated the maze. The mice were dissected at 17 months of age after behavioral testing and the brains were processed for analysis. CpG ODN treated mice had fewer plaques compared to Tg2576 AD mice.















In addition to the analysis of A?? burden, researchers evaluated the treatment effect of CpG ODNs on microglial (cells that act as the first form of active immune defense in the central nervous system) in Tg2576 AD mice. CpG ODNs treatment resulted in overall cortical and hippocampal brain reduction in immunoreactivity at 17 months.


"In evaluating the efficiency of CpG ODN treatment in the AD mice model, we found that simulation of TLR9 signaling led to a remarkable reduction of amyloid burden which was paralleled by a reduction in the numbers of activated defensive immune responses in the central nervous system (CNS)," said Dr. Wisniewski. "Thus the effect of CpG ODNs on immune cells may induce heightened levels of surveillance and activity by these cells and thus increased influx into the brain and clearance of A??. Activation of immune cells may elicit entrance of other cells into the CNS and induce either A?? clearance or induce CNS cell signaling leading to recruitment of cells capable of clearing A??."


Researchers noted that the findings show administration of CpG ODNs clearly was beneficial, leading to reductions in both amyloid deposition and cognitive decline. This shows that modulation of the immune system may be beneficial for human AD patients but the methods used must be modified to prevent toxicity.


About NYU Langone Medical Center


Located in the heart of New York City, NYU Langone Medical Center is a premier center for health care, biomedical research, and medical education. For over 167 years, NYU physicians and researchers have contributed to the practice and science of medicine. Today the Medical Center consists of NYU School of Medicine; Rusk Institute of Rehabilitation Medicine, the first and largest facility of its kind; NYU Hospital for Joint Diseases, a leader in musculoskeletal care; and such nationally recognized programs as the NYU Cancer Institute, the NYU Child Study Center, and the NYU Cardiac and Vascular Institute.


New York University Langone Medical Center

1 Park Ave.

New York

NY 10016

United States

med.nyu

More Change Needed To Match Growing Challenge Of Dementia

As much as ??8.2 billion is been spent inefficiently on dementia care every year a report by the National Audit Office (NAO) said yesterday.


'Improving Services for People with Dementia' found that while dementia is a national priority, it often isn't at a local level, despite the condition costing more than heart disease, stroke and cancer combined. The report looks at progress of the National Dementia Strategy for England 12 months on from its launch and finds that significant steps have been made but more needs to be done to improve care and save millions.


New research in the report finds that over half of GPs surveyed haven't had adequate training and almost a third remain unconfident in diagnosing dementia. Only 21 per cent of consultants said a senior clinician had taken the lead for improving dementia in their hospital and only 15 per cent of psychiatrists reported that their PCT had invested extra funds into their service. The report recognised much groundwork has been done but concludes that the Department of Health must put in place the levers necessary to deliver the strategy.


Andrew Ketteringham, Director of External Affairs of Alzheimer's Society says,


'This influential report shows just how big the dementia crisis is. Change can't come soon enough for the millions of families battling daily with this devastating condition. The Strategy will transform lives but only if local health authorities are compelled to give dementia the priority it deserves. Millions depend on the Strategy succeeding. It's a race against time.'


Dawn Edmonds, 53, of Shropshire who cares for her husband Dave, 62, added,


'I love Dave but caring for a person with dementia is the most difficult job in the world. Every step has been a struggle, I've had to sell my house and even move to a different postcode to get the care Dave needed. I haven't worked in ten years and like millions of carers I have been pushed into poverty. The strategy is a chance for real change but across the country people have sat in rooms talking for too long. The time for talking is over. We now need action to get us out of this mess.'


Key findings of the report include


- Few frontline staff could identify leaders championing dementia. Nurses surveyed said they had received no information on the Strategy.


- Joined up working between health and social care is patchy and people are still being admitted to hospital unnecessarily, have longer length of stays and enter residential care prematurely.


- Only two Strategic Health Authorities were actively working with the care homes sector.


- There has been no improvement in GP knowledge and awareness over five years. Dementia is not included in the core requirements for nursing degrees.


- 37 per cent of consultants surveyed said a multi-agency group had been formed in their area to plan implementation of the Strategy (41 per cent were unsure).


- 58 per cent of consultants have an older people's mental health liaison team in their general hospital.


- Only 11 per cent of consultant psychiatrists could point to an agreed joint care pathways in their area (41 per cent were unsure).


- Dementia is not a priority in the 2010 - 2011 NHS Operating Framework, nor is it featured in a set of national priorities against which local organisations performance is monitored

Source
Alzheimer's Society

Alzheimer's Test That Can Be Administered In Family Practitioners' Offices Offers Better Opportunities For Early Detection

Early detection is key to more effective treatment for Alzheimer's disease and other forms of cognitive impairment, and new research shows that a test developed at the University of Tennessee is more than 95 percent effective in detecting cognitive abnormalities associated with these diseases.



The test, called CST -- for computerized self test -- was designed to be both effective and relatively simple for medical professionals to administer and for patients to take.



Rex Cannon, an adjunct research assistant professor of psychology at UT Knoxville, and Dr. John Dougherty, an associate professor in the UT Graduate School of Medicine, worked with a team of researchers to develop CST. The impetus for the test came from data showing that 60 percent of Alzheimer's cases are not diagnosed in the primary care setting, and that those delays lead to missed treatment opportunities.



"Early detection is at the forefront of the clinical effort in Alzheimer's research, and application of instruments like CST in the primary care setting is of extreme importance," said Cannon.



The CST is a brief, interactive online test that works to asses various impairments in functional cognitive domains - in essence, it's a "fitness test" of sorts for the basic functions of thinking and processing information that are affected by Alzheimer's and milder forms of cognitive impairment.



Cannon and Dougherty's research, published in the April issue of the Journal of Alzheimer's Disease and in an early online edition of the journal, showed that the CST was substantially more effective and more accurate in detecting the presence of Alzheimer's and other forms of cognitive impairment in patients than other existing tests. The CST had a 96 percent accuracy rate compared to 71 percent and 69 percent for the tests that are currently in use.



Part of the goal in developing the test, according to Cannon, was to ensure that the test is useful in the primary care setting, where physicians may not have detailed training in recognizing cognitive impairments, but where an early diagnosis may do the most good for patients.



"Computerized testing is a developing and exciting area for research," said Cannon, who noted that the test can provide an objective way to determine what diseases may affect the patient and provide information to begin treatments that can blunt the effects of Alzheimer's.



Cannon and Dougherty, who also are affiliated with the Cole Neuroscience Center at the UT Medical Center, collaborated with Medical Interactive Education in developing the CST over the past two years.



The journal article is titled "The Computerized Self Test (CST): An Interactive, Internet Accessible Cognitive Screening Test For Dementia"



Source:

Whitney Holmes

University of Tennessee at Knoxville

Black, Hispanic Caregivers More Likely To Misinterpret Signs Of Alzheimer's, Survey Finds

Hispanic and black caregivers are more likely than other ethnic groups to misinterpret symptoms of Alzheimer's disease as normal signs of aging, according to a recent survey by the Alzheimer's Foundation of America, HealthDay/Washington Post reports. The survey found that 37% of black caregivers and 33% of Hispanic caregivers believed that the disease's symptoms were a normal part of aging, compared with 23% of caregivers from other racial or ethnic groups. The survey also found that black and Hispanic caregivers were more likely to report that they knew little about Alzheimer's.

Misinterpretation of the disease's symptoms "often leads to delays in seeking care, when early treatment might make a difference in the progression" of the condition, HealthDay/Post reports. Experts said the survey's findings indicate a need for more culturally competent education on Alzheimer's disease. Eric Hall, founding CEO of AFA, called the findings "distressing," adding, "In the absence of a cure, care becomes a critical issue to sustain the highest quality of life for the longest time."

According to Angela Geiger, vice president of constituent relations for the Alzheimer's Association, Alzheimer's has different effects in different racial and ethnic groups. For example, the disease is more prevalent in blacks than whites, and Hispanics are more likely to display symptoms earlier. Such differences prompted the organization to create "a series of culturally appropriate publications tailored" to blacks and Hispanics, she said (Doheny, HealthDay/Washington Post, 4/20).


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.

Recent Study Documents The Spread Of A Disease Process Thought To Signal The Onset Of Alzheimer's Disease

Research unveiled at SNM's 57th Annual Meeting shows that scientists are drawing closer to documenting the progression of a disease process believed to cause Alzheimer's disease. This research could eventually lead to life-saving preventative measures for millions of patients who suffer from this chronic neurodegenerative disorder.



"Alzheimer's is a relentless disease that kills once it is established in the brain, but we are tantalizingly close to a cure," said Mark Mintun, M.D., professor of radiology and director of the Center for Clinical Imaging Research at Washington University, St. Louis, Mo. "The build-up of a naturally-occurring protein called beta-amyloid appears to be associated with the initiation of the disease. There is significant interest in understanding how to image this process and develop potential pharmaceuticals to prevent or remove beta-amyloid from the brain before the onset of dementia."



In one of the few large-scale, longitudinal studies of its kind, scientists used positron emission tomography (PET) to document changes in the accumulation of beta-amyloid, which forms into a plaque in the neural tissues of those diagnosed with Alzheimer's. Research reveals that by the time patients are diagnosed and once-healthy neurons have begun to deteriorate, it may be too late to effectively treat Alzheimer's disease and restore brain function. PET and other molecular imaging techniques are helping researchers to understand the initial pathology of the disease in order to determine the best course of treatment for each patient - even before symptoms occur, such as diminished memory and critical thinking and eventually the ability to perform simple tasks.



Using molecular imaging to monitor changes in beta-amyloid levels in the brains of elderly patients, scientists will be able to develop drugs that could potentially prevent Alzheimer's disease, and physicians will be able to determine at what stage of the disease treatment should begin. "With this type of research, physicians could be able to recommend treatment before irreversible damage occurs," added Mintun.



The study involved 129 participants, ages 45 to 86 with a mean age of 67 and with no signs or symptoms of cognitive disorder. Subjects underwent two PET scans within a five-year period using 11C Pittsburgh Compound-B (11C-PIB), a PET imaging agent that binds to beta-amyloid in the brain. The average length of time between scans was two-and-a-half years. Changes in beta-amyloid deposits were documented and used to determine the progression of potential preclinical disease. Results revealed that beta-amyloid deposits were abnormally high in 19 of the 129 subjects on the very first PET scan, and eight of the remaining 110 subjects became abnormal by the second scan. In these 27 subjects with abnormal beta-amyloid deposits, there were highly significant increases in the level of beta-amyloid between the two scans. Researchers hope to ultimately use this and other data to develop a method of detecting the onset and progression of very early stages of Alzheimer's disease.



Scientists now suspect that Alzheimer's disease begins developing an estimated 10 years before the appearance of cognitive dysfunction. According to the World Health Organization, approximately 18 million people are currently living with Alzheimer's disease worldwide. This number is projected to almost double by 2025.



Scientific Paper 382: M.A. Mintun, A. Vlassenko, D. Head, L.J. Casmaer, Y.I. Sheline, A. Goate, J.C. Morris, Washington University, St. Louis, Mo. "Quantifying the rate of beta-amyloid accumulation in cognitively normal participants using longitudinal [11C] PIB PET imaging," SNM's 57th Annual Meeting, June 5, 2010, Salt Lake City, Utah.



Source:

Amy Shaw


Society of Nuclear Medicine

Role Of Cholesterol In Alzheimer's Disease Unclear, Reports The 'Harvard Men's Health Watch'

It sounds simple: The lower
your cholesterol, the better your heart health. But a man's heart and his
head don't always agree. In fact, the relationships among cholesterol
levels, psychological function, and neurologic disorders are complex and
sometimes controversial, reports the March 2007 issue of Harvard Men's
Health Watch.



There are two major forms of dementia: vascular dementia and
Alzheimer's disease. Vascular dementia results when blood vessel damage
deprives the brain of oxygen. Brain cells die as a result, and mental
function suffers. Some studies link high cholesterol levels to an increased
risk of cognitive impairment, but others report the opposite. More research
is needed to sort this out, but even now, investigations of HDL (good)
cholesterol and mental function have consistently reported that high HDL
levels appear to help preserve mental function in older people.



The connection between Alzheimer's disease and cholesterol is even more
complex. Scientists have learned much of the damage of Alzheimer's comes
from deposits of a sticky protein, called beta-amyloid, in vital areas of
the brain. In some studies, high cholesterol levels appear to accelerate
the formation of beta-amyloid plaques. People with the genetic trait that
increases the level of a particular cholesterol transport protein have a
greatly increased risk of late-onset Alzheimer's.



The urgent question is whether cholesterol-lowering drugs, such as
statins, can reduce the risk of Alzheimer's disease. In the most recent
studies, people who took statins did not appear to be at lower risk for the
disease. Additional research is under way. Right now, it is too early for
firm conclusions on the relationships among cholesterol, cognitive
function, and statin therapy.


Harvard Health Publications

health.harvard/men

UM Genetic Researchers Release New Findings On Alzheimer's Disease

Researchers at the University of Miami Miller School of Medicine led by Margaret A. Pericak-Vance, Ph.D., and Jonathan L. Haines, Ph.D. at Vanderbilt University Medical Center, have identified nine genes that may increase susceptibility for Alzheimer's disease and confirmed a region on chromosome 12q long believed to harbor an Alzheimer's risk gene. The findings were posted online today and will appear in the January issue of the American Journal of Human Genetics. This project represents the first essential step in the application of modern genomic approaches to complex diseases and is one of four studies of its kind.



A research team at the Miller School's Miami Institute for Human Genomics and the Vanderbilt Center for Human Genetics Research performed a genome-wide association study using state-of-the-art genotyping technology that allows scientists to interrogate 550 thousand genetic variations in approximately 500 people with Alzheimer's disease and 500 people without the disease. The results were validated in an independent dataset.


"Results from this study open the door for increased understanding of this important neurological disorder," said Dr. Pericak-Vance, director of the Miami Institute for Human Genomics and the Dr. John T. Macdonald Foundation Professor of Human Genomics. "We now have exciting new directions to explore."


The findings show that the amyloid precursor protein, accepted as a risk gene for early-onset Alzheimer's disease, is also involved in late-onset Alzheimer's disease. The study also provides evidence of a risk locus at 12q13. Chromosome 12 has been of intense interest to geneticists in search of Alzheimer's risk genes. The locus implicated by this study is in close proximity to the vitamin D3 receptor gene. Low vitamin D levels have been reported in patients with cognitive impairment and Alzheimer's disease.


A variation in the vitamin D3 receptor gene that causes low vitamin D levels may also increase risk for Alzheimer's disease. According to Dr. Haines, "the vitamin D3 receptor finding on chromosome 12 is really exciting because it implicates a potential biological pathway that has been of interest in neurological disorders."



For the past decade, Alzheimer's disease genetics has been at an impasse. In the early 1990s, Dr. Pericak-Vance's discovery of the association of apolipoprotein E with Alzheimer's disease gave hope that the genetic etiology of a host of commons diseases would rapidly unravel. Scientists were able to identify genes of large effect, because they are present in a great enough portion of the population to be detected with available technologies. Disease genes present in smaller portions of the population, however, could not be confirmed.


Genome-wide association studies have improved researchers' ability to find disease genes of smaller or more moderate effect. Thanks to this powerful new tool, there will be several new candidate genes to pursue. "Data from the Miami Institute for Human Genomics genome-wide association study will invigorate the field and form a foundation for future investigations into the genetics of Alzheimer's disease," said Pericak-Vance. "We are now closely studying a number of candidate genes associated with Alzheimer's risk in our data."



The identification of new Alzheimer disease genes may lead to a better understanding of the complex causes of Alzheimer's disease and lead to improved diagnostic tools, enhanced preventive measures, and find new targets for treatment.


Other key investigators include John R. Gilbert, Ph.D.; Eden R. Martin, Ph.D.; Michael A. Slifer, M.D., Ph.D., at the Miller School's Miami Institute for Human Genomics; and Yi-Ju Li, Ph.D., at Duke University.



Jeanne Antol Krull

miami

Reduced Brain Volume May Predict Dementia In Healthy Elderly People

Reduced volume, or atrophy, in parts of the brain known as the amygdala and hippocampus may predict which cognitively healthy elderly people will develop dementia over a six-year period, according to a study in the January issue of Archives of General Psychiatry, one of the JAMA/Archives journals.


New strategies may be able to prevent or delay the onset of Alzheimer's disease (AD), the most common cause of dementia among older adults, according to background information in the article. Accurate methods of identifying which people are at high risk for dementia in old age would help physicians determine who could benefit from these interventions. There is evidence that adults with AD and mild cognitive impairment, a less severe condition that is considered a risk factor for AD, have reduced hippocampal and amygdalar volumes. However, previous research has not addressed whether measuring atrophy using magnetic resonance imaging (MRI) can predict the onset of AD at an earlier stage, before cognitive symptoms appear.


Tom den Heijer, M.D., Ph.D., of the Erasmus Medical Center, Rotterdam, the Netherlands, and colleagues used MRI to assess the brain volumes of 511 dementia-free elderly people who were part of the Rotterdam Study, a large population-based cohort study that began in 1990. They screened the participants for dementia at initial visits in 1995 and 1996 and then in follow-up visits between 1997 and 2003, during which they asked about memory problems and performed extensive neuropsychological testing. The authors also monitored the medical records of all participants. During the follow-up, 35 participants developed dementia and 26 were diagnosed with AD.


People with severe amygdalar or hippocampal atrophy had the highest risk of developing dementia or AD over the course of the study, which followed participants for an average period of six years. "Concerning the extent of atrophy, we found in those destined to develop dementia volume reductions between 17 percent and 5 percent, depending on how long before the diagnosis of dementia the MRI was conducted," the authors report. "In persons with mild to moderate Alzheimer disease, volume reductions compared with healthy elderly persons are between 25 percent and 40 percent, suggesting that atrophy rates accelerate in patients with Alzheimer disease."


"Our study suggests that structural brain imaging can help identify people at high risk for developing dementia, even before they have any memory complaints or measurable cognitive impairment," they write. "However, we must bear in mind that most people with atrophy did not develop dementia, even after six years. Further prospective population studies are therefore required to find additional biomarkers, including other brain imaging parameters, that alone or in combination with clinical and genetic characteristics can help separate those who are at risk for developing dementia from those who are not."


(Arch Gen Psychiatry. 2006;63:57-62)


Editor's Note: This research was financially supported by the Netherlands Organisation for Scientific Research and the Health Research and Development Council, The Hague, the Netherlands.


Monique M. B. Breteler

m.bretelererasmusmc.nl

JAMA and Archives Journals

jamamedia

Depression Is A Risk Factor Rather Than Early Sign Of Alzheimer's Disease

A new study by researchers at Rush University Medical Center supports the idea that depression is truly a risk factor for Alzheimer's disease rather than a subtle early sign of its underlying pathology. The study, published in the April issue of the Archives of General Psychiatry, found no evidence of an increase in depressive symptoms during the prodromal phase before the clinical diagnosis of Alzheimer's disease.



Numerous observational studies have found higher levels of depressive symptoms in old age to be associated with increased incidence of Alzheimer's disease and mild cognitive impairment. However, previous studies have not been able to answer the question of whether depressive symptoms actually contribute to the development of dementia (risk factor hypothesis) or are a consequence of the disease (reverse causality hypothesis.)



Robert S. Wilson, PhD, a neuropsychologist at the Rush Alzheimer's Disease Center, and colleagues examined data from the Rush Religious Orders Study, a cohort of 917 older Catholic clergy without dementia at study onset, to examine the change in depressive symptoms of Alzheimer's disease before and after the emergence of the cognitive symptoms of the disease.



For up to 13 years, the study participants underwent annual clinical evaluations that included assessment of depressive symptoms, cognitive testing, and clinical classification of mild cognitive impairment (MCI) and Alzheimer's disease. During the study period, 190 participants developed Alzheimer's disease.



Consistent with earlier findings in the Rush Religious Orders Study, having more depressive symptoms at baseline was associated with increased incidence of Alzheimer's disease and MCI.



However, the study found that those who developed Alzheimer's disease showed no increase in depressive symptoms before clinical diagnosis. Researchers were able to observe patients during a mean of approximately four years before the onset of dementia. Additionally, researchers saw no increase in depression during the three to four years preceding the onset of MCI, which antedates the onset of dementia by several years.



"If depressive symptoms are a consequence of dementia or a reaction to declining function, depressive symptoms would likely increase at some point before dementia is clinically evident," said Wilson. "We observed no such increase."



The study also found that even after the diagnosis of Alzheimer's disease was made there was no general increase in depression, but rather an increase that was confined to individuals with certain personality traits.



"Depressive symptoms may be associated with distinctive changes in the brain that somehow reduce neural reserve, which is the brain's ability to tolerate the pathology associated with Alzheimer's disease," said Wilson. "Understanding how depression contributes to the development of Alzheimer's disease may suggest new approaches to disease prevention."







The research was supported by grants from the National Institutes on Aging, which leads the Federal effort to support and conduct basic, clinical, and social and behavioral studies on aging and on Alzheimer's disease. The Rush Alzheimer's Disease Center is one of 29 NIA-supported Alzheimer's Disease Centers across the United States. For more information on the Rush Alzheimer's Disease Center, visit rush/.



Source: Kim Waterman


Rush University Medical Center