New Insight Into Brain Disorders

The function of an enzyme in the brain - strongly linked to a number of major brain diseases such as Alzheimer's, schizophrenia and bi-polar disorder - has been identified for the first time by researchers at the University of Bristol, UK.



These findings, published in Neuron, will help in the understanding of how memories are laid down and what goes wrong in these disorders.



The research showed how controlling the activity of glycogen synthase kinase-3 (GSK3) might prevent a memory being erased by improving the strength of connections between neurons in the brain, thus allowing better consolidation of new information.



Professor Collingridge from the University of Bristol said: "While GSK3 has previously been implicated in major neurological disorders, until now its role in normal neuronal function has been largely unknown. Our new understanding will help pharmaceutical companies develop drugs to inhibit it when things go wrong."



Professor Graham Collingridge and his team, with colleagues from the University of British Columbia, revealed that the activity of GSK3 facilitates a form of 'cross-talk' between the two major forms of synaptic plasticity in the brain.



Synaptic plasticity is the strength of a connection between neurons and forms the basis of learning and memory.







Contact: Cherry Lewis


University of Bristol

High Adherence To Mediterranean-Type Diet, Increased Physical Activity Associated With Reduced Risk Of Alzheimer Disease

Elderly individuals who had a diet that included higher consumption of fruits, vegetables, legumes, cereal and fish and was low in red meat and poultry and who were physically active had an associated lower risk of Alzheimer disease, according to a study in the August 12 issue of JAMA. In a second study, higher adherence to a Mediterranean diet was associated with slower cognitive decline, but was not associated with a decreased risk of dementia.



Research regarding the effect physical activity can have on the risk of Alzheimer disease (AD) or dementia has shown mixed results, as has the effect of dietary habits. Their combined association has not been investigated, according to background information in the article.



Nikolaos Scarmeas, M.D., of Columbia University Medical Center, New York, and colleagues examined the association between physical activity and risk of AD and also the effect of physical activity and adherence to a Mediterranean-type diet on AD risk. The study included 2 groups that consisted of 1,880 community-dwelling elderly residents of New York city without dementia at the start of the study, for whom there was both diet and physical activity information available. Standardized neurological and neuropsychological measures were administered approximately every 1.5 years from 1992 through 2006.



The participants received measurements of their adherence to a Mediterranean-type diet (scale of 0-9; categorized as low, middle, or high) and their physical activity (sum of weekly participation in various physical activities, weighted by the type of physical activity [light, moderate, vigorous]; categorized into no physical activity, some, or much, also low or high), separately and combined. A higher score for diet was obtained with higher consumption of fruits, vegetables, legumes, cereals, and fish; lower consumption of meat and dairy products; a higher ratio of monounsaturated fats to saturated fats and mild to moderate alcohol consumption.



Individuals were followed up for an average of 5.4 years, during which a total of 282 developed AD. In considering only physical activity, the researchers found that more physical activity was associated with lower risk for developing AD. "Compared with physically inactive individuals, report of some physical activity was associated with a 29 percent to 41 percent lower risk of developing AD, while report of much physical activity was associated with a 37 percent to 50 percent lower risk," the authors write.



When considered simultaneously, both physical activity and Mediterranean diet adherence were significantly associated with AD incidence. According to the researchers, "Belonging to the middle diet adherence tertile was associated with a 2 percent to 14 percent risk reduction, while belonging to the highest diet adherence tertile was associated with a 32 percent to 40 percent reduced risk. Similarly, compared with individuals with no physical activity, individuals reporting some physical activity had a 25 percent to 38 percent lower risk for AD, while individuals reporting much physical activity had a 33 percent to 48 percent lower risk for AD."



The authors also write, "Compared with individuals with low physical activity plus low adherence to a diet (absolute AD risk, 19 percent), high physical activity plus high diet adherence was associated with a 35 percent to 44 percent relative risk reduction (absolute AD risk, 12 percent). ??¦ Absolute AD risks declined from 21 percent in the group with no physical activity plus low diet adherence to 9 percent in the group with much physical activity plus high diet adherence."



"In summary, our results support the potentially independent and important role of both physical activity and dietary habits in relation to AD risk. These findings should be further evaluated in other populations."


JAMA. 2009;302[6]:627-637.


Source
Journal of the American Medical Association

British Researchers Identify Link Between Childhood IQ And Vascular Dementia

Scottish researchers funded by the UK's leading dementia research charity, the Alzheimer's Research Trust, have found a link between childhood IQ and vascular dementia later in life.


Their research, published in the journal Neurology, found that lower childhood intelligence increases the risk of vascular dementia, a disease which currently affects 112,000 people in the UK. The results suggest that interventions to lower blood pressure and smoking targeted from early in life to those with a lower IQ could reduce the numbers of people developing dementia in old age. They also help scientists to understand what is happening in the brains of people with dementia and the best way to tackle different dementias.


Researchers based at the University of Edinburgh compared the records of 173 people who participated in the Scottish Mental Survey of 1932, when almost every child aged 11 years in Scotland took a mental ability test. They showed that lower childhood IQ increased the risk of vascular dementia, but not Alzheimer's disease. Because the difference was not seen in Alzheimer's, this suggests that increased risk of 'dementia' may be due to vascular causes.


Lead researcher, Dr Brian McGurn, formerly from the University of Edinburgh now based at Hairmyres hospital, East Kilbride said, "Our work suggests a possible link between mental ability in early life and risk of developing vascular dementia. The unique data available from the Scottish Mental Survey means the link can be demonstrated independent of factors like socio-economic status and education."


Rebecca Wood, Chief Executive of the Alzheimer's Research Trust said, "This research confirms that vascular risk factors are very important in tackling dementia. If we live a healthier lifestyle and reduce our risk of high blood pressure, cholesterol and don't smoke, then this gives us a much better chance of avoiding dementia later in life.


With 700,000 people in the UK with dementia today, we urgently need to fund more research to find ways to prevent, treat or cure dementia, but research is seriously under-funded".


Notes


- The Alzheimer's Research Trust is the UK's leading research charity for dementia. For free information on dementia and the treatments available, visit alzheimers-research.uk or phone 01223 843899.


- Vascular dementia is the second most common form of dementia after Alzheimer's disease and is linked to high blood pressure, high cholesterol or smoking. There are 112,000 people with vascular dementia and 417,000 with Alzheimer's disease, and a total of 700,000 people with all types of dementia in the UK.


- The research 'Childhood cognitive ability and risk of late-onset Alzheimer and vascular dementia' by Dr Brian McGurn, Prof Ian Deary and Prof John Starr at the University of Edinburgh and is published in Neurology on 25th June 2008.

Alzheimer's Research Trust

Number Of People Diagnosed With Dementia In England Still Falling Short

New NHS statistics highlighting the number of people diagnosed with dementia do not accurately reflect the real number of people with the condition, according to Alzheimer's Society.


Figures released by the NHS (Quality and Outcomes Framework, QOF) show that almost 249,463 in England have been formally diagnosed with dementia which is a far cry from the true figure of 575,000 who have the condition.


Andrew Chidgey, Head of Policy and Campaigns at Alzheimer's Society, says,


'The shockingly low diagnosis rates in England highlight that people are not visiting their GPs and even if they do, diagnoses are not being made. It is clear that there is a shortfall and we must increase understanding of dementia amongst the public and GPs to ensure a swift and timely diagnosis.'


Alzheimer's Society says there are currently 750,000 people living with dementia in the UK, yet only a third of them have had a diagnosis. GPs are an important part of the diagnosis process and the low number of diagnoses is in part due to the lack of training in dementia available to GPs. Research also shows that many people concerned about memory problems put off going to see their GP.


Low awareness of the early signs of dementia and the treatment and support available are among the other reasons why people may not receive a diagnosis. Public and GP awareness of the symptoms of dementia and how people can live well with the condition needs to be improved.


However, people worried about their memory should still seek the help of their GP.


Andrew Chidgey adds,


'Forgetfulness is not uncommon amongst most people, but when it begins to affect daily life it is important to get it checked out as soon as possible. Memory loss can be a symptom of dementia, along with confusion and mood changes. The sooner people seek help the sooner they can get support and information.'


Earlier this year, Alzheimer's Society re-launched its Worried about your memory? campaign, which stresses the importance of seeking help if people are worried about their own memory or that of someone close to them. It involved leaflets and posters being delivered to 10,000 GP surgeries - almost every surgery in England, Wales and Northern Ireland. Since the re-launch in August, 4,000 people have requested an information booklet.


Notes


- The QOF is a voluntary annual reward and incentive programme for GPs across the England. It records the number of people diagnosed with dementia by GPs. Its aim is to improve the quality of care patients are given by rewarding practices for the quality of care they provide.


- There are more than 8,000 GP surgeries in the England and over 10,000 across the UK.


- The initiative follows the successful launch of Worried about your memory? in 2009 which reached 80,000 people after leaflets were delivered to GPs across the country. Of those who requested further information, one in five went on to get a diagnosis. The campaign was relaunched in August 2010.


- To find out more about dementia visit here.


Fact about dementia


- Dementia is not a single illness but a group of symptoms caused by damage to the brain. The symptoms include loss of memory, mood changes and confusion


- Dementia affects everyone in different ways, but you should seek help without delay if your memory is not as good as it used to be and especially if you:


- struggle to remember recent events, although you can easily recall things that happened in the past


- find it hard to follow conversations or programmes on TV


- forget the names of friends or everyday objects


- cannot recall things you have heard, seen or read


- notice that you repeat yourself or lose the thread of what you are saying


- have problems thinking and reasoning


- feel anxious, depressed or angry about your forgetfulness


- find that other people start to comment on your forgetfulness


- feel confused even when in a familiar environment.


- One in three people over 65 will die with dementia


Source:

Alzheimer's Society

Synosia Therapeutics Begins Phase I Trial Of A New Generation Treatment For Cognitive Impairment In Alzheimer's Disease And Schizophrenia

Synosia Therapeutics announced today that it has started a Phase I clinical trial of SYN-120, its new generation 5-HT6 antagonist under development for the treatment of cognitive impairment associated with Alzheimer's and schizophrenia. The study will assess the safety and tolerability of single ascending doses of SYN-120 in healthy volunteers.


Dr Ian Massey, Chief Executive Officer and President of Synosia Therapeutics said: "It's a tribute to our team to be launching this study within months of acquiring SYN-120 through our partnership with Roche. It demonstrates our ability to efficiently and rapidly initiate and conduct clinical trials and to shorten the product development cycle".


Alzheimer's is an incurable disease, predominantly occurring in the elderly. Driven by the ageing population, prevalence of the disease is expected to double by 2025. Industry analysts Lead Discovery state that revenues of approved Alzheimer's disease drugs across major markets (US, Japan, France, Germany, Italy, Spain and the UK) totalled over $3bn in 2006, with revenues expected to exceed $5bn by 2012.


Schizophrenia is a severe form of mental illness, affecting about 24 million people worldwide. Cognitive impairment has long been recognised as a core feature of schizophrenia. It is present in the majority of patients, independent of symptoms such as delusions and hallucinations, and a major cause of poor social and vocational outcome. There are currently no medications approved for the treatment of cognitive impairment in schizophrenia.


About SYN-120



SYN-120, a potent and selective antagonist of the 5-HT6 receptor, was discovered by Roche and is now under development by Synosia for the treatment of cognitive impairment. Antagonism of 5-HT6 receptors, which are expressed exclusively in regions of the brain associated with cognition, results in increased concentrations of acetylcholine and glutamate in these regions. Currently, acetylcholinesterase inhibitors are the mainstay for treatment of Alzheimer's. SYN-120 is anticipated to be more efficacious than the acetylcholinesterase inhibitors and also to be devoid of the side effects (e.g. nausea and vomiting) of this class that result from non-selective increases in acetylcholine in organs other than the brain. Preclinical studies in a variety of models have shown that 5-HT6 antagonists have the potential to help reverse the cognitive losses brought about by Alzheimer's disease and to improve executive function in schizophrenics.


Source
Synosia

Good enzyme for Alzheimer disease ADAM

A disintegrin-metalloproteinase prevents amyloid plaque formation and hippocampal defects in an Alzheimer disease mouse model.


Alzheimer Disease (AD), a progressive neurological disorder, is characterized by the presence of amyloid plaques in the brain. These plaques are comprised of aggregates of amyloid beta-peptides (AB peptides), which are believed to play a central role in disease development. Most strategies to prevent AD have been aimed at reducing the generation of amyloid beta-peptides.


This is done by targeting specific enzymes, beta- and gamma-secretase, in the amyloid precursor protein (APP) degradation pathway, which sequentially cleave APP to form the Ab peptide. Falk Fahrenholz and colleagues at the University of Mainz, Germany, now provide evidence that targeting and alternative enzyme, alpha-secretase, might be a useful alternative strategy for reducing AB peptide.


In the APP processing pathway, alpha-secretase cleavage of APP generates an alternative breakdown product of the protein that cannot generate AB peptide. Here the researchers use a mouse model deficient in or over expressing the gene ADAM10, which codes for alpha-secretase protein.

In these studies, they find that moderate increased expression of ADAM10 in mice reduced AB peptide formation, prevented plaque formation, and, from a functional standpoint provided improvement in both long-term potentiation and cognitive impairment. On the other hand, mice lacking ADAM10 had increased number and size of amyloid plaques.

The data here provide evidence that a-secretase might be a useful therapeutic target for AD, and also suggest that impairment of this enzyme might underlie some forms of the disease.



An accompanying commentary by Christian Haas and Stefan F. Lichtenthaler provides details on the APP degradation pathway and places this work and AD in this context.



TITLE: A disintegrin-metalloproteinase prevents amyloid plaque formation and hippocampal defects in an Alzheimer disease mouse model


AUTHOR CONTACT:

Falk Fahrenholz

University of Mainz, Mainz, Germany.




View the PDF of this article at: https://the-jci/press/20864.pdf


ACCOMPANYING COMMENTARY: Amyloid at the cutting edge: activation of a-secretase prevents amyloidogenesis in an Alzheimer disease mouse model


AUTHOR CONTACT:

Christian Haass

Ludwig-Maximilians-Universitat, Munich, Germany.




View the PDF of this commentary at: https://the-jci/press/21746.pdf


Contact: Laurie Goodman

press_releasesthe-jci

212-342-4159

Journal of Clinical Investigation

Study Finds Possible Link Between Tooth Loss, Dementia

Tooth loss may predict the development of dementia late in life, according to a study by University of Kentucky researchers.


The researcher, led by Pamela Sparks Stein in the UK College of Medicine's Department of Anatomy and Neurobiology, used data collected from 144 participants in the Nun Study, a study of aging and Alzheimer's disease among Catholic sisters of the School Sisters of Notre Dame.


"Of the participants who did not have dementia at the first examination (of annual exams over a 12-year period), those with few teeth zero to nine had an increased risk of developing dementia during the study, compared with those who had 10 or more teeth," the researchers reported in a paper published in the October issue of the Journal of the American Dental Association (JADA).
The researchers relied on dental records and annual cognitive exams of the Nun Study participants in the order's Milwaukee province. The participants' ages ranged from 75 to 98 years old.


Numerous past studies have shown that patients with dementia are more likely to have poor dental health than patients without dementia. Few researchers, however, have examined whether poor oral health may contribute to the development of dementia.


The UK research team which includes Mark Desrosiers of the UK Sanders-Brown Center on Aging, Sara Jean Donegan of the Marquette University School of Dentistry, Juan F. Yepes of the UK colleges of Dentistry and Medicine, and Richard J. Kryscio, chair of the Department of Biostatistics in the UK College of Public Health proposes several possible reasons for the association between tooth loss and dementia, including periodontal disease and early-life nutritional deficiencies, infections or chronic diseases that may result simultaneously in tooth loss and brain damage.


The researchers caution that further study is needed to confirm whether tooth loss has any real role in bringing on dementia. "It is not clear from our findings whether the association is causal or casual," they write, urging further study.


JADA, a monthly journal, is the ADA's flagship publication and the best-read scientific journal in dentistry.


In striving to become a Top 20 public research institution, the University of Kentucky is a catalyst for a new Commonwealth a Kentucky that is healthier, better educated, and positioned to compete in a global and changing economy. For more information about UK's efforts to become a Top 20 university, please go to uky/OPBPA/Top20.html


University of Kentucky

102A Mathews Bldg.

Lexington, KY 40506-0047

United States

uky

Vascular Pathology In Familial Alzheimer Disease

A group led by Dr. Gregory A. Elder of the James J. Peters Veteran's Affairs Medical Center, Bronx, NY has demonstrated that presenilin-1 plays a role in the vascular pathology found in Alzheimer disease. Their report can be found in the January 2010 issue of the American Journal of Pathology.



Alzheimer disease accounts for half of all dementias diagnosed each year. Mutations in presenilin-1 (PS-1), which cleaves amyloid precursor protein, are one of the most common causes of early onset cases of familial Alzheimer disease (FAD), which accounts for 5-10% of all Alzheimer disease sufferers.



Alzheimer disease is accompanied by vascular pathology, where blood vessels and microvessels are damaged. To determine if mutated PS-1 contributes to the vascular pathology observed in FAD, Gama Sosa et al generated a mouse model that overexpressed either wild-type or mutated human PS-1. They found age-related vascular pathology in these FAD model mice that was especially prominent in the microvasculature. However, the basis for this pathology appears to lie in the neurons, as neurons but not vascular endothelial or glial cells express PS-1 in these mice. Taken together, these results implicate a role for neuronal to vascular signaling in the pathogenesis of vascular pathology in FAD.



In future studies, Dr. Elder and colleagues plan to use their mouse model to "uncover the role of PS-1 FAD mutants in neurovascular signaling and provide insights into how neurovascular signaling may be disrupted in sporadic [Alzheimer disease] as well."



Gama Sosa MA, De Gasperi R, Rocher AB, Wang AC-J, Janssen WGM, Flores T, Perez GM, Schmeidler J: Age-Related Vascular Pathology in Transgenic Mice Expressing Presenilin 1-Associated Familial Alzheimer's Disease Mutations. Am J Pathol 2010, 176: 353-368



Source: Dr. Angela Colmone


American Journal of Pathology

Nursing Home Residents with Alzheimer's Disease Benefited from Continuous Treatment with ARICEPT(reg) (donepezil HCl tablets)

A new retrospective analysis reported that Alzheimer's patients in nursing homes who were treated with ARICEPT(reg) for at least six months showed greater benefits in cognitive and functional status than patients who discontinued therapy. The findings, based on data obtained from an assessment tool used nationally by nursing homes, were presented at the American Geriatrics Society Meeting (AGS) today.



Continued treatment was also associated with more patient time spent in leisure activities and lower average daily labor costs, compared with discontinuing treatment.*



"This analysis supports the need to treat nursing home residents who have Alzheimer's disease to help them with their ability to perform daily activities," said Jonathan Musher, M.D., corporate medical director, Beverly Healthcare Corporation, a national long-term care provider for the elderly.



The analysis of nursing home residents was the first to examine the impact of Alzheimer's treatment with ARICEPT(reg) using data from the Minimum Data Set (MDS) assessments. This national assessment tool includes measures to evaluate Alzheimer's disease patients, including aspects of cognitive and functional status.



The one-year retrospective analysis collected MDS data to evaluate changes over baseline in patients receiving continued ARICEPT(reg) treatment (n=210) and those who discontinued treatment (n=210). Patients in each cohort were matched demographically and with respect to a variety of factors, including cognitive status, function, behavior, medical status and selected medications used, enabling comparisons across the treatment groups in addition to evaluation within each group. Measures included cognitive and functional status, time spent in leisure activities, behavior and average daily labor costs associated with patient care.



For all patients in the analysis, a baseline MDS assessment was completed within the first 60 days of treatment. In the continuing treatment group, MDS data were collected six to 12 months following initiation of treatment. In the discontinued group, data were collected at least 90 days after treatment was discontinued and within 12 months of initial treatment.



The analysis also showed that, for patients who continued treatment with ARICEPT(reg), the frequency of problematic behaviors declined compared to baseline. Further, the average difference in daily labor cost (in 2001-2002 dollars) was $6.90 less per day, per patient in patients who continued treatment compared to those who discontinued treatment. Average daily labor cost per resident is based on the resident's acuity (i.e., severity of impairment). The higher the acuity, the more labor the resident requires.



Information About ARICEPT(reg) (donepezil hydrochloride tablets) Treatment


While there is no cure for Alzheimer's disease, medical treatments are available to manage symptoms of the disease. Once-a-day prescription ARICEPT(reg) is indicated for mild to moderate Alzheimer's disease.
















In a progressively degenerative disease such as Alzheimer's, improvement, stabilization or a less-than-expected decline over time is considered a positive response to treatment. These types of responses have been observed in patients treated with ARICEPT(reg) in clinical trials for Alzheimer's disease. Individual responses to treatment vary, and some patients may not respond.



ARICEPT(reg) is well tolerated but may not be for everyone. Some people may experience nausea, diarrhea, insomnia, vomiting, muscle cramps, fatigue, or loss of appetite. In studies, these side effects were usually mild and temporary. Some people taking ARICEPT(reg) may experience fainting.



ARICEPT(reg) is the number one prescribed Alzheimer's disease therapy worldwide, with more than 1 billion patient days of ARICEPT(reg) therapy sold. More than 1.7 million people in the United States alone have begun ARICEPT(reg) therapy.



ARICEPT(reg) is co-promoted in the United States by Eisai Inc. and Pfizer Inc, which are dedicated to advances in Alzheimer's therapy.



For more information about managing Alzheimer's disease and about ARICEPT(reg), and for prescribing information on ARICEPT(reg), please call (888) 999-9616, or visit aricept. Full prescribing information is available at that Web site.



About Eisai Inc.


Eisai Inc. is a U.S. pharmaceutical subsidiary of Eisai Co., Ltd., a research-based human health care company that discovers, develops, and markets products in more than 30 countries.



Established in 1995, Eisai Inc. began marketing its first product in the United States in 1997 and has rapidly grown to become an integrated pharmaceutical business with sales of more than $1.5 billion in fiscal year 2002 (year ending March 31, 2003).


Eisai Inc. employs a total of more than 850 people at its headquarters in Teaneck, N.J., at its state-of-the-art pharmaceutical production and formulation research and development facility in Research Triangle Park, N.C., and in the field. Between 1998 and 2003, Eisai Inc. moved up rapidly in the rankings of U.S. pharmaceutical companies (based on revenues) from No. 44 to No.23.



About Pfizer


Pfizer Inc discovers, develops, manufactures, and markets leading prescription medicines, for humans and animals, and many of the world's best-known consumer products.



*The labor cost per resident is based on the resident's acuity (i.e., severity of impairment). The higher the acuity, the more labor the resident requires. The cost accounting system uses the acuity and the total labor charges to generate an average daily labor cost per resident.


eisai

Wallace And Gromit Makers Join Fight Against Obesity

Alzheimer's Society welcomes the new advert by Aardman Animations at the centre of a ??75m government marketing campaign to raise awareness of the link between obesity and life-shortening disease.


Neil Hunt, Chief Executive of Alzheimer's Society, comments,


'It is great news that the makers of Wallace and Gromit are joining the fight against Obesity. Obesity doubles risk of dementia and even modest increases in weight can increase risk of dementia by up to 30%.


If we do nothing now, one million people will develop dementia in the next 10 years. We hope this advert and the Change4Life campaign will help reduce the rising numbers of people living with this devestating condition in future. With the right investment, dementia can be defeated.'



Alzheimer's Society


Alzheimer's Society is the leading care and research charity for people with all forms dementia and their carers. It provides information and education, support for carers, and quality day and home care. It funds medical and scientific research and campaigns for improved health and social services and greater public understanding of dementia.


Alzheimer's Society

Non-Drug Treatments For Dementia Show Promise, Experts Say

Memory training and other non-drug treatments may one day help older adults ward off declines in mental function, according to researchers from Wake Forest University School of Medicine in an editorial in the current issue of the Journal of the American Medical Association.



"The latest research suggests that mental training and physical activity both have promise for preventing declines in cognition," said Sally A. Shumaker, Ph.D., lead author on the editorial. "It's possible to envision a future treatment approach that combines lifestyle and drug treatments to meet the specific needs of each individual."



Shumaker, a professor of public health sciences and associate dean for research at Wake Forest, said the findings suggest opportunities for studying other non-drug treatments, such as meditation, to prevent or slow declines in cognition, which includes concentration, language, memory and abstract reasoning.



"Cognitive decline is a rapidly growing problem because of our aging population," said Shumaker. "It is probably one of the biggest fears that older adults have - the loss of your mind and your competency and independence. It seriously threatens the ability of the aging population to live independently."



In the editorial, Shumaker and co-authors Claudine Legault, Ph.D., and Laura H. Coker, Ph.D., also from Wake Forest, discuss the results of a recent multicenter study involving cognitive training, as well as other advances in the field.



The Advanced Cognitive Training for Independent and Vital Elderly (ACTIVE) study involved almost 3,000 participants. Half received 10 sessions of cognitive training and half received no special training. Participants who had the training showed immediate improvements in memory, reasoning and speed of processing. When the participants were tested five years later, the improvements had been sustained.



Other recent research showing that sedentary older adults perform less well on measures of memory suggests that physical activity may also be able to improve memory, according to the editorial.



There are an estimated 24 million people in the world with dementia and 4.6 million new cases are diagnosed each year. Declines in certain mental functions, such as memory, predict future inability to perform activities of daily living, such as dressing and feeding themselves.



"These studies illustrate the promise of non-drug treatments," said Shumaker. "The medications available today produce only low to moderate improvements in mental function. And they can have adverse side effects. Showing that cognitive training can protect mental function means that individuals who cannot tolerate existing drugs would have additional treatment options."



"The ACTIVE study is an important step toward demonstrating the feasibility of enrolling older adults in a long-term study of a cognitive training intervention," according to the editorial.



The authors say that matching cognitive training with an individual's risk factor profile is an intriguing possibility. For example, training that focuses on memory may be best for those at risk for Alzheimer's disease.



"Once they are standardized and developed for mass markets, cognitive training programs might be available to seniors through churches, schools and senior centers," said Shumaker.



"Importantly, cognitive training programs may give individuals a greater sense of control over the disturbing prospect of cognitive decline and have a beneficial effect on their quality of life," says the editorial.



As a researcher, Shumaker served as national principal investigator for the Women's Health Initiative Memory Study, which showed that estrogen and progestin doubled the risk of dementia in older women.






Wake Forest University Baptist Medical Center is an academic health system comprised of North Carolina Baptist Hospital and Wake Forest University Health Sciences, which operates the university's School of Medicine. U.S. News & World Report ranks Wake Forest University School of Medicine 18th in family medicine, 20th in geriatrics, 25th in primary care and 41st in research among the nation's medical schools. It ranks 35th in research funding by the National Institutes of Health. Almost 150 members of the medical school faculty are listed in Best Doctors in America.



Contact: Karen Richardson


Wake Forest University Baptist Medical Center

Subjects At Risk Of Developing Alzheimer's Disease May Now Be Able To Delay The Onset Of Their First Symptoms By Several Years

The human brain loses 5 to 10% of its weight between the ages of 20 and 90 years old. While some cells are lost, the brain is equipped with two compensatory mechanisms: plasticity and redundancy. Based on the results of her most recent clinical study published today in the online version of Brain: A Journal of Neurology, Dr. Sylvie Belleville, PhD in neuropsychology, the principal author of this study and Director of Research at the Institut universitaire de g?©riatrie de Montr?©al (IUGM), which is affiliated with the Universit?© de Montr?©al, has found that for elderly subjects at risk of developing Alzheimer's disease, hope may lie in brain plasticity.


"Brain plasticity refers to the brain's remarkable ability to change and reorganize itself. It was long thought that brain plasticity declined with age, however, our study demonstrates that this is not the case, even in the early stages of Alzheimer's disease", declares Sylvie Belleville.


These findings open countless new avenues of research including the possibility of improving the plasticity of affected areas of the brain, and slowing the decline in plasticity through pharmacological means or lifestyle changes, thereby allowing subjects with Alzheimer's disease to enjoy several more symptom-free years.


The hypothesis behind this research was that certain cells traditionally involved in other brain processes could, through a simple memory training program, temporarily take over since they themselves are not yet affected. According to Dr. Belleville: "Our research has validated our hypothesis. Not only were we able to use functional imaging to observe this diversification, but we also noted a 33% increase in the number of correct answers given during a post-training memory task by subjects with mild cognitive impairment (MCI) who, incidentally, are ten times more likely to develop Alzheimer's disease".


The training program that was used was designed to help elderly subjects with MCI develop strategies, such as the use of mnemonics, for example, and promote encoding and retrieval, such as word lists, for example, using alternative areas of the brain. "The hypothesis had already been raised, but our team was the first to provide scientific support, using a functional neuroimaging protocol", added Sylvie Belleville.


Researchers worked with thirty elderly subjects: 15 healthy adults and 15 with MCI. Magnetic resonance imaging was used to analyse brain activity in the two groups 6 weeks prior to memory training, one week prior to training and one week after training. Before the memory training, magnetic resonance imaging in both the healthy elderly subjects and those with MCI showed activation in areas of the brain traditionally associated with memory. As expected, decreased activation was observed in subjects with MCI. After training, brain areas in elderly subjects with MCI showed increased activation in areas typically associated with memory, but also in new areas of the brain usually associated with language processing, spatial and object memory and skill learning.


According to Dr. Belleville: "Analysis of brain activity during encoding as measured before and after the training program, indicates that increased post-training activation in the right inferior parietal gyrus is associated with post-intervention improvement. The healthy area of the brain has taken over for the area that is compromised."


Sources: Universit?© de Montr?©al, AlphaGalileo Foundation.

Stimulating The Brain's Immune Response May Provide Treatment For Alzheimer's Disease

A new target for the prevention of adverse immune responses identified as factors in the development of Alzheimer's disease (AD) has been discovered by researchers at the University of South Florida's Department of Psychiatry and the Center of Excellence for Aging and Brain Repair.



Their findings are published online in the Journal of Neuroscience.



The CD45 molecule is a receptor on the surface of the brain's microglia cells, cells that support the brain's neurons and also participate in brain immune responses.



Previous studies by the USF researchers showed that triggering CD45 was beneficial because it blocked a very early step in the development of Alzheimer's disease. In the present study, the researchers demonstrated in Alzheimer's mouse models that a loss of CD45 led to dramatically increased microglial inflammation.



Although the brain's immune response is involved in Alzheimer's disease pathology, "this finding suggests that CD45 on brain immune cells appears critically involved in dampening harmful inflammation," said study senior author Jun Tan, MD, PhD, a professor of psychiatry and Robert A. Silver chair at the Rashid Laboratory for Developmental Neurobiology, USF Silver Child Development Center and research biologist for Research and Development Service at the James A. Haley Veteran's Hospital.



The investigators also found an increase in harmful neurotoxins, such as A beta peptides, as well as neuron loss in the brains of the test mice.



"In short, CD45 deficiency leads to increased accumulation of neurotoxic A beta in the brains of old Alzheimer's mice, demonstrating the involvement of CD45 in clearing those toxins and protecting neurons," Dr. Tan said. "These findings are quite significant, because many in the field have long considered CD45 to be an indicator of harmful inflammation. So, researchers assumed that CD45 was part of the problem, not a potential protective factor."



The next step is to apply these findings to develop new Alzheimer's disease treatments, said Paula Bickford, PhD, a professor in the USF Department of Neurosurgery and senior career research scientist at the James A. Haley Veteran's Hospital.



"We are already working with Natura Therapeutics, Inc. to screen for natural compounds that will target CD45 activation in the brain's immune cells," Dr. Bickford said.


Notes:


Other researchers involved in this study were: Dr. Yuyan Zhu, Dr. Huayan Hou, Dr. Kavon Rezai-zadeh, Dr. Brian Giunta, Ms. Amanda Ruscin, Dr. Carmelina Gemma, Dr. JingJi Jin, Dr. Natasa Dragicevic, Dr. Patrick Bradshaw, Dr. Suhail Rasool, Dr. Charles G. Glabe (University of California, Irvine, CA), Dr. Jared Ehrhart, Dr. Takashi Mori (Saitama Medical Center/Saitama Medical University, Japan), Dr. Demian Obregon, Dr. Terrence Town (Cedars-Sinai Medical Center, Los Angeles, CA). Drs. Yuyan Zhu and Huayan Hou contributed equally to this work.



Their work was supported by the National Institute on Aging and the National Institute of Neurological Disorders and Stroke, National Institutes of Health.



Source:

Randolph Fillmore

University of South Florida (USF Health)

Increases In TST Related To CPAP Treatment Improve Cognition In Alzheimer Patients With OSA

Increases in total sleep time related to the treatment of obstructive sleep apnea (OSA) with continuous positive airway pressure (CPAP) are associated with improvements in cognition in patients with Alzheimer disease, according to a research abstract presented on Tuesday at SLEEP 2008, the 22nd Annual Meeting of the Associated Professional Sleep Societies (APSS).



The study, authored by Jana R. Cooke, MD, Sonia Ancoli-Israel, PhD and colleagues from the University of California San Diego, focused on 52 participants with an average age of 77.8 years who had Alzheimer disease and OSA. The participants were randomized to six weeks of therapeutic CPAP or three weeks placebo CPAP followed by three weeks therapeutic CPAP. The participants underwent cognitive testing at baseline, three weeks and six weeks. Sleep was analyzed and scored for sleep stage, total sleep time, amount of time awake during the night, and the amount of oxygen in the blood.



According to the results, when Alzheimer's disease patients with OSA were treated with CPAP, an increase in the total amount of sleep at night, not improvement in oxygen levels, was associated with improvements in cognition.



"This finding implies that the cognitive dysfunction associated with OSA in patients with dementia may be in part an effect of short sleep time rather than a function of low levels of oxygen during sleep," said Dr. Cooke.



OSA is a sleep-related breathing disorder that causes your body to stop breathing during sleep. OSA occurs when the tissue in the back of the throat collapses and blocks the airway. This keeps air from getting into the lungs. OSA is more common among older adults and among people who are significantly overweight. OSA can increase a person's risk for high blood pressure, strokes, heart disease, and cognitive problems.



Not sleeping well can lead to a number of problems. Older adults who have poor nighttime sleep are more likely to have a depressed mood, attention and memory problems, excessive daytime sleepiness, more nighttime falls and use more over-the-counter or prescription sleep aids. In addition, recent studies associate lack of sleep with serious health problems such as an increased risk of obesity, cardiovascular disease and diabetes.



While most people require seven to eight hours of sleep a night to perform optimally the next day, older adults might find this harder to obtain. Older adults must be more aware of their sleep and maintain good sleep hygiene by following these tips:
Establishing a routine sleep schedule.















Avoiding utilizing bed for activities other than sleep or intimacy.


Avoiding substances that disturb your sleep, like alcohol or caffeine.


Not napping during the day. If you must snooze, limit the time to less than one hour and no later than 3 p.m.


Stick to rituals that help you relax each night before bed. This can include such things as a warm bath, a light snack or a few minutes of reading.


Don't take your worries to bed. Bedtime is a time to relax, not to hash out the stresses of the day.


If you can't fall asleep, leave your bedroom and engage in a quiet activity. Return to bed only when you are tired.


Keep your bedroom dark, quiet and a little cool.

First introduced as a treatment option for sleep apnea in 1981, CPAP is the most common and effective treatment for OSA. CPAP provides a steady stream of pressurized air to patients through a mask that they wear during sleep. This airflow keeps the airway open, preventing the pauses in breathing that characterize sleep apnea and restoring normal oxygen levels.







CPAP Central (SleepEducation/CPAPCentral), a Web site created by the AASM, provides the public with comprehensive, accurate and reliable information about CPAP. CPAP Central includes expanded information about OSA and CPAP, including how OSA is diagnosed, the function of CPAP, the benefits of CPAP and an overview of what to expect when beginning CPAP, the position of experts on CPAP, and tools for success. CPAP Central also features an interactive slide set that educates the public about the warning signs of OSA.



Although sleep patterns change as people age, disturbed sleep and waking up tired every day are not part of normal aging. Those who have trouble sleeping are advised to see a sleep specialist at a facility accredited by the AASM.



More information about "sleep and growing older" is available from the AASM at sleepeducation/Topic.aspx?id=30, and OSA at sleepeducation/Disorder.aspx?id=7.



The annual SLEEP meeting (9-12 June, 2008) brings together an international body of 5,000 leading researchers and clinicians in the field of sleep medicine to present and discuss new findings and medical developments related to sleep and sleep disorders.



More than 1,000 research abstracts will be presented at the SLEEP meeting, a joint venture of the AASM and the Sleep Research Society. The three-and-a-half-day scientific meeting will bring to light new findings that enhance the understanding of the processes of sleep and aid the diagnosis and treatment of sleep disorders such as insomnia, narcolepsy and sleep apnea.



SleepEducation, a patient education Web site created by the AASM, provides information about various sleep disorders, the forms of treatment available, recent news on the topic of sleep, sleep studies that have been conducted and a listing of sleep facilities.



Source: Kathleen McCann


American Academy of Sleep Medicine

Ending Two-Year Waiting Period For Medicare

Ending the Medicare Disability Waiting Period Act of 2007 (S 2102), offered by Sen. Jeff Bingaman (D-N.M.), would provide much needed assistance to those under age 65 diagnosed with early-onset Alzheimer's who lose their jobs and their employer- based health insurance.


There are as many as 500,000 individuals under age 65 with early-onset Alzheimer's or a related dementia who may qualify for Medicare benefits under Social Security Disability Insurance (SSDI) but must suffer through the 24 months after the date their SSDI begins for Medicare benefits to start. Over a 10-year period, this legislation would phase out the waiting period and would also, in the interim, create a process by which those with life-threatening diseases like Alzheimer's could get an exception to the waiting period.


Providing immediate access to Medicare benefits for people disabled by Alzheimer's disease would reduce the problem of lack of health insurance and high out-of-pocket expenditures for this vulnerable population. It ensures access to critical health care services, including prescription drugs that can help manage the disease. According to national data from the Health and Retirement Survey (HRS), prescription drugs can cost people with Alzheimer's as much as four times that for people with normal cognitive status.


Additionally, HRS data suggests almost one-third (29 percent) of people age 55-64 with disabling cognitive impairments have no health insurance; this landmark legislation could help remedy this troublesome problem.


Alzheimer's disease poses tremendous burdens on individuals and families, burdens made worse by lack of health care coverage. As the leading organization representing people with Alzheimer's disease, the Alzheimer's Association applauds Senator Bingaman for his leadership and urges swift enactment on this important legislation to provide invaluable health coverage and peace of mind for those with Alzheimer's and other disabling, fatal diseases.


Sen. Bingaman's news release


About the Alzheimer's Association


The Alzheimer's Association is the leading voluntary health organization in Alzheimer care, support and research. Our mission is to eliminate Alzheimer's disease through the advancement of research; to provide and enhance care and support for all affected; and to reduce the risk of dementia through the promotion of brain health. Our vision is a world without Alzheimer's.

alz/

Evotec's EVT 101 Well Tolerated In Four Week Higher Repeat Dose Safety Study

Evotec AG (Frankfurt Stock Exchange: EVT; NASDAQ: EVTC) announced top-line results of a double-blind, 4-week Phase Ib study with EVT 101, an orally active NR2B-subtype selective antagonist of NMDA receptors with potential in Alzheimer's disease, neuropathic pain and other indications. The study showed in both young and elderly subjects that the drug was well tolerated up to the highest dose tested.


The study was designed to evaluate safety/tolerability, pharmacokinetics, and pharmacodynamics during prolonged dosing with EVT 101 as com-pared to placebo, but at higher dose levels and for a longer duration that the previously completed Phase I study. The study was conducted and completed as planned per protocol.



EVT 101 was administered to 48 young and elderly healthy subjects over four weeks. Up to the highest dose level (12 mg/day in elderly, 15 mg/day in young subjects) EVT 101 was well tolerated by both populations. No severe or serious adverse events were reported, and only few transient, mostly mild, adverse events occurred. This safety and tolerability profile is extremely encouraging as the doses evaluated are predicted to be well into the anticipated therapeutic range. As previously reported (see press re-lease, March 28, 2008), this trial contained a sub-study in which drug CSF levels were measured to determine the extent of brain penetration.


Psychometric tests, examining different aspects of cognitive function, revealed a mixed pattern of minor transient changes, as expected from populations of healthy subjects performing optimally in cognitive tasks.


"Together with results from the fMRI brain imaging which we announced in March, these results provide a robust Phase Ib package. We have found doses of this highly specific compound that achieve a high level of brain exposure to achieve a high level of NR2B receptor blockade. These doses produce specific modulation of relevant brain areas and, importantly, are also well tolerated. This provides a good foundation for moving forward with the clinical development of this compound and enables us to investigate EVT 101 in relevant patient groups," commented Dr Tim Tasker, Executive Vice President Clinical Development, Evotec AG.



About Evotec AG


Evotec is a leader in the discovery and development of novel small molecule drugs. Both through its own discovery programs and through research collaborations, it is generating the highest quality research results to its partners in the pharmaceutical and biotechnology industries. In proprietary projects, Evotec specializes in finding new treatments for diseases of the Central Nervous System. Evotec has three programs in clinical development: EVT 201, a partial positive allosteric modulator (pPAM) of the GABAA receptor complex for the treatment of insomnia, EVT 101, a subtype selective NMDA receptor antagonist for the treatment of Alzheimer's disease and/or pain, and EVT 302, a MAO-B inhibitor in development for smoking cessation. Evotec's proprietary preclinical research programs focus on the purinergic receptors, P2X3 and P2X7, for the potential treatment of pain and inflammatory diseases. In addition, Evotec has worldwide collaboration and license agreements with Pfizer to research, develop and commercialize small molecule vanilloid receptor (VR1) antagonists.

evotec

Alzheimer's Foundation Of America Showcases New Jewelry Line To Honor Caregivers

The Alzheimer's Foundation of America
(AFA) has introduced a jewelry line that, in addition to being highly
fashionable, makes more than merely a fashion statement: it is designed to
recognize the heroic act of caregiving and to raise awareness of
Alzheimer's disease and related dementias.


The line consists of a necklace, bracelet and lapel pin -- each with a
sterling silver pendant modeled after AFA's logo of arms embracing a heart.
The logo reflects the organization's mission of providing optimal care to
individuals with dementia and their families.


"Caregivers give from the deepest recesses of their hearts. Our goal is
to recognize the selflessness and strength of these exceptional human
beings in light of the enormity of their role," said Eric J. Hall, AFA's
chief executive officer.


AFA expects the jewelry to especially touch caregivers of individuals
with Alzheimer's disease or other illnesses, and their families, as well as
to have universal appeal due to its artistic look.


An estimated five million Americans have Alzheimer's disease, which
results in loss of memory and other cognitive functions; the incidence is
expected to triple by mid-century. There is an estimated one to four
caregivers for each person with the disease.


A recent AFA survey of caregivers of individuals with Alzheimer's
disease, conducted by Harris Interactive, highlighted caregivers' massive
responsibilities: More than 70 percent attend appointments with their loved
ones, help plan and organize their lives, and aid in day-to-day activities.
The survey also found that 76 percent of caregivers have learned that they
are stronger than they thought.


Proceeds from the jewelry will support AFA's programs, including grants
to member organizations to enhance local services. The Alzheimer's
Foundation of America, a nonprofit organization based in New York City,
unites hundreds of member agencies nationwide that provide hands-on
services to individuals with Alzheimer's disease and related illnesses, and
their families.


Alzheimer's Foundation of America

alzfdn

Most Neuropsychological Tests Don't Tell Alzheimer's Disease From Vascular Dementia

Most of the cognitive tests that have been used to decide whether someone has Alzheimer's disease or vascular dementia have not been very helpful when used alone. A new report published by the American Psychological Association concluded that when older people are confused and forgetful, doctors should base their diagnoses on many different types of information, including medical history and brain imaging.


Both Alzheimer's disease and vascular dementia affect learning and memory, behavior and day-to-day function. Even so, they're caused by different problems in the brain and require different medical approaches. It's important to tell them apart accurately, stresses the study in July's Neuropsychology. Valid diagnoses can help doctors treat patients more effectively, and help patients and families better understand their situations.


Jane Mathias, PhD, and Jennifer Burke, M.Psych.(Clinical), both from the University of Adelaide, analyzed 81 previously published studies that compared the cognitive testing of people diagnosed with dementia of the Alzheimer's (4,867) and vascular type (2,263). The average age across participants was 75.


Of the 118 different tests that were used in more than one study, Mathias and Burke found that only two were able to adequately differentiate between Alzheimer's and vascular dementia.


The Emotional Recognition Task (the ability to identify facial expressions in photographs and match emotional expressions to situations, at which people with Alzheimer's were better) and Delayed Story Recall (at which people with vascular dementia were better), were the only tests that appeared to reliably tell the two groups apart.


Even so, whether due to individual variability (people start at different baselines) or possible undiagnosed mixtures of Alzheimer's and vascular disease, there was enough overlap between the two groups to signal the need for more information. Because of these muddied waters, "The combined picture is what's important, so we need to look at how we can improve diagnosis by combining different measures," said Mathias.


Of note, many commonly used tests -- such as Digit Span (repeating a set of numbers forward, backward), verbal fluency (generating words by first letter or category, such as animals), drawing tasks and more - were unable to distinguish between dementia types. "While these tests may assist in diagnosing dementia, they do not adequately discriminate between Alzheimer's disease and vascular dementia," wrote the authors. Teasing apart different types of dementia is often harder than deciding whether someone is showing cognitive decline in the first place, Mathias explained.


Although the two tests that worked best would most reliably contribute to a clinical diagnosis, "All cognitive tests should be used cautiously and only in conjunction with other information (imaging, medical history) when diagnosing patients," the authors said.


Article: "Cognitive Functioning in Alzheimer's and Vascular Dementia: A Meta-Analysis," J. L. Mathias, PhD, and J. Burke, M.Psych.(Clinical), University of Adelaide; Neuropsychology, Vol. 23, No. 4.


Source

The American Psychological Association

Alzheimer's Society Backs 'Caring With Confidence', UK

Alzheimer's Society has welcomed the launch of 'Caring with Confidence', a new learning programme that will deliver knowledge and skills to carers across England.


Seven learning sessions aimed at improving support for carers will be launched in locations across the country from yesterday. In addition, Alzheimer's Society has won a tender to provide special sessions for carers of people with dementia. These sessions will be available later in the year in Sussex, Somerset, Devon and Hampshire.


Research by Caring with Confidence highlighted that:


- More than 60% of people believe their caring role affected their health (16% a lot 46% a little)


- One in five people caring 50 plus hours a week are also juggling a full-time job, and 23% of those people asked had been caring for at least 10 years


- Support or provision should explain how to deal with the benefits and healthcare system (46% and 41% said these topics would be very or extremely useful) as well as providing practical information and advice about the condition they are dealing with (38% very or extremely useful)


Neil Hunt, chief executive, Alzheimer's Society says,


'This research confirms the difficult situation that carers face and shows us that a little help can go a long way. Hundreds of carers call the Alzheimer's Society Dementia Helpline every year telling us they need more support and advice to help them cope.
Caring with Confidence is an important step towards delivering support when people need it most. We are very excited to be part of the programme. Alzheimer's Society will shortly provide a Caring with Confidence session specifically for carers of people with dementia in four locations across England. We hope this will be the beginning of opportunities to make the programme available for carers everywhere.'


Stephen Jacobs, OBE, Caring with Confidence Project Board Chair, adds,


'The contribution made by carers is huge, but it is a role that is often taken on at short notice and without preparation, leaving carers to struggle with the vital responsibilities that they have assumed - this is where Caring with Confidence can help.'


Notes


- The research referred to in the press release was conducted by an independent market research company for Caring with Confidence during February, March and April 2008. The study saw 1084 carers contacted and six detailed group discussions were held.


- 700,000 people in the UK have a form of dementia, more than half have Alzheimer's disease. In less than 20 years nearly a million people will be living with dementia. This will soar to 1.7 million people by 2051.


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


- The Alzheimer's Society needs to raise money to care for people today and to find a cure for tomorrow. You can donate now by calling 0845 306 0898 or visiting alzheimers.uk


- Alzheimer's Society provides a National Dementia Helpline, the number is 0845 300 0336 or visit alzheimers.uk

Source
Alzheimer's Society

Brain Activity, Drugs Could Affect Alzheimer's Progression

The activity of connections among brain cells significantly affects levels of the toxic protein beta-amyloid (A?) that is a major cause of Alzheimer's disease (AD), researchers have found. A? is produced by the cleavage of amyloid precursor protein (APP) within brain cells.



Findings suggest that the kind of mental activity people practice or drugs they might take for depression or anxiety could affect their AD risk or the disease progression.


In an article in the December 22, 2005, issue of Neuron, David Holtzman and colleagues detailed studies in which they determined how neuronal activity affected the level of A? in the "interstitial fluid" (ISF) between cells. The brain damage of AD is caused in considerable part by high levels of A? in the ISF, where it aggregates into the brain-clogging plaque that kills brain cells.


In studies with mice, they found that stimulating brain cells while sampling ISF revealed a significant increase in A? levels. Conversely, when they administered drugs that blocked neuronal activity, A? levels dropped.


Their studies also revealed that A? appeared to be released from the same kinds of sac-like vesicles in neurons that transport the chemical signals called neurotransmitters that one neuron uses to triggers a nerve impulse in its neighbor. Such vesicles launch their cargoes across the connections called synapses between neurons.


One important question arising from their findings, noted the researchers, is the effect of cognitive activity--such as that produced by an enriched environment--on A? levels. Both animal and human studies have suggested that such activity affects A? plaque levels.


"One hypothesis is that enrichment may increase overall synaptic activity in some brain regions and decrease it in others, depending on the environmental alteration," wrote Holtzman and his colleagues. "For example, certain memory tasks in humans simultaneously increase and decrease activity within different brain areas. Increased activity might result in increased susceptibility to A? deposition if the activated neural circuits contain high levels of human APP expression, thereby increasing A? release from those pathways. Conversely, if synaptic activity decreases in a brain area that is normally vulnerable to A? pathology, then there may be reduced A? deposition as a consequence of enrichment," they wrote.


Overall, the researchers concluded that "these findings are consistent with the possibility that physical and environmental changes resulting in altered neuronal/synaptic activity throughout life can modulate the amount of A? that accumulates in plaques in a region-dependent manner.


"That synaptic activity and A? levels are directly linked in vivo may have important treatment implications," they wrote. "Drugs used to treat neuropsychiatric disorders, such as depression or anxiety, among many others, directly influence neurotransmitters, and their receptors, thereby altering synaptic activity," they wrote. "Thus, it is likely that these drugs might influence A? levels within specified neuronal networks as well. If so, such drugs could potentially influence risk or progression of AD. Understanding the effects of drugs on ISF A? may enable the design of ways to decrease soluble A? levels, including synaptotoxic A? oligomers, in specific brain regions.


"Defining the relationship between normal brain function and the metabolism of a key protein involved in a neurodegenerative disease may provide new clues into the factors that regulate the biology of AD as well as other disorders of the nervous system," they wrote.


John R. Cirrito, Kelvin A. Yamada, Mary Beth Finn, Steven Mennerick, and David M. Holtzman of the Washington University School of Medicine in St. Louis, Missouri; Robert S. Sloviter of the University of Arizona in Tucson, Arizona; Kelly R. Bales, Patrick C. May, Darryle D. Schoepp, and Steven M. Paul of Lilly Research Laboratories in Indianapolis, Indiana. This work was supported by National Institutes of Health grants AG13956 (D.M.H.), AG11355 (D.M.H.), and DA07261 (J.R.C.); an Alzheimer's Association Zenith Award (D.M.H.); MetLife Foundation (D.M.H.); and Eli Lilly and Co. The authors have declared a conflict of interest. K.R.B., P.C.M., D.D.S., and S.M.P. are employees and shareholders of Eli Lilly and Co.


Cirrito et al.: "Synaptic Activity Regulates Interstitial Fluid Amyloid-b Levels In Vivo." Publishing in Neuron, Vol. 48, 913-922, December 22, 2005, DOI 10.1016/j.neuron.2005.10.028 neuron.


Heidi Hardman

hhardmancell

Cell Press

cellpress

Age Concern And Help The Aged Comment On Dementia Research, UK

Michelle Mitchell, Charity Director for Age Concern and Help the Aged, said:


'The fact that dementia research remains so disproportionately underfunded will be deeply concerning to older people, their families and anyone who has experienced this cruel disease.


'The financial burden of this disease is already very high and this will increase further as the population ages unless we find a cure or learn how to prevent dementia.


'Dementia is not going to go away and it is therefore of paramount importance to both sufferers now and society as a whole, that we invest in research.


'This is why Age Concern and Help the Aged are a major funder of dementia research and we strongly support calls for more funding for this vital work.'


Visit our Disconnected Mind website to find out about our research into the causes of mental decline.



Notes


Age UK is the new force combining Age Concern and Help the Aged. We will be known by our new name from Spring 2010. The Age UK family includes Age Scotland, Age Cymru and Age NI.


Source
Help The Aged

Number Of Older People Being Admitted To Hospital Increased By Two Thirds In A Decade, Alzheimer's Society Comment

The number of people aged 60 and over in hospitals is increasing at a faster rate than any other age range according to a report released yesterday.


According to the Hospital Episode Statistics: Admitted Patient Care - England 2009/10, the number of patients aged 75 and over has risen by two thirds (66 per cent) in the past decade. The number of 60-74 year olds being admitted also rose by 48 per cent. This compared to an average increase of 38 per cent.


Alzheimer's Society comment:


'It is important we don't accept these steep increases in the number of older people being admitted to hospital as an inevitable consequence of an ageing population. Many of these admissions could be avoided if better help and support was available at an earlier stage, preventing the need for expensive and distressing crisis care later on.


'People with dementia represent a very large proportion of these admissions. As many as one in four people on hospital wards have the condition and many stay in hospital far longer than necessary. Investing in care in the community now would enable many of these people to stay at home for longer and could help save the NHS millions of pounds.'


Ruth Sutherland

Interim Chief Executive


Source:

Alzheimer's Society

Four New Research Studies Describe Experimental Immunotherapies For Alzheimer's

The primary therapeutic target in Alzheimer's disease has been the beta amyloid peptide, which clusters outside cells in the brain to form sticky clumps known as plaques. Recently, more attention has been given to the tau protein, which aggregates inside the brain cells of people with Alzheimer's, forming neurofibrillary tangles. Precisely how these proteins interact in causing the disease is unclear.


Four new research studies reported today at the Alzheimer's Association International Conference on Alzheimer's Disease 2010 (AAICAD 2010) in Honolulu, HI describe experimental immunotherapies for Alzheimer's two of which target tau directly and two of which may reduce tau even though their primary target was beta amyloid.


"It is very important that we have a variety of therapeutic targets in the fight against Alzheimer's disease," said William Thies, PhD, Chief Medical and Scientific Officer at the Alzheimer's Association. "The more opportunities that we investigate to intervene and change the relentless and progressive course of Alzheimer's, the better chance that we will find something that works."


"Importantly, these studies teach us more not only about tau-targeted therapies but also about the progression of Alzheimer's disease," Thies added. "It may be that amyloid changes in the brain happen early in the disease and tau-related changes happen 'downstream' where they have a more direct effect on cognitive function. However, this is still to be determined."


"We need more basic research about what causes Alzheimer's, as well as therapy-related studies, to fill the front end of the drug pipeline and get us the better treatments and prevention strategies that we so desperately need to head off the epidemic of Alzheimer's," Thies said.


Beta Amyloid Immunotherapy with Bapineuzumab in Alzheimer's May Also Reduce Tau


Bapineuzumab (Janssen Alzheimer Immunotherapy and Pfizer) is an antibody to the beta amyloid plaques that are associated with Alzheimer's disease, and is currently in Phase 3 testing as a treatment for mild to moderate Alzheimer's. An abnormal form of the tau protein known as phospho-tau (P-tau) forms into tangles which are the other established lesions in the brain of people with Alzheimer's. The amount of P-tau in cerebrospinal fluid (CSF) is believed to be a marker of active loss of brain cells in people with Alzheimer's; prior studies have shown increases in P-tau in people with mild cognitive impairment who later develop Alzheimer's. P-tau was studied as a therapeutic biomarker in the Phase 2 clinical trials of bapineuzumab.


The pooled exploratory analysis reported at AAICAD 2010 by Kaj Blennow, MD, PhD, of the University of Gothenburg, Sweden, and colleagues included a subgroup of participants from two randomized, multicenter, double-blind, placebo-controlled, multiple-ascending-dose studies conducted in the United States (Study 201) or in the United Kingdom and Finland (Study 202). Study 201 enrolled 35 patients (20 bapineuzumab, 15 placebo) in the CSF substudy, and Study 202 enrolled 11 patients (7 bapineuzumab, 4 placebo) in the CSF substudy. CSF was collected at baseline and 2 weeks after the week 52 infusion.















The researchers found that Study 201 showed a trend (p=0.0564) towards a decrease in CSF P-tau in bapineuzumab-treated compared with placebo-treated cases. In Study 202, no significant treatment effects were seen. When they combined data from both studies, they found a statistically significant decrease (p=0.0270) in P-tau in bapineuzumab-treated compared with placebo-treated patients.


"These observations suggest that immunotherapy treatment targeting amyloid may also alter neurodegenerative processes that occur later in the disease process and that are more directly associated with loss of function," Blennow said. "However, this was a small study and these findings need to be confirmed."


Another Immunization Therapy for Alzheimer's with Beta Amyloid Also Reduces Tau


AN1792 (Elan) showed early promise as a beta amyloid immunotherapy for Alzheimer's. In 2002, a Phase 2 trial reported that about 6 percent of participants developed serious brain inflammation symptoms resembling meningoencephalitis. The trial was stopped as was further clinical development. However, participants in the first AN1792 trial continue to be observed.


Delphine Boche, PhD, of the University of Southampton's School of Medicine, UK, and colleagues studied the levels of beta amyloid and phospho-tau in six regions of cerebral grey matter that are affected by Alzheimer's pathology in the brains of 10 people with Alzheimer's who were immunized with AN1792 and compared the findings with 28 unimmunized Alzheimer cases. They had previously shown a reduction of beta amyloid in people treated with AN1792 and now looked to see if it had any effect on tau.


The researchers found statistically significant reductions in tau and beta amyloid in the immunized patients compared with untreated Alzheimer's. The reduction in tau appeared to be specifically in the dendrites, which are the branched projections of a neuron that conduct the electrochemical stimulation received from other nerve cells to the cell body. In contrast, tau in the bodies of the nerve cells, where the tangles form, seemed unaffected.


"The findings show that treatment aimed at beta amyloid may also modify tau changes in Alzheimer's," Boche said. "The lack of change in tau in the bodies of nerve cells might explain why the people in the original AN1792 trial didn't experience an improvement in cognitive functioning even though we saw amyloid clearance."


"This study demonstrates a link between these two Alzheimer's-related proteins, which has been suspected but not clearly demonstrated in the human brain. The findings give us more basic information about the interaction between beta amyloid and tau in Alzheimer's and may clarify how the disease progresses in the brain," Boche said.


Tau Antibodies Reduce Brain Tangles in Alzheimer-Model Mice


Allal Boutajangout, PhD, of the New York University School of Medicine, and colleagues previously reported that active tau immunization clears tau tangles from the brain and reduces or prevents functional impairments in two different tangle-model mice. In a study reported at AAICAD 2010, they assessed the efficacy of passive immunization for 13 weeks with the PHF1 antibody to tau in a mouse model of Alzheimer's tangles.


The researchers found that weekly injections of PHF1 in the tangle mice reduced the amount of tau aggregates in the brain and decreased functional impairment. The treated mice performed better than controls on the traverse beam task (p

Alzheimer's Disease: Modulating Enkephalin May Reduce Cognitive Deficits

Alzheimer's disease (AD) is an incurable disease that is increasing in prevalence and will increase even more rapidly as the Baby Boom generation enters the age of highest risk. The available AD drugs are only partially effective in some patients. New strategies are urgently needed.



In a new study, published in the Journal of Neuroscience, researchers in the laboratory of Lennart Mucke, MD, director of the Gladstone Institute of Neurological Disease (GIND), have determined in mouse models that modulating the activity of enkephalin peptides in the brain might reduce the cognitive deficits seen in Alzheimer's disease.



Enkephalins are part of the endogenous opioid system, which modulates learning and memory and other brain functions. They are produced by several different cell types in the brain, particularly in areas affected by AD. Enkephalins are derived by enzymatic cleavage from a precursor protein, preproenkephalin, and stored in vesicles. Upon stimulation, enkephalins are released with neurotransmitters, such as glutamate.



"The enkephalin pathway is an intriguing candidate for us because it is involved in many functions that are affected by Alzheimer's and other neurodegenerative diseases," said Dr. Mucke. "We were not sure, though, whether it contributed causally to the disease or acts as a compensatory mechanism."



To better understand the activities of the enkephalins in AD, the Mucke team examined their functions in a transgenic mouse model of AD. These mice express two proteins associated with AD - human amyloid precursor protein (hAPP) and its cleavage product, A??? peptides - in neurons and exhibit several characteristics of AD.



The team found increased levels of preproenkephalin mRNA and of enkephalin in brain regions important for memory that are affected in early stages of AD.



When they genetically manipulated the mice to make them more or less susceptible to neuronal damage, the scientists found that the enkephalin levels were also affected. Furthermore, as levels of the enkephalins increased, the ability of mice to complete behavioral tests declined. Compounds that blocked opioid receptors, through which enkaphalins exert their effects, reduced cognitive deficits. AD patients also showed increased levels of enkephalins in brain regions affected by the disease.



"Our results indicate that the high levels of enkephalins may contribute to cognitive impairments in hAPP mice and maybe also in AD patients," said Dr. Mucke. "Although these are early results, they are encouraging and may lead the way to a new AD therapy based on limiting enkephalin production or signaling."







William J. Meilandt , Gui-Qiu Yy, Jeannie Chin, Erik D. Roberson, Jorge. J. Palop, Tiffany Wu, and Kimberly Scearce-Levie also contributed to the study. The research was supported by the National Institutes of Health and the Gladstone Institutes.



About the Gladstone Institutes:

The J. David Gladstone Institutes, affiliated with the University of California, San Francisco (UCSF), is dedicated to the health and welfare of humankind through research into the causes and prevention of some of the world's most devastating diseases. Gladstone is comprised of the Gladstone Institute of Cardiovascular Disease, the Gladstone Institute of Virology and Immunology, and the Gladstone Institute of Neurological Disease. More information can be found at gladstone.ucsf/



Source: Valerie Tucker


Gladstone Institutes

Depression Increases Risk Of Alzheimer's Disease

People who have had depression are more likely to develop Alzheimer's disease than people who have never had depression, according to a study published in the April 8, 2008, issue of Neurology®, the medical journal of the American Academy of Neurology.


The study involved 486 people age 60 to 90 who had no dementia. Of those, 134 people had experienced at least one episode of depression that prompted them to seek medical advice.


The participants were followed for an average of six years. During that time 33 people developed Alzheimer's disease. People who had experienced depression were 2.5 times more likely to develop Alzheimer's disease than people who had never had depression. The risk was even higher for those whose depression occurred before the age of 60; they were nearly four times more likely to develop Alzheimer's than those with no depression.


"We don't know yet whether depression contributes to the development of Alzheimer's disease or whether another unknown factor causes both depression and dementia," said study author Monique M.B. Breteler, MD, PhD, with the Erasmus University Medical Center in Rotterdam, the Netherlands. "We'll need to do more studies to understand the relationship between depression and dementia."


One theory was that depression leads to loss of cells in two areas of the brain, the hippocampus and the amygdala, which then contributes to Alzheimer's disease. But this study found no difference in the size of these two brain areas between people with depression and people who had never had depression.


The study also assessed whether the participants had symptoms of depression at the start of the study. But those with depressive symptoms at the start of the study were not more likely to develop Alzheimer's than those with no depression at the start of the study.


The study was supported by the Netherlands Organization for Scientific Research and the Health Research and Development Council.


The American Academy of Neurology, an association of more than 21,000 neurologists and neuroscience professionals, is dedicated to improving patient care through education and research. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as stroke, Alzheimer's disease, epilepsy, Parkinson's disease, and multiple sclerosis.


For more information about the American Academy of Neurology, visit aan.


American Academy of Neurology (AAN)

1080 Montreal Ave.

St. Paul, MN 55116

United States

neurology

Two New Studies Show Dementia Care Fails People With Sight Loss

The sight loss charity, Thomas Pocklington Trust (1), calls for a fresh approach to dementia care after new research confirms a lack of attention to sight loss. A sensory model of care practice should be developed, says the charity after two new studies revealed a widespread failing to acknowledge the importance of sight loss.



The first study, "People with dementia and sight loss: a scoping study of models of care," (2) exposes pressing and persistent problems in the care of those with dementia and sight loss. It finds that both the most widely used model of care, and the leading best-practice literature display "a fundamental lack of sensitivity about sight loss."



The second study, "Visual Hallucinations in Sight Loss and Dementia", (3) describes people with joint dementia and sight loss as a forgotten group, and finds that many cases are missed or misdiagnosed because of failures to assess for both conditions.



Says Dr. Angela McCullagh, Research and Development Director, Thomas Pocklington Trust, "Sight loss plays a major role in people's experience of dementia, yet it is almost entirely excluded from current models of care. A change in policy and practice is needed, where sight loss is made visible in dementia care."



The first study (Models of Care) looked at major texts, interviewed practitioners and audited care homes. It found that while front-line care workers try to respond to the problems of dementia and sight loss, neither official policy nor guidance provides the means to fully address the issue.



Eight leading models of practice were assessed. One specifically gives importance to visual cues. Of the rest, only two explicitly mention visual impairment. The most common model used in the UK (4), which is embedded in dementia policy, fails to take sight loss into account.



Dementia policy, says the study:


- Pays too little attention to the physical environment to be sensitive to joint dementia and sight loss.

- Overlooks sensory solutions that help groups of people such as good lighting, contrasting and tactile signage and positive sounds.

A new model of care - a sensory model - is needed, say the researchers (5).



In dementia care literature it is generally assumed that people can see:


- Issues related to joint dementia and sight loss are not highlighted or debated.

- Key words that might be expected - visual impairment, lighting, optometrists, eye care/health - are not even indexed in "best practice" texts.

- Opportunities to highlight issues of sight loss are overlooked. Eg: Multi-sensory methods such as aromatherapy and music therapy are discussed with no mention of their potential value to those with sight loss.



In dementia care practice:















- Sensitivity to and awareness of sight loss issues varies amongst practitioners.

- In care homes, inspectors often rely on notice boards to provide information.

- The importance of wearing spectacles, having eye examinations and taking up free NHS tests can be overlooked. One care home had not had an optometrist visit for over a year and managers were sceptical about the value of eye tests for people with dementia.



Interest in developing effective models of care is clear: the researchers quickly brought together over 30 organisations and staff looking for better ways to support people who have sight loss and dementia.



The second study (Hallucinations), carried out by researchers at the Institute of Psychiatry, King's College, London, reviewed existing literature on hallucinations in sight loss and dementia and found the three conditions occur together more frequently than previously recognised.



From their study the researchers predict that 30% of those with combined sight loss and dementia will have hallucinations - around 35,000 people in the UK. However, the study also led them to question whether previous research has overlooked the fact that sight loss and dementia may act together to cause hallucinations. In this case, some 118,000 people could be affected - 100% of those with joint dementia and sight loss. Despite this the study could find no evidence of initiatives, guidelines or co-ordinated working between professionals in the two fields. Many cases of combined sight loss and dementia are missed, says the study, as routine assessments for both conditions are rare. This means that someone with sight loss may be wrongly diagnosed with dementia or a diagnosis of dementia may be missed in someone with sight loss.



"Once again, people who have joint sight loss and dementia are missing out on a combined approach to care," says Dr. McCullagh. "The research shows a clear need for greater coordination amongst professionals. Now more research is needed both to widen our knowledge of this forgotten group and to develop professional practices that address their particular experiences."



Source
Thomas Pocklington Trust

'Growing' New Approach In Training To Improve Dementia Care

Growing, the last book in Alzheimer's Society's Feelings Matter Most series, will be launched at the third national Dementia Congress in Bournemouth.


The series challenges current practises and urges dementia care trainers to give dementia care the time it needs. Growing highlights the need to grow training from simple awareness raising to developing evidence-based learning.


Author David Sheard sets clear guidelines for organisations to develop a person-centred learning and development training strategy. In Growing, David offers health professionals a unique ten point workshop programme designed for practical delivery by accomplished trainers in the dementia care environment.


Neil Hunt, Alzheimer's Society Chief Executive said,


Dementia is not a natural part of ageing; it is caused by diseases of the brain and robs people of their lives. This series takes a fresh look at how we can best support people with dementia and confronts preconceived ideas about how to ensure the best quality care for the 700,000 people living with the condition in the UK.


The publication is part of a series of books being produced by Alzheimer's Society. To order a copy of any Alzheimer's Society publications please telephone 01736 336995 or visit alzheimers.uk


Notes


- Pictures of the publication available on request

- 1 in 3 older people will end their lives with a form of dementia

- 700,000 people in the UK have a form of dementia, more than half have Alzheimer's disease. In less than 20 years nearly a million people will be living with dementia. This will soar to 1.7 million people by 2051. 1 in 6 people over 80 have dementia

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

- As a charity, Alzheimer's Society depends on the generosity of the public to help it care, research and campaign for people with dementia. You can donate now by calling 0845 306 0898 or visiting alzheimers.uk

Alzheimer's Society

University Of Florida To Lead National Effort To Help Patients With Rare Brain Disease

Even with devastating brain diseases such as Alzheimer's and Parkinson's, doctors can reach into their medical bags to find something to help a patient.



But they come up empty-handed when they try to help the vast majority of patients with ataxia - disabling disorders that rob people of their balance and coordination.



University of Florida neurologists are trying to change that with the help of a $1 million Challenge grant from the National Institute of Neurological Disorders and Stroke to establish a nationwide network of physician-scientists with expertise in clinical ataxia research.



"A lot of times I explain to patients the symptoms of ataxia are similar to what happens when someone gets too much alcohol into their system," says S.H. Subramony, M.D., a professor of neurology in the UF College of Medicine. "In either case there is slurred speech, inability to walk straight, falling, blurry vision - symptoms that indicate damage to a part of the brain called the cerebellum."



Ataxia - from the Greek "a taxis," meaning without order or coordination - can leave a patient unable to coordinate their eye blinks, let alone move. It can be hereditary or it could be brought on by strokes, tumors or other medical problems. One form, called sporadic ataxia, appears without apparent explanation in adults with no family history of the disease.



"Our first goal is to find a treatment to make patients' lives easier," said Tetsuo Ashizawa, M.D., chairman of the UF department of neurology and principal investigator and leader of the national effort, called the Clinical Research Consortium for Spinocerebellar Ataxias. "But the common thread ataxia shares with diseases such as Alzheimer's, Parkinson's, Huntington's and ALS is that neurons are dying. By studying ataxia, we can create insight into the neurodegenerative process in all of those diseases."



With laboratory and clinical research expertise from Ashizawa, Subramony and Michael Waters, M.D., Ph.D., director of the neurology department's stroke program, UF will lead nine other consortium institutions, including the Johns Hopkins University and Harvard University. The institutions are strategically placed across the nation so patients who have difficulty traveling can find close and state-of-the-art health care.



The ataxia consortium is part of the NIH's Rare Diseases Clinical Research Network, which will be awarding more than $117 million over the next five years to explore the natural history, epidemiology, diagnosis and treatment of more than 95 rare diseases.



By definition, a rare disease affects fewer than 200,000 persons in the United States. But put them all together - 6,500 rare diseases have been identified - and an estimated 25 million Americans are affected. Diabetes, in comparison, affects an estimated 24 million people.
















"Collectively rare diseases can become very huge public health problem even though the reach of each individual disease is small," Ashizawa said. "I think the NIH recognized the need to provide outreach and medical care to patients, in addition to the need for research. Now we have a huge responsibility to achieve our goals for the taxpayers."




UF researchers will be working with cell cultures, animal models and patient samples to find targets to alleviate ataxia problems. In the meantime, scientists will build a natural history database to bring this devastating disease into more precise focus.



"We want to know how a patient will progress from day to day and hour to hour if they have degenerative ataxia disorders," Ashizawa said. "We want to know what factors worsen or improve the condition. For example, when patients are calm, they seem to do better. When they're upset and rushed, they do terribly. If they drink alcohol, they are much worse."



Creating or finding a drug that would help these patients is one of the consortium's goals. Ashizawa notes that it may be possible that deep brain stimulation surgery, a technique UF has expertise in that uses tiny electrical pulses to influence movement or moods, may be beneficial.



The first step is to identify the patients and create a nationwide registry funded by the NIH and the National Ataxia Foundation. In addition, the consortium is collaborating with ataxia groups in Europe, South America and Japan.



"Collaboration is a critical element of rare diseases research and the partnerships represented in this program have tremendous potential to make great strides in understanding these diseases," according to a statement by Stephen C. Groft, Pharm.D., director of NIH's Office of Rare Diseases Research. "The network emphasizes collaboration not just among investigators from multiple research sites but between investigators and patient advocates as well."



Challenge grants are part of the American Recovery and Reinvestment Initiative and address specific scientific and health research challenges that will benefit from two-year jumpstart funds.




Source
The University of Florida Health Science Center

New Guide Strives To Improve Care Of Neurological Conditions, UK

A ground-breaking guide aimed at promoting the benefits of specialist nurses in the care of people with long term neurological conditions is launched today.


The important document results from a unique partnership between three of the UK's leading charities for neurological conditions, the MS Society, Epilepsy Action and the Parkinson's Disease Society, with the Department of Health, Royal College of Nursing and NHS National Workforce Projects.


The guide, Long Term Neurological Conditions . A Good Practice Guide to the Development of the Multidisciplinary Team and the Value of the Specialist Nurse, will be launched at the Harrogate International Conference Centre.


The guidance document is being launched exactly one year on from a specialist nursing summit held on 1 May 2007 with Ivan Lewis, Minister for Care Services. This highlighted the vital role of specialist nurses in helping people with multiple sclerosis (MS), epilepsy and Parkinson's disease. The outcome of the meeting was that a guidance document would be prepared to outline best practice and educate health commissioners on the benefits of protecting the specialist nurse post.



It is aimed at commissioners and service providers for people with long term neurological conditions to help them offer the right service, delivered by an appropriate workforce, to meet patients' needs. It outlines why services for neurological conditions are important, demonstrates the value of multi-disciplinary teams and clarifies the contribution of specialist nurses. For example:


- An MS nurse could save an average PCT up to ??18,000 a year by treating relapses at home rather than in hospital


- Misdiagnosis of epilepsy in England cost ??134 million in 2004. An epilepsy nurse can save ??184 per patient per year by improving diagnosis - a major saving across a primary care trust (PCT) with, on average, more than 80 epilepsy patients


- More than one in three people with Parkinson's disease are admitted to hospital every year. A Parkinson's disease nurse can have a significant impact in reducing hospital admissions and length of stay, addressing inequalities in access to neurologists ensuring specialist care is delivered and improving overall care and treatment.


Ann Keen MP, Minister for Health Services, said: "This guide is bound to become invaluable for service managers, staff and commissioners aspiring to excellence in the treatment of long term conditions. It shows that being able to deliver effective care does not necessarily mean spending more money but ensuring that the best methods of teamwork, planning and treatment are in place."


The MS Society funds more than 100 of the UK's MS specialist nurses and worked with the UK MS Specialist Nurses Association to contribute to the guide.


MS Society chief executive Simon Gillespie said: "The support of an MS nurse can make a massive difference to someone living with this devastating condition. Their range of knowledge and expertise is unique. This guide is an important step forward in safeguarding existing nurses and in making the case for more."


Epilepsy Action has been funding epilepsy specialist nurses (ESNs) through its Sapphire Nurse Scheme since 1995. There are currently approximately 200 ESNs in England; 80 of which are Sapphire Nurses.


Epilepsy Action chief executive Phil Lee said: "We are delighted to have been able to play an important part in producing this guide. It is a very positive step forward for people with epilepsy in that it will hopefully lead to more epilepsy specialist nurses. This in turn would go towards improving care."


The Parkinson's Disease Society has invested more than ??8m in specialist Parkinson's nursing services since 1994 and there are currently more than 230 of them working across the UK.


Steve Ford, chief executive of the Parkinson's Disease Society, said: "Access to a Parkinson's disease nurse specialist is the number one campaign priority for people with Parkinson's. These nurses not only ensure patients are able to manage their symptoms effectively, they also offer the local health organisations opportunities to innovate how care is delivered."


The document can be viewed here.

Health Care Workforce