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The standard explanation for what causes Alzheimers is known as the amyloid hypothesis, which posits that the disease results from of an accumulation of the peptide amyloid beta, the toxic protein fragments that deposit in the brain and become the sticky plaques that have defined Alzheimers for more than 100 years.

Billions of dollars are spent yearly targeting this toxic peptide but what if this is the wrong target? What if the disease begins much earlier, fueled by a natural process? Reporting in the current edition of the journal Neurobiology of Aging, UCLA professor of psychiatry George Bartzokis argues just that and says that a better working hypothesis is the “myelin model.”

“The greatest promise of the myelin model of the human brain is its application to the development of new therapeutic approaches,” Bartzokis said.

Like insulation around wires, myelin is a fatty sheath that coats our nerve axons, allowing for efficient conduction of nerve impulses. It is key to the fast processing speeds that underlie our higher cognitive functions and encoding of memories.

But the lifelong, extensive myelination of the human brain also makes it uniquely vulnerable to damage. The myelin models central premise is that it is the normal, routine maintenance and repair of myelin throughout life that ultimately initiates the mechanisms that produce degenerative diseases like Alzheimers. That is, the amyloidbeta peptide and the tau peptide, which is also implicated in Alzheimers, as well as the signature clinical signs of the disease, such as memory loss and, ultimately, dementia, are all byproducts of the myelin breakdown and repair processes.

“The pervasive myelination of our brain is the single most unique aspect in which the human brain differs from other species,” said Bartzokis, who is a member of the Laboratory of Neuro Imaging in the UCLA Department of Neurology and a member of UCLAs Brain Research Institute. Myelin is produced by oligodendrocytes, specialized glial cells that themselves become more vulnerable with age.

Bartzokis notes that myelination of the brain follows an inverted Ushaped trajectory, growing strongly until our 50s, when it very slowly begins to unravel as we age. The myelin that is deposited in adulthood ensheaths increasing numbers of axons with smaller axon diameters and so spreads itself thinner and thinner, Bartzokis said. As a result, it becomes more susceptible to the ravages of age in the form of environmental and genetic insults and slowly begins to break down faster than it can be repaired.

The exclusive targeting of the amyloidbeta peptide for many years is understandable because the same genes and enzymes involved in controlling myelination and myelin repair are, ironically, also involved in the production of amyloidbeta proteins. Bartzokis point is that the amyloid beta may actually develop as a result of the natural process of the repair and maintenance of myelin.

“So the breakdown that leads to Alzheimers and other agerelated brain diseases, such as Parkinsons, may begin much earlier, before the formation of the protein deposits that are used to define these diseases,” Bartzokis said.

Most drugs being developed for Alzheimers are targeting amyloid beta, but little if any clinical improvement is being seen. This is, according to Bartzokis, “similar to cleaning up a house thats been flooded by water but never repairing the actual pipe that created the flood.

“For drug development then, the targets should be much further upstream, earlier in the process before the AB plaques even develop,” he said.

Instead of focusing on reducing amyloid beta, Bartzokis argues, the myelin model suggests entirely different approaches to treatment and prevention of Alzheimers disease that precede plaque formation. With modern brain imaging technology, clinicians could track the dynamic changes taking place in the brain and intercede well before any signs of Alzheimers are seen.

“With earlier intervention,” Bartzokis said, “we could reduce and potentially eliminate the increasingly catastrophic burden of dementia on the individual and their family, the health care system, and our society.”

The research was supported by the National Institutes of Health, the RCS Alzheimers Foundation and the U.S. Department of Veterans Affairs. The author reports no conflicts of interest.

The UCLA Department of Psychiatry and Biobehavioral Sciences is part of the Semel Institute for Neuroscience and Human Behavior at UCLA, an interdisciplinary research and education institute devoted to the understanding of complex human behavior, including the genetic, biological, behavioral and sociocultural underpinnings of normal behavior, and the causes and consequences of neuropsychiatric disorders. In addition to conducting fundamental research, the institute faculty seeks to develop effective treatments for neurological and psychiatric disorders, improve access to mental health services, and shape national health policy regarding neuropsychiatric disorders.

Source University of California, Los Angeles

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

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

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

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

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

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

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

Source
Cristina Wångblad

In an effort to tackle major health policy issues in the United States, the Robert Wood Johnson Foundation® (RWJF) has announced the selection of this years recipients of its Investigator Awards in Health Policy Research. Sixteen scholars affiliated with major universities across the country will receive funding to support 10 new research projects. The winning researchers are tackling a wide range of health policy issues such as ways to treat children with Attentiondeficit hyperactivity disorder (ADHD) more effectively and improve their quality of life; the way we define and assess risk for developing Alzheimers Disease; consumer understanding of health claims made about food and beverages; the connections between child and adult health; and the politics surrounding research that compares the effectiveness of medical treatments.

“This program stimulates thinking that is creative and crosses disciplinary boundaries in search of solutions to vexing issues affecting health and health care in the United States,” says David Mechanic, Ph.D., national program director for the Investigator Awards in Health Policy Research.

RWJF created the Investigator Awards in Health Policy Research program to support talented researchers whose crosscutting and bold new ideas promise to contribute meaningfully to improving U.S. health policy. Funded projects produce enduring insights, sophisticated analyses of pressing problems, potential solutions for improving health and health care, and evidence that informs policymakers, the media, and the public. Since 1992, the Foundation has supported 157 projects involving 202 investigators.

Source
Barrett Whitener

Alzheimers Society has teamed up with the BBCs Lab UK to launch Brain Test Britain, a unique trial that will seek an answer to the question Does brain training really work?

Launching on BBC One tonight (1930, Monday, 7 September 2009), Brain Test Britain will investigate the effects of brain training on mental fitness. Initial results will be announced in a Bang Goes the Theory special, early next year. The experiment will continue for a further nine months looking closely at whether brain training can maintain or even improve the brain. Alzheimers Society hopes results will be a step towards solving whether brain training can reduce the risk of dementia.

Celebrities and BBC presenters will be pitched against each other as they get brain fit. Supporters include BBC Ones Evan Davis and Alzheimers Society ambassadors Richard McCourt of Dick and Dom, Tania Bryer and Russell Grant.

Richard McCourt of Dick and Dom, Alzheimers Society Ambassador says,I always wondered if any of these brain training gadgets and games really work. Im looking forward to being trained up and finding out a lot more about how our brains function. The more we know about the brain, the nearer well come to finding a cure for dementia and thats the reason why I want to be involved.

Professor Clive Ballard, Director of Research, Alzheimers Society says, Every week thousands of people spend time exercising their brain using some form of computerbased brain training, but the jurys still out on whether exercising your brain can boost your brain power. As Brain Test Britain asks the question, everyone can help with the answer. With one million people set to develop dementia in the next 10 years, its vital we understand the truth behind the old saying use it or lose it. Join us today and have fun while helping to solve one of the biggest mysteries of the brain. Does brain training really work?

Brain Test Britain will be powered by Lab UK, a BBC website that enables the public to participate in groundbreaking scientific experiments online. Volunteers are being asked to train their brains for 10 minutes at a time, three times a week, for at least six weeks. A oneoff Bang Goes The Theory special will reveal the results of the Brain Test Britain experiment early next year. Alzheimers Society advises that leading a healthy lifestyle is the best way to reduce your risk of dementia. The best evidence is to eat a healthy diet, keep active, dont smoke, get blood pressure and cholesterol checked and keep a healthy weight.

“N60″ might not be the first thing that comes to mind when people think of Alzheimers disease, but thanks to researchers from the United States, South Korea and France, this might change. Thats because these researchers have found that the N60 section of a protein called “RanBP9″ might be the key that unlocks an entirely new class of Alzheimers drugs, and with them, hope. In a research report published online in The FASEB Journal, these scientists describe how the N60 fragment of the RanBP9 protein increases the production of the amyloid beta protein, which is present in excessive amounts in the brains of people with Alzheimers disease.

Most experts believe that if the creation of amyloid beta protein can be halted or slowed, the devastating effects of Alzheimers disease may also be stopped or slowed too. Knowing which portion of the RanBP9 protein to target is particularly important because it gives researchers a more specific focus for developing new Alzheimers drugs.

According to David Kang, assistant professor of neurosciences at the University of California, San Diego, and one of the researchers involved in the work, “Our study suggests that targeting RanBP9 expression and/or N60 fragment generation may lead to novel strategies to combat this devastating disease.”

To make this discovery, Kang and colleagues examined extracts from brains with Alzheimers disease and agematched healthy controls and found that the N60 section of RanBP9 was increased in Alzheimers brain. When control DNA, fulllength RanBP9 DNA, and RanBP9N60 DNA were individually expressed in cultured cells, they found that cells expressing the full length RanBP9 protein had an increased amount of the amyloid beta protein that was 3fold over control, and cells expressing the RanBP9 protein and N60 section had an increased amount of the amyloid beta protein that was 5fold over control.

“Alzheimers might seem hopeless to some, but this research shows that were closer than ever to unraveling both the protein tangles and mysteries surrounding this devastating disease,” said Gerald Weissmann, M.D., EditorinChief of The FASEB Journal.

According to the U.S. Centers for Disease Control and Prevention, Alzheimers disease is the most common form of dementia among older adults, affecting as many as 5 million Americans. Alzheimers disease involves parts of the brain that control thought, memory, and language and can seriously affect a persons ability to carry out daily activities. The disease usually begins after age 60, and risk goes up with age. About 5 percent of men and women ages 65 to 74 have Alzheimers disease, and nearly half of those aged 85 and older may have the disease.

Details
Madepalli K. Lakshmana, John Y. Chung, Supul Wickramarachchi, Eileen Tak, Elisabetta Bianchi, Edward H. Koo, and David E. Kang. A fragment of the scaffolding protein RanBP9 is increased in Alzheimers disease brains and strongly potentiates amyloid peptide generation FASEB J. doi10.1096/fj.09136457. fasebj.org/cgi/content/abstract/fj.09136457v1

Source
Cody Mooneyhan

A researcher at the University of Illinois at Chicago College of Medicine has been awarded more than $9.8 million to head a fiveyear National Institute on Aging Program Project Grant.

The project will bring together a “dream team” of researchers from five institutions to examine the biology of the most important risk factor in Alzheimers disease, the cholesterolcarrying protein apolipoprotein E (apoE), and its receptors in the central nervous system.

Mary Jo LaDu, associate professor of anatomy and cell biology in the UIC College of Medicine, was one of the first researchers to investigate the role of apoE in neuronal injury and death. She showed that these lipoproteins in the central nervous system are distinct in structure and function from those found elsewhere in the body.

LaDu said she recognized that learning how apoE and its receptors affect the progression of AD may be the key to understanding the disease. So she decided to use her longterm association with other researchers in the field to develop a project that could tackle the biology of apoE and apoE receptors from all angles.

“I was able to bring together researchers who had overlapping interests and diverse expertise to attack the problem,” LaDu said. Although not all of her collaborators knew each other, they all were excited about the project and immediately meshed as a team, she said.

“This is the first time that an NIH Program Project Grant has brought together investigators from so many institutions,” said LaDu.

Other investigators include Steve Estus at the University of Kentuckys SandersBrown Center on Aging, who studies the molecular genetics of AD; cell biologist Guojun Bu of Washington University School of Medicine in St. Louis, an expert on apoE receptors; neurobiologist William Rebeck of Georgetown University, who studies the cellular mechanisms of signal transduction relevant to AD; and Edwin Weeber of the University of South Florida, a behaviorist and electrophysiologist who focuses on learning and memory and studies changes in synaptic function and animal behavior in genetically altered mice.

The grant will fund the work of the researchers, project administrators, and core facilities. A symposium is planned for next June in St. Louis.

Source
Jeanne GalatzerLevy

The UK will play a leading role in coordinated European action to tackle dementia from.

A new initiative launched by the European Commission has adopted proposals to tackle Alzheimers disease, dementias and other neurodegenerative conditions.

The UK is one of ten countries that will lead research aimed at tackling shared health and social care problems. According to the Commission there are over seven million people with Alzheimers disease and related disorders in Europe and it is predicted that this number will double in the next 20 years.

Todays actions mark new steps both in the Commissions Europe for Patients campaign and the new approach of Joint Programming in research.

Dr Susanne Sorensen, Head of Research, Alzheimers Society says,

Building on successful high impact dementia research, the UK will play a critical role in this initiative, leading the fight to defeat dementia. By uniting to find a cause, cure and fund care, we can galvanise our efforts and offer hope to millions of people. But while Europe strives forward, the UK government still lags behind the US, Germany and France in providing dementia research funding and there is still no specifically targeted dementia research funding. Yesterday the government promised to develop a strategy for investment in dementia research. It must make good on its promises or we will all pay the price.

In an open letter to the government yesterday, 31 leading dementia researchers united to call for a national plan for dementia research and a tripling of current investment.

Experts estimate that over 24 million people worldwide suffer from dementia, and many of these people live in low and middleincome countries. Recently, there has been growing interest in whether dietary factors, particularly oily fish and meat, might influence the onset and/or severity of dementia. Oily fish are rich in omega3 longchain polyunsaturated fatty acids, which some studies suggest are positively related to cognitive function in later life. Conversely, there is a suggestion from some studies that increased meat consumption may be related to cognitive decline. To examine this, a group of international researchers studied older people in 7 middle to lowincome countries. You can read the results of their study in the August 2009 issue of the American Journal of Clinical Nutrition.

Data from 14,960 participants (≥65 y of age) living in China, India, Cuba, the Dominican Republic, Venezuela, Mexico, and Peru were analyzed. Dietary habits were assessed by using standard, culturally appropriate facetoface interviews, and dementia was diagnosed by using validated culturally and educationally fair criteria.

In each of the study countries, except India, there was an inverse association between fish consumption and dementia prevalence. These data extend to low and middleincome countries previous conclusions from industrialized countries that increased fish consumption is associated with lower dementia prevalence in later life. The authors propose that this relation is not due to poor overall nutritional status in those with dementia, because meat consumption tended to be higher in this group. The relation between meat consumption and dementia remains unclear.

Source
Suzanne Price

Dimebolin, originally administered as an antihistamine, has previously been found to help slow the decline of cognitive ability in participants.

This study analysed tau and how dimebolin affects build up of the toxic beta amyloid protein, which is widely believed to be linked to the development of dementia.

This research showed that while dimebolin had a beneficial effect it actually caused an increase of the beta amyloid in mouse models.

This head scratching research has thrown up surprising results and suggests that while dimebolin provides cognitive benefits it may actually increase levels of toxic beta amyloid in the brain. One possible explanation may be that dimebolin is accelerating the process of beta amyloid development, which may reduce its toxicity. The questions surrounding whether beta amyloid causes nerve death in Alzheimers or is a biproduct of the process must be addressed by further research.

One in three people over 65 will die with dementia. Further, more robust research is needed to clarify whether dimebolin is an effective treatment for Alzheimers in the long term and if these puzzling increases in beta amyloid are also seen in human brains. With the right investment, dementia can be defeated. Alzheimers Society funds research to improve the lives of people today and to find a cure for tomorrow.

Professor Clive Ballard
Director of Research
Alzheimers Society

Reference Samuel Gandy, Dimebon regulates amyloid beta metabolism in cultured cells, isolated nerve terminals and interstitial fluid of living rodent brain.

Elderly people with no memory or thinking problems are more likely to later develop thinking problems if they have a growing amount of “brain rust,” or small areas of brain damage, according to a study published in the July 14, 2009, print issue of Neurology®, the medical journal of the American Academy of Neurology.

For the study, researchers followed 49 people age 65 and older who had no memory or thinking problems for an average of 9.5 years. The participants had at least three brain scans and annual tests of thinking skills. During the study, 24 of the participants developed persistent cognitive impairment, or memory problems that are a potential precursor to Alzheimers disease or another type of dementia.

The study found that those who had the fastest rate of growth in the amount of small areas of brain damage, or white matter hyperintensities, were more likely to later develop permanent thinking problems that in many cases led to dementia than those with a slow rate of growth in these types of brain lesions. Every cubic centimeter (less than a quarter of a teaspoon) increase in the amount of brain lesions was associated with a 94 percent increased risk of developing cognitive impairment.

The total amount of brain lesions at the beginning of the study was not a predictor of risk of developing cognitive impairment after taking into consideration the rate of change of these brain lesions over time.

“We need to determine factors that can decrease the accumulation of white matter hyperintensities over time,” said study author Lisa Silbert, MD, MCR, of Oregon Health & Science University in Portland and a member of the American Academy of Neurology. “We also need to determine how to identify those who are vulnerable to this accumulation so they can be targeted for potential early prevention or treatment methods.”

The study was supported by the Department of Veterans Affairs, National Institutes of Health, Paul B. Beeson Career Development Award in Aging, Max Millis Fund for Neurological Research, and Storms Family Fund at the Oregon Community Foundation.

The American Academy of Neurology, an association of more than 21,000 neurologists and neuroscience professionals, is dedicated to promoting the highest quality patientcentered neurologic 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, Alzheimers disease, epilepsy, Parkinsons disease, and multiple sclerosis.