Professor David Nutt has been appointed to the newly created Edmond J. Safra Chair in Neuropsychopharmacology and as head of the new Department of Neuropsychopharmacology and Molecular Imaging. The chair was funded by the Edmond J. Safra Philanthropic Foundation and Lily Safra. The department is the joint effort of Imperial College and the Central and North West London NHS Foundation Trust.

Nutt’s particular expertise is in how brain circuitry works, particularly as regards anxiety, depression and addiction. He said would like to use advanced PET scanning techniques to have pilot studies under way for new treatments in five years.

Researchers have long looked at plaque in the brain built up by amyloid proteins as a cause of Alzheimer’s. Nutt said he hopes to examine the role inflammation might play in the poorly understood process of why the plaque builds up.

In earlier research, Nutt demonstrated faults in the brain’s main systems inhibiting brain signals in those suffering from alcoholism or severe anxiety.

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The U.K.’s Alzheimer’s Research Trust paid for the study which was published in the most recent issue of The Lancet Neurology. The research was conducted by a team led by Clive Ballard of King’s College in London.

The study focused on 165 patients in Alzheimer’s care homes. All of the subjects had been taking antipsychotic drugs to battle the effects of dementia. For the research, about half the patients kept taking the antipsychotic medication while the other half began receiving a placebo.

After three years, about two-thirds of patients taking the placebo were still alive while only one-third of those taking the medication lived. Specifically, after 24 months, the survival rate for those on medication was 41 percent as opposed to 71 percent for those withdrawn from medication. After 36 months, 30 percent of those on medication survived while 59 percent on the placebo were still alive.

A report compiled for a British Member of Parliament last year showed that about 100,000 Alzheimer’s patients with dementia routinely receive antipsychotic medication. The drugs target the symptoms of dementia such as aggression and delusion.

Ballard said the lesson of the study is that the research and care-giving communities need to seek more benign treatments for dementia symptoms.

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Dr. Siegfried Hekimi of the school’s Department of Biology said the drug clioquinol directly effects the CLK-1 protein and could act to slow aging. While exactly how the drug affects CLK-1 is unknown, Hekimi said a possible explanation is the fact that clioquinol is known to affect metal in the bloodstream, leading him to theorize that metals are involved some way.

Researchers tested the compound on mice and some invertebrates and demonstrated that it inhibited CLK-1 and impacted the progression of Alzheimer’s and two other age-related disease.

However, Hekimi advised caution, saying far more research is required.

The drug, clioquinol, was used widely in Asia and Europe for gastrointestinal disorders. However, in the ’60s in Japan, it was linked to an outbreak of subacute myelo-optic neuropathy (SMON) and taken off the market. But some researchers point out that the incident was never studied and that the drug has been used safely since, casting doubt on the link between it and SMON, according to McGill.

At right: Dr. Siegfried Hekimi

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Yuji Goto works at the Institute for Protein Research at Japan’s Osaka University and along with fellow researchers has been using lasers to better observe tangles of protein known as amyloids. Their goal was to study how the tangles formed.

In the lab, Goto and associates added a dye that specifically attaches to amyloids then made it fluorescent by hitting it with a laser. But in addition to making it easier to observe the fiber tangles, they found that in certain circumstances the laser-hit fibers stopped growing and some even degraded. The dye is called thioflavin T.

What causes this? According to the American Society of Biological Chemistry, Goto thinks that exciting the dye with the laser causes it to transfer its energy to oxygen nearby. The resulting active oxygen then affects the protein fibers.

Goto’s research is being published in the current issue of the Journal of Biological Chemistry.

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Lord James Black, the Nobel Prize-winning developer of beta blockers, recently addressed business and biotech leaders in London and pointed to a troubling trend. As he has approached pharmaceutical companies with ideas for new drugs and sought funding to work on them, he said he found the companies increasingly reluctant to take a chance on projects that previously they would have supported.

The reasons for the reluctance are complicated:

• First, major drug makers long depended on profits from top-selling products to fund research and development on new medication. The cost of the R&D could run into the billions industry wide, with company executives aware that most of the projects would not bear fruit while the few “blockbuster” products would cover the costs. Now many of their best products have patents that are about to expire and few have promising drugs to bring to market in place of them.
• A second cause of the drying up of research funds, according to industry experts, is that the government review process has become longer, slower and more rigorous.
• Finally, the investment community, particularly in the current financial environment, is less supportive of companies taking big risks in hopes of hitting the home run with a major medical breakthrough.

This is particularly concerning as regards research into diseases for which a hoped-for cure is a long way off, such as Alzheimer’s, because the money will flow in increasing amounts to projects that promise a faster and more certain return.

One solution being considered in England is for investors and companies to form biotech joint ventures that are smaller, less costly and can focus entirely on one project. While money for such joint ventures has been harder to come by recently, the British government, working with major corporations, is considering a $3 billion fund to jump-start the effort.

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Initially, researchers believed the shortage of donated brains was a result of people being uncomfortable with the thought of it. However, following a recent outreach program, they are now convinced the issue is one of education and awareness.

One thing is clear and that is the need. Dr. Payam Rezaie told the BBC recently that the Open University’s Neuropathology Research Lab only had 20 brains for research, where more than a hundred are needed. He labeled those numbers “drastically awful.”

Scientists need brains of disease sufferers and healthy individuals as well, and the head of England’s Human Tissue Authority, that oversees donations, said it is more difficult to find healthy donors.

Interestingly, a recent “brain bank” established in Scotland by the Tissue Authority showed that making people aware of the problem is the key to solving it. When officials approached friends or relatives of potential doners who were required to have an autopsy to verify cause of death, more than 90 percent authorized the donation.

Oddly enough, the effort has been hampered somewhat by the country’s organ donor program. The researchers say many who have signed donor cards to donate organs upon their death believe that covers the brain. It doesn’t. Donor cards cover organs donated for transplant only, not research.

For immediate action, Britain’s Medical Research Council is coordinating the data gathered by all brain banks nationally.

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Previous research with mice has shown that medications developed with amyloid beta protein can spur the body to produce an antibody labeled “A?” that slows progression of the disease and might even improve cognition. Amyloid beta is thought to play a major role in contributing to Alzheimer’s disease. The antibody appears to break down the amyloid plaques linked to Alzheimer’s.

There also have been tests on humans, but for safety reasons, those had to be stopped. Researchers believe a way to make the medication safer for humans would be to use a vaccine that is close to the human protein but not the same, much the way smallpox is battled with a cowpox virus.

Robert Friedland and his co-workers developed a protein that is found in potato virus. Then they tested the vaccine on mice with additional shots for four months. The results of the tests, which were published in the Journal of Biological Chemistry, showed that the mice began developing antibodies. The mice also developed the antibody called “A?” after receiving shots with vaccine from potato leaf versus vaccine from purified sources.

Friedland pointed out that potato virus is common and offers no humans risk.

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The research could result in new treatments for a variety of debilitating illness and injuries including Alzheimer’s disease. The Foundation’s goal with the gift is to speed the pace of development of groundbreaking applications of stem cell research.

It is the third major gift in this area of research by the Foundation, which was created by Eli Broad after having earned his money through insurance and construction activities. The Foundation earlier gave UCLA $20 million and the University of Southern California $30 million for stem cell research.

Total cost of the new lab in San Francisco facility is projected at $123 million. It was at UC-San Francisco in 1981 that biologist Gail Martin helped identify embryonic stem cells in mice.

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Pratchett is the creator of the Discworld series with more than 60 million books in print which have been translated into more than three dozen languages. He had received the Order of the British Empire in 1998.

It was just last year that Pratchett went public with the fact that he was seeing signs in himself of Alzheimer’s in its early stages. He promised to continue writing, but he has done more than that.

In addition to raising public awareness of the disease, Pratchett has spoken to British Prime Minister Gordon Brown at his Downing Street home to request more funding for research into the effects of Alzheimer’s, such as dementia. He also donated more than $700,000 to the Alzheimer’s Research Trust. Finally, he has become an official celebrity patron of the trust.

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David K. Johnson at KU said the links between healthy levels of exercise and avoiding physical disability have long been established. However, his research seems to indicate physical fitness may have benefits for cognition as well. Johnson is an assistant professor of psychology and works in gerontology as an assistant research scientist.

The university’s Medical Center in Kansas City has been conducting neuroimaging studies through its Alzheimer’s and Memory Program in Kansas City and at the Neuropsychology and Aging Laboratory in Lawrence. Johnson has been working with this effort. It was financed by the National Institute on Aging and established a positive relationship between seniors and aerobic workouts.

Scientists conducted studies with 150 elderly residents of the area between the ages of 65 and 95. The research has been under way for five years and used memory and MRI tests.

Johnson said the results indicated that physical activity may be two to three times more effective than mental exercises – such as crossword puzzles – in helping memory. He added that the exercise does not have to be vigorous, but could begin with increasing the amount of normal activity such as walking or climbing stairs.

Johnson cautioned that the research is in an early stage, and he is recruiting now for additional studies.

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Eef Hogervorst, a professor at Loughborough University, recently headed a study on the issue that will be published in Dementias and Geriatric Cognitive Disorders in January. Funding for the study came from the Alzheimer’s Research Trust in the U.K. and allowed researchers to work with colleagues in Indonesia.

Scientists studied the eating habits of 719 advanced-age citizens of Java living in both rural and city setting. The results indicated that for those 68 years old and older, deterioration of memory is linked to eating high tofu in high quantities.

Hogervorst pointed out that products made with soy are micronutrient-rich, but that the effects of these micronutrients – commonly called phytoestrogens – are not clear.

Oddly, better memory seemed linked with high consumption of a product made from fermented soy products called tempe. Hogervorst postulated that the positive side effects of tempe could be tied to the fact that the product has a high level of folate, known to lessen the risk of dementia.

Hogervorst advocates additional research to better understand how the product or a combination of it with other products can reduce the effects of memory loss in the elderly.

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Dr. Richard Hodes, who is the director of the National Institute on Aging, said that scientists have taken great strides in their knowledge of how Alzheimer’s disease works, adding that they are working diligently toward treatments for it. Despite that desire to find answers, however, he said their study showed no preventive effect by the ginkgo supplement on Alzheimer’s disease.

The study and researchers were backed financially by five organizations from the National Institutes of Health, including: National Center for Complementary and Alternative Medicine; National Institute on Aging; National Heart, Lung, and Blood Institute; National Institute of Neurological Disorders and Stroke, and the Office of Dietary Supplements.

The study was titled the Ginkgo Evaluation of Memory (GEM) study, and with eight years of work at four sites, it was the largest clinical test of the effects of ginkgo against dementia.

In the study, 3,069 participants were included. Participants had to be 75 or older and have normal cognition or only mild impairment. No patients with dementia were included in the study. After screening, two groups were randomly created with one receiving a ginkgo extract and the other a placebo twice daily.

Evaluation of the results of up to seven years of testing showed no difference in the number from each group who developed more serious cognitive impairment.

According to Dr. Stephen DeKosky, the lead researcher for GEM study, the results confirmed the value of trials and tests such as those conducted. But, he added, older patients who are using dietary supplements like ginkgo and hoping they will prevent dementia should get with their health care providers to look for the best plan of treatment.

Image: Stanford University

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“This finding is significant because it suggests that improving blood flow to the brain might be an effective therapeutic approach to prevent or treat Alzheimer’s,” said the study’s primary author, Robert Vassar, a professor of cell and molecular biology at Northwestern’s Feinberg School School of Medicine.

The study shows that a brain not getting enough sugar glucose launches a process ultimately producing sticky clumps of protein thought to be related to causing Alzheimer’s. This glucose lack can happen in those suffering from cardiovascular disease that restricts arterial blood flow to the brain.

Specifically, a deficient supply of energy to the brain alters a protein, called eIF2alpha, and that in turn boosts production of an enzyme that “flips a switch” starting production of the sticky clumps, Vassar said. His research was conducted on human and mice brains and was published in the journal Neuron.

The good news is relatively simple preventive measures can improve blood flow to the brain. The measures include:

• getting exercise
• reducing cholesterol
• managing hypertension.

“If people start early enough, maybe they can dodge the bullet,” Vassar said, adding that for those already showing symptoms of the reduced blood flow, vasodilators, which increase it, could boost oxygen and glucose delivery to the brain.

It was Vassar who 10 years ago found the enzyme that triggers formation of the sticky clumps of protein outside neurons that disrupt the neuron’s message-transmitting ability. What causes the dangerous levels of the protein has not been known. This study points to energy deprivation as a possible trigger.

Funding Vassar’s research were the National Institute on Aging, the MetLife Foundation and Northwestern University.

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“Doctors should pay close attention when following these patients, as their observations could help define the precursors of diseases such as Parkinson’s, Alzheimer’s, Lewy body dementia, or multiple system atrophy,” said Dr. Jacques Montplaisir of the University of Montreal and Montreal’s Sacre-Cour Hospital, who was the lead researcher on the study.

Montplaisir worked with Dr. Rondald Postuma from the Research Institute of the McGill University Health Center.

While strides are being made in diagnosing such ailments before their advanced stages, there is still insufficient data concerning early warning signs, the study’s proponents said. The study showed that patients included in the research who had REM, or Rapid Eye Movement, sleep disorders had a 52.4 percent chance of developing a neurodegenerative disease within 12 years.

Their findings have been published in the Neurology, which is the official publication of the American Academy of Neurology.

Other results of the study include that patients with REM sleep disorder have a 17.7 percent chance of developing a neurodegenerative disease within five years of diagnosis and a 40.6 per cent in 10 years.

“These results establish a clear link and indicate that these sleep disorders could be a predictor of neurodegenerative disease,” Postuma said.

The study included 93 subjects. And while treatments exist for REM sleep disorders, those medications don’t delay onset of neurodegenerative disease, the study said.

Image: Memorial Regional South Hospital

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The Picower Foundation announced it would shut down after almost 20 years because of losses it sustained when a prominent New York money manager’s fund, in which the foundation had invested, collapsed. The foundation provided $50 million in initial funding for the Massachusetts Institute of Technology’s Picower Institute for Learning and Memory.

“It’s obviously terrible news,” an MIT official said. “The Picowers have made an enormous contribution to neuroscience. Everyone here was shocked and very much saddened.”

As recent as last May, the foundation gave the Picower Institute $4 million, which created the Picower Institute Innovation Fund. The target of the fund was to provide support for cutting-edge research by neurologists on the Picower Institute faculty.

For example, the research included the use of lasers on brain cells to restore memories.

But this week, the foundation announced it would shut down because of losses it sustained, which it said were associated with New York money manager Bernard Madoff’s investment fund.

While the initial $50 million grant was fully funded, the MIT official had no comment on the status of other grants from the foundation to the school.

Founded in 2002 to study neurological disorders including Alzheimer’s, the institute was initially called the Picower Center for Learning and Memory. It was renamed in 2005. At the time, the $50 million represented the school’s largest single gift from any foundation.

Image: MIT

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Researchers published the results of a study in Nature Cell Biology. They believe it documents a link between reduction in blood flow and the amyloid beta buildup, which were previously unknown to be related.

“This is quite unexpected,” said the study’s lead author Dr. Berislav Zlokovic. “On the other hand, both of these processes are mediated by the smooth muscle cells along blood vessel walls, and we know that those are seriously compromised in patients with Alzheimer’s disease, so perhaps we shouldn’t be completely surprised.”

The new findings are the result of a seven-year collaboration between two laboratories. Heading up the University of Rochester’s Center for Neurodegenerative and Vascular Brain Disorders, Zlokovic focused on research investigating possible root causes of Alzheimer’s at the molecular level. After noting a similarity in gene research by cardiovascular scientists and those studying Alzheimer’s patients, Zlokovic teamed with Dr. Joseph Miano of Aab Cardiovascular Research Institute, who co-authored this study with him.

In Alzheimer’s patients, the blood system that normally easily flushes excess amyloids doesn’t do the job, allowing a harmful buildup of the protein, damaging brain cells.

The study looked at two proteins that when working together activate genes that inhibit the removal of the built-up toxic protein.

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The good news is wine is among the most effective of those items. The bad news is too much of this good thing can have the opposite effect and impair cognitive ability.

“Those overdoing it at Christmas should note that while moderate alcohol consumption is associated with better cognitive function and reduced risk of Alzheimer’s disease and dementia, heavy alcohol intake could be one of many causes of dementia – as well as a host of other health problems,” researchers were quoted as saying in a recent Oxford release on the subject.

Researchers found that in addition to wine, chocolate and tea are among foods with flavonoids that can improve cognition.

Studies were conducted on 2,031 people between the ages of 70 and 74 with the subjects filling out a survey on their normal eating habits. They also took cognitive tests. The research was conducted by the Oxford Department of Physiology, Anatomy and Genetics in cooperation with colleagues from Norway.

The study showed that those who ate or drank wine, tea or chocolate scored “significantly better” on the cognitive tests. Results were published in The Journal of Nutrition.

The research follows an increased interest in the effects of micronutrients in cognitive decline typically associated with advancing age. Scientists are examining the role played by foods and drinks that are sources micronutrients – called polyphenols – in plant-derived foods.

The most effective food or drink in this study was wine. But while the results above appear to support the effectiveness of wine and other foods in improving cognition, researchers said more study is required.

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Starting in 2009, researchers will be able to access a giant “biobank” of health and environmental data to study contributing factors to a variety of current health concerns, including Alzheimer’s disease.
The data repository will be built and maintained by Kaiser Permanente using an $8.6 million grant from the Pioneer Portfolio of the Robert Wood Johnson Foundation.

“The unequaled size and power of this biorepository will drive research that can dramatically improve the health and health care of millions of Americans,” according to Dr. Risa Lavizzo-Mourey, president and CEO of the foundation. “We are proud to help establish this as a premier resource for the nation that can significantly advance medical knowledge and treatments.”

The Northern California Division of Research of Kaiser Permanete will use the grant to accumulate and store the first 200,000 DNA samples, using the samples to create a database of health and environmental information. The foundation and Kaiser Permanente hope to grow the database to 500,000 samples over the next three years. The goal is to create a sufficient statistical sample so that “even subtle effects of environmental and genetic factors in less common health conditions such as mental health disorders or autoimmune diseases” can be identified, according to a foundation press release.

The grant also is to be used to create and put in place policies and procedures allowing access to the to researchers worldwide.
Biobanks critics worry that public access to genetic information could result in discrimination. However, a new federal law prohibits such discrimination, the foundation said. Additionally, the foundation release said, “All biorepository data and DNA samples are de-identified and stored in secure locations with limited authorized access.”

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Dr. Jordan Tang

It was nine years ago that Dr. Jordan Tang discovered the enzyme that causes the symptoms – such as memory loss – associated with Alzheimer’s disease. Today, just when that discovery will lead to a cure – or if it will lead to one – remains uncertain, Tang told The Oklahoman newspaper.

The true answer is nobody really knows,” the researcher, who is associated with the Oklahoma Medical Research Foundation, was quoted in the paper.

Tang estimated that the drug company eventually developing a cure could be looking at a windfall of $20 billion to $30 billion. But even if a possible effective treatment is discovered, there remains a long process of clearing it through the Food and Drug Administration.

That process could take up to three years, assuming initial tests prove to slow onset of the disease’s symptoms. But if a drug gets into testing, Tang told the paper that pressure from the senior community could expedite the process.

That’s what happened with HIV,” he was quoted as saying. “It was an accelerated process. It conceivably could happen.”

Another challenge in testing and proving the effectiveness of a cure is the length both of the testing process – typically 18 months – and the slow rate at which Alzheimer’s symptoms can reveal themselves. The challenge would be to document the progress of the effects of the disease, comparing subjects suffering from it with others who do not have it, over the year and a half time period. The catch being those suffering from Alzheimer’s might not evidence the symptoms during the test period at a rate sufficient to make the test meaningful.

The reality is this issue might require a three-year study versus and 18-month test, Tang said.

Tang told the paper he believes that an effective treatment will be found. Ironically, during his period of work on Alzheimer’s, two researchers on the team have had parents die while suffering from the disease.

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“We advocate, based on these findings, that the criteria for the diagnosis of Alzheimer’s disease should include MRI scans,” said Dr. Ranjan Duara, who was the lead author of a study by Florida’s Alzheimer’s Disease Research Center. “By incorporating MRIs into the assessment of patients with memory problems, early diagnosis can be standardized and done far more accurately.”

Duara works at Miami’s Wien Center for Alzheimer’s Disease and Memory Disorders at Mount Sinai Medical Center where he is medical director.

As the most common cause of dementia, Alzheimer’s disease is often indicated by memory loss, disorientation, and deterioration of reading and speaking skills. Because other syndromes or disease’s share these symptoms, often the only way, previously, to confirm Alzheimer’s disease in a patient was by autopsy, which would show the affected brain area.

Previously doctors only used a brain scan to rule out other possible causes of the Alzheimer’s symptoms, such as a stroke.

Researchers studied 260 people in the Miami and Tampa, Florida, areas who were suffering some memory loss. The MRI showed atrophy in the brain regions commonly associated with Alzheimer’s and helped researchers accurately diagnose that the memory loss was from the disease and not from other sources.

Additionally, the study showed that MRIs can spot shrinkage in the brain of people not yet showing signs of Alzheimer’s. These patients began showing this signs as little as two years later, suggesting the scans can be an early predictor of the disease.

The study was funded in part by a National Institute on Aging grant.

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