Alzheimer Related News Items

News as of 2/08/04

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Top Items

Cloning Creates Human Embryos - Scientists in South Korea report that they have created human embryos through cloning and extracted embryonic stem cells, the universal cells that hold great promise for medical research. Their goal, the scientists say, is not to clone humans but to advance understanding of the causes and treatment of disease. The work was led by Dr. Woo Suk Hwang and Dr. Shin Yong Moon of Seoul National University and will be published 2/13/04 in the journal Science. The paper provides a detailed description of how to create human embryos by cloning. Experts in the field not involved with the work said they found the paper persuasive. It is what patients with diseases like Parkinson’s and diabetes had been waiting for, the start of so-called therapeutic cloning. The idea is to clone a patients cells to make embryonic stem cells that are an exact genetic match of the patient. Then those cells, patients hope, could be turned into replacement tissue to treat or cure their disease without provoking rejection from the body’s immune system. Even though the new work clears a significant hurdle, scientists caution that it could take years of further research before stem cell science turns into actual therapies. By Gina Kolata NY Times 2/12/04 Article at http://www.nytimes.com/2004/02/12/science/12CELL.html?hp Free abstract and link to free copy for registered users of Science at http://www.sciencemag.org/cgi/content/abstract/1094515

published online 12 Feb. 2004; 10.1126/science.1094515

Vitamin E, C Supplements May Prevent AD - A study involving more than 4700 participants strongly suggests that the combination of vitamin C and E lowers the risk of developing AD. As the lead investigator Dr. Peter P. Zandi at The Johns Hopkins University Bloomberg School of Public Health in Baltimore told Reuters Health, properly conducted prevention trials are needed to confirm the results. However, “because vitamins E and C are relatively non-toxic and are believed to have wide-ranging health benefits, they may offer a very attractive strategy for preventing AD.” The findings come from the Cache County Utah Study, which looked at the prevalence of AD and other dementias in terms of genetic and environmental risk factors. As part of the study, people aged 65 and older were assessed for dementia between 1995 and 1997 and again between 1998 and 2000. According to the team’s analysis use of vitamin E and C supplements in combination lowered the odds of having AD at the start of the study by about 78 percent, and the odds of developing the disease by about 64 percent during the follow-up period. There was also a trend toward reduced AD risk among people who took vitamin E and multivitamins containing vitamin C. In contrast, there was “no evidence of a protective effect with the use of vitamin E or C supplements alone, with multivitamins alone, or with vitamin B-complex supplements.” Currently, the recommended daily allowance for vitamin E is 22 IU (15 mg) and for vitamin C, 75 to 90 mg, the team points out. Although multivitamin preparations typically contain approximately these levels, individual supplements commonly contain doses up to 1000 IU of vitamin E and 500 to 1000 mg or more of vitamin C. “Our findings suggest that vitamins E and C may offer protection against AD when taken together in the higher doses available from individual supplements,” the researchers conclude. Zandi also pointed out that there may be a biological reason why the two vitamins together produce a benefit, related to the different duration of their antioxidant effects. “Vitamin E is a lipid-soluble vitamin that sticks around in fat tissues of the body for a relatively long time,” he explained. “In contrast, vitamin C is a water-soluble vitamin and is rapidly excreted from the body. Vitamin C may act to ‘recharge’ the antioxidant capacities of vitamin E so that the vitamin E can sustain its job of soaking up free radicals and relieving oxidative stress in the body.” By Megan Rauscher Reuters Health 1/19/04 Archives of Neurology 2004, 61:18-19.

Drugs

Namenda(TM) (memantine HCl), First Drug Approved For Treatment of Moderate to Severe AD Now Available Nationwide - Forest Laboratories, Inc. announced 1/13/04 that Namenda(TM) (memantine HCl), the first and only medication approved for patients with moderate to severe AD, is now available to physicians, patients, and pharmacies nationwide. Namenda was approved by the U.S. Food and Drug Administration (FDA) on October 16, 2003. Healthcare providers, patients and caregivers should call their local pharmacies to determine if Namenda is available in their area. Namenda is a low to moderate affinity NMDA (N-methyl-D-aspartate) receptor antagonist. It is thought that overexcitation of NMDA receptors by the neurotransmitter glutamate may play arole in AD since glutamate plays an integral role in the neural pathways associated with learning and memory. The excitotoxicity produced by abnormal levels of glutamate is thought to be responsible for the neuronal cell dysfunction observed in AD. Namenda is thought to selectively block the excitotoxic effects associated with abnormal transmission of glutamate, while allowing for the physiological transmission associated with normal cell functioning. PR 1/13/04

Drug Team May Stem AD Effects - Two drugs that act differently on the brain’s chemistry worked in tandem to help stave off the brain-robbing symptoms of AD, researchers said 1/20/04. The patients in a yearlong study were afflicted with moderate-to-severe AD and had been taking the drug donepezil, which prevents the breakdown of an important chemical messenger in the brain, acetylcholine, which commonly occurs with AD. But patients who also took the drug memantine scored better on tests for cognition and some quality-of-life measures than patients given a placebo along with donepezil. Memantine is a drug that counteracts the overproduction of the brain cell-killing chemical glutamate. The interactions between the two drugs were not clear, researchers said. But “to find a new medication that can provide substantial benefit to patients at this stage of the disease, either alone or in combination with another AD drug, is certainly good news,” said Dr. Pierre Tariot, professor of psychiatry, medicine and neurology at the University of Rochester, and one of the study’s authors. Donepezil is sold under the brand name Aricept by Eisai Inc. and Pfizer. Memantine is sold under the name Namenda by Forest Laboratories, which helped finance the study. By Reuters 1/20/04 The Journal of the American Medical Association 2004;291:275

Checking Brain Chemical Key for Memory - Low levels of a key chemical messenger, acetylcholine, in the brain are crucial during sleep if you are going to form long-term memories. That’s the conclusion of German researchers at the University of Lubeck, Germany. They suggest their discovery might warrant a closer look at how certain medications are given to AD patients. For decades, scientists have known that levels of the chemical messenger acetylcholine must be adequately high during wakefulness for learning new things. “Our study now is the first one to show that for memory consolidation -- that is, strengthening newly acquired memories -- low levels of acetylcholine in the brain during sleep are a prerequisite,” says lead researcher Steffen Gais, with the department of neuroendocrinology. While Gais concludes the current practice of giving AD patients medicine to keep their acetylcholine levels high during sleep should be re-evaluated, an AD expert says much more study is needed before medication changes are warranted. By Kathleen Doheny HealthDay Reporter 1/28/04 Proceedings of the National Academy of Sciences

Brain Protein Discovery May Herald ‘Memory Pill’ - A pill to prevent people forgetting things has come a step closer with the discovery of a protein in the brain that stimulates nerve cell growth. Scientists believe that the protein chemical, cypin, is involved in learning and memory because of the role it plays in forming connections between brain cells. It may be possible to develop memory-enhancing drugs that mimic the protein’s natural effect, or at least stimulate it to work when something goes wrong, they said. Cypin appears to be crucial for the growth of fine filaments between nerve cells, which could explain how memories are formed, said Professor Bonnie Firestein of Rutgers State University of New Jersey. When nerve cells, or neurons, fail to form new branches it may lead to debilitating conditions such as the gradual memory loss suffered by AD patients, Professor Firestein said. “The identification of cypin and understanding how it works in the brain opens up new avenues for the treatment of serious neurological disorders,” she said. Cypin was first identified in humans in 1999, but only in the latest study was it found to be present in the brain as an active enzyme - a molecule that speeds up biological reactions. Cypin works by glueing structural “building blocks” together inside the long filaments, or dendrites, that grow out of neurons, the scientists discovered. Researchers have previously shown that these dendrites and the connections they make are crucial for making and storing memories. By Steve Connor, Science Editor Independent News UK 1/19/04 Nature Neuroscience 2004:7;2 pp145-152

Saegis Pharmaceuticals Completes Exclusive License Agreement for AD Drug - Saegis Pharmaceuticals, Inc., announced 1/6/04 it has been granted an exclusive license to develop and market its lead AD candidate, SGS742, from Novartis Pharma AG. Under the terms of the agreement, Novartis received an equity stake in Saegis. Saegis was granted an option to an exclusive license on SGS742 from Novartis in 2001 and successfully completed a Phase II clinical trial of the compound in mild cognitive impairment (MCI), a type of age-related memory loss that is often a precursor to AD. Saegis is now initiating a Phase II clinical trial of SGS742 in mild to moderate AD. Rodney Pearlman, President and CEO of Saegis Pharmaceuticals, said . “On the basis of our clinical work with the compound to date, we believe that SGS742 has the potential to be a useful treatment in mild cognitive impairment and AD.” PR 1/6/04

Genes & Genetic Issues

Gene Could Lead to Heart-Healthy Foods - Scientists have pulled off a feat of gene engineering that could lead, in theory at least, to juicy steaks and fluffy omelets that are good for your heart. The scientists inserted a worm gene into mice and made the rodents produce significant amounts of omega-3 fatty acids, a heart-friendly substance normally found in salmon and other oily fish. The researchers at Boston’s Massachusetts General Hospital now are trying to breed gene-engineered chickens that would lay omega-3 eggs. And they said the obvious follow-up would be transferring the gene to livestock to see if they can produce meat and milk rich in omega-3. “It would be little bit more difficult in a cow or pig,” said the study’s senior author, Jing X. Kang. “Overall, it would be quite similar and I think the outcome would be the same.” Omega-3 fatty acids are thought to prevent heart disease by helping to reduce the inflammation involved in hardening of artery walls. They also may reduce blood pressure and chemically regulate the electrical impulses of the heart’s rhythm. Omega-3s also are important to brain development and may reduce the risk of AD. By Joseph B. Verrengia, AP Science Writer 2/4/04 Nature 427, 504 (05 Feb. 2004).

Sumitomo Finds Gene Against AD, Down Syndrome - Sumitomo Chemical Co has found a gene that could lessen the symptoms of AD and Down syndrome, a major Japanese daily reported 2/1/04. The company is seeking patents on the gene, code-named NXF, in and outside Japan, and hopes to develop medicine based on the gene, the Asahi Shimbun said. The NXF gene promotes the production of proteins necessary for nerve operation, as opposed to a gene responsible for Down syndrome, which is caused by extra genetic material in the 21st chromosome. Researchers also found that the amount of a protein unique to AD patients decreases when measured in cells in which the NXF gene is artificially grown. Kyodo News 2/2/04

Caregivers

Tests Tell When AD Patients Should Stop Driving - Tests that evaluate spatial relationships between objects and driving simulations are helpful in identifying drivers with AD who shouldn’t be behind the wheel, a new study finds. Typical “neuropsychological tests” include block design and picture completion tasks. In these tests, patients must match designs or complete pictures using colored blocks. There is ample evidence that drivers with dementia are at increased risk for car crashes and getting lost while driving. The researchers reviewed 27 studies on dementia and driving that had been published between 1988 and 2003. Their goal was to find the most effective tests for predicting driving performance. The best ones were specific skills tests and simulated on-road and non-road tests that evaluated mental status and “visuospatial” skills and predicted driving performance, the study says. The results of these tests were a more reliable measure of driving ability than observations from family members, the researchers note. The investigators also found tests that look at attention and concentration were less helpful and not as accurate in predicting driving performance. These findings have implications for families trying to decide if a relative with early AD should be driving, says study author Mark Reger, a fellow in psychiatry and behavioral science at the University of Washington School of Medicine. “Families concerned about whether their loved one is safe to drive might consider neuropsychological testing as a part of driving risk assessment,” he says. By Steven Reinberg HealthDay Reporter 1/26/04 January 2004 issue of Neuropsychology

Nursing Home Injury Victims Often Demented - Study - Nursing home residents injured by other residents often may be the most mentally impaired people who wander into others’ “personal space,” researchers said on 2/3/04. “Injured residents were more likely, perhaps unknowingly, to ‘put themselves in harm’s way,’ be verbally aggressive, and be cognitively impaired,” wrote Tomoko Shinoda-Tagawa of the Harvard School of Public Health in Boston. Cases of mentally impaired patients “wandering” into confrontations and being injured were most likely to occur in AD wards, which can be overcrowded, the report said. The report suggested using “soft barriers” such as netting to keep patients apart. The researchers reviewed more than 1,100 cases of violence among Massachusetts nursing home patients in 2000 and identified 294 that involved lasting injuries ranging from broken bones to cuts. “Our finding suggested that it is possible that some of the residents who sustained injuries may have provoked the attacks ... (by) wandering into another resident’s ‘personal space,’ ” the report said. It also was possible that a small group of patients who inflict injuries were responsible for most of the violence, they said. Reuters 2/3/04 Journal of the American Medical Association 2004;291: 591 2/4/04

Testing

New Imaging Agent Could Help Diagnose AD - A new imaging agent that homes in on the gummy plaque believed to destroy the brains of AD patients may finally allow the disease to be diagnosed before it kills, researchers at the University of Pittsburgh said 1/21/04. The agent, a radioactive dye called Pittsburgh Compound B, can also be used to test new drugs being developed to fight AD by the use of positron emission tomography. Using the new agent, “we will likely be able to follow the progression of the disease and speed the development of promising new therapies aimed at halting the build-up of amyloid in the brain,” Dr. William Klunk of, who led the study, said in a statement. “We will not only find out when plaques begin to form, we will be able to see directly if a medication is preventing or reversing plaque formation over the long term,” Klunk said. The dye, an adjusted version of the dye used by pathologists to find AD in brain samples from dead patients, is harmless. In two hours it is gone from the body. Reuters 1/21/04 Annals of Neurology published online 10.1002/ana.20009

St. Joseph’s Among First in U.S. to Use New Technology in Genetic Testing for AD -Researchers at St. Joseph’s Hospital and Medical Center are among the first in the country to use a new molecular diagnostic tool to help develop genetictests for AD. St. Joseph’s DNA Diagnostic Laboratories validated the test in collaboration with Nanogen, Inc. , a company that develops and commercializes molecular diagnostic products for the gene-based testing market. Using the company’s NanoChip© Molecular Biology Workstation and analyte specific reagents, researchers can detect the specific genetic form, or allele, of the ApoE gene, which is associated with an increased risk for developing AD. Currently, this mutation is detected with more conventional technology that is not widely available. Nanogen licensed the detection of ApoE alleles for use with the NanoChip device in April 2003. “The relationship between St. Joseph’s and Nanogen allows us to offer predisposition testing for AD to patients throughout Arizona in a timely, accurate and cost-effective manner. Currently, patients can wait up to six weeks for results,” says Dr. John Stone, Laboratory Director. “We anticipate that this collaboration will soon lead to the development of similar tests.” PR 1/6/04

Failure to Spot Early Symptoms Still Stalling Growth of AD Drug Market - Decision Resources, Inc., a research and advisory firms focusing on pharmaceutical and health care issues, finds that lack of public awareness of early symptoms and inaccurate diagnosis are constraining the AD drug market. According to a new Pharmacor study entitled AD, in many countries there is still a stigma associated with AD, and memory loss is considered a part of the natural aging process. These attitudes hold back those suffering from signs of AD from getting early treatment. However, early and accurate diagnosis of the disease is also a problem. “Early and accurate diagnosis of AD is especially challenging for nonspecialists, who manage the care of the majority of AD patients,” said Nancy Macdonald, Ph.D., analyst at Decision Resources. “Until new diagnostic tools become available, many patients will receive a misdiagnosis or wait two to four years after onset of AD symptoms for a correct diagnosis.” PR ½7/04

Other Items

Low Blood Pressure Linked to Dementia in Elderly - A low blood pressure is associated with an increased risk of dementia in people over 75 years of age, according to a new report. This risk seems to pertain only to AD type dementia and is highest in subjects with persistently low pressures. The findings are based on a study of 406 community-dwelling elderly subjects who were dementia-free at study entry and were followed for up to 21 years. Systolic and diastolic blood pressures, the first and second numbers, respectively, in a blood pressure measurement, were determined in all subjects. During the study, 122 subjects developed dementia, lead author Dr. J. Verghese and colleagues, from Albert Einstein College of Medicine in New York, note. The authors found that a diastolic blood pressure below 70 raised the risk of dementia. Specifically, for each 10-point drop in pressure, the risk of dementia increased by 20 percent. Low pressures were only linked to an increased risk of AD-type dementia, not the type that occurs as a result of blocked blood vessels in the brain. Further analysis revealed a decreased risk of AD-type dementia for patients with moderately high systolic pressures. However, this association was not very strong. Compared with other subjects, people with consistently low blood pressures throughout the first two years of the study were twice as likely to develop dementia. “Our results suggest that low blood pressure may be both the cause and the consequence of dementia,” the researchers state. “If our results are replicated, intervention studies are required to study whether maintaining blood pressure at optimal levels reduces the risk of dementia in elderly individuals.” Reuters Health 1/8/04 Neurology 2003;61:1667-1672

AD Risk in Men Tied to Low Testosterone - Low levels of testosterone are linked with a higher risk of developing AD, a new study claims. In a large group of men, researchers looked at the levels of free testosterone, which is the amount of testosterone circulating in the blood. The researchers found a 26 percent decrease in the risk of AD for every 50 percent increase in the amount of free testosterone measured in the blood. While levels of testosterone do decrease with age, levels dropped significantly more in men who developed AD. In addition, men who developed AD had about half the amount of testosterone compared to men who didn’t get the disease. And for some men, this drop in testosterone was found 10 years before AD was diagnosed. “This is one more piece that we need to understand whether testosterone will protect men from developing AD,” says study author Dr. Susan Resnick, an investigator with the National Institute on Aging (NIA). “The logical next step would be to see if men should be raising their levels of testosterone. We don’t know the answer to that yet.” In the study, 574 men were followed for about 19 years as part of the Baltimore Longitudinal Study of Aging. Their testosterone levels were checked periodically, and none of the men had AD at the beginning of the study. During the follow-up period, 54 of the men developed AD. In earlier studies, Resnick and her team found older men with high levels of free testosterone have better visual and verbal memory and perform spatial tasks better then men with lower levels of testosterone. “In the current study, we found that higher levels of free testosterone were associated with a significant reduction in the risk for AD,” Resnick says. However, Resnick adds it is a complicated problem, and simply raising testosterone levels might not do the trick. “There may be some optimal level of testosterone that is beneficial, but levels that are too high or too low may not be beneficial,” she explains. By Steven Reinberg HealthDay Reporter 1/26/04 Neurology 2004;62:188-193

New Clues to Genesis of AD - German scientists say they may have found a missing link in the chain of events that trigger AD. University of Bonn researchers are pointing the finger at a protein called abeta, which often shows up in large quantities in the cerebral cortex of patients with AD. Their study appears in the February issue of Traffic. Despite the presence of abeta in the brains of AD patients, scientists weren’t certain whether the protein could enter the cell plasma and cause damage. In this new study, Bonn University scientists say they discovered abeta can enter the cell plasma but, as a rule, decomposes once it’s in the cell plasma. But the scientists suggest that if this decomposition does not occur properly, abeta can accumulate and destroy cells. HealthDayNews 1/14/04 Traffic

Slowing Down AD - Two proteins appear to work together in mice to prevent the formation of the brain plaques that are characteristic of AD. Researchers at Washington University School of Medicine in St. Louis report 1/22/04 in the that the proteins clusterin and apolipoprotein E (apoE) seem to orchestrate the removal of potentially hazardous molecules from the brain. Ironically, previous research implicated these same proteins in a key stage of brain plaque formation. “This is one of the first demonstrations in living animals that these proteins affect amyloid clearance,” Dr. David H. Holtzman, head of the neurology department, says in a prepared statement. “Our findings suggest it is worthwhile to explore the use of drugs or therapies to alter or perhaps increase the expression of these proteins as a potential treatment for AD,” Holtzman says. HealthDayNews 1/22/04 Neuron vol. 41, 193-202 22 Jan. 2004

New Brain Disease Could Be Affecting Many Thousands - A newly discovered neurodegenerative disease could be affecting tens of thousands of men around the world, say researchers. The disease closely resembles AD, Parkinson’s and senile dementia, but appears to be caused by a genetic defect linked to fragile X syndrome. Until now carrying the defect was not thought to be harmful. Researchers believe the new disease, named FXTAS (fragile X-associated tremor/ataxia syndrome), may affect up to one in 3000 men, with most sufferers being over 50 years old. “FXTAS may be one of the most common causes of tremor and balance problems in the adult population and yet it is being misdiagnosed” says Paul Hagerman, a biochemist at the University of California, Davis and one of the research team. “Thankfully it can now be identified with a standard DNA test.” “Many of the patients we studied were thought to have Parkinson’s disease, AD, or were just suffering from normal ageing,” he told New Scientist. “In some cases patients with the disease even had surgery. Now that FXTAS has been identified these people will no longer receive the wrong treatment.” FXTAS is characterised by tremors, balance problems and dementia that become increasingly severe with age. Initial signs of the disorder include difficulty writing, using eating utensils, pouring water and walking. Other features include short-term memory loss and anxiety. By Danny Penman NewScientist.com news service 1/27/04 Journal of the American Medical Association 2004;291:460-469

Stroke Risk Linked to Decline in Mental Powers - A high risk for stroke predicts a deterioration in mental functioning, even when dementia and clinical stroke do not occur, investigators reported 1/15/04 at a media briefing by the American Medical Association. “Factors that increase the risk of stroke affect planning and organizational abilities,” lead researcher Dr. Merrill F. Elias said. Such risk factors include type 2 diabetes, abnormal heart rhythms, heart enlargement, high blood pressure, and smoking. The Framingham Stroke Risk Profile (FSRP) is a validated score that measures the risk of having a stroke, based on a variety of factors such as blood pressure, smoking, having diabetes, and so on. Dr. Elias, at Boston University, and his colleagues examined FSRP scores in 2,175 members of the Framingham Offspring Cohort, none of whom had a history of stroke or dementia. The participants also underwent a battery of mental tests The researchers found that as stroke risk increased, performance went down on tests of abstract reasoning, visual-spatial memory, tracking and organization, and attention. Functions not associated with FSRP were verbal learning and memory, Dr. Elias said. Since stroke risk profile factors play a role in dementia, “it is very likely that they play a role in AD,” he added. “The importance of our work is that it establishes a relationship between high risk for stroke and early cognitive deficit,” the investigator explained. “The greatest opportunity to intervene is at the beginning when the cognitive deficit is mild. As the deficit increases, our opportunity to intervene decreases significantly.” Behavioral interventions and medications to treat risk factors such as hypertension and hypercholesterolemia “are both essential,” he told Reuters Health. This report will be published in the February issue of the medical journal Stroke. Dr. Vladimir Hachinski, editor-in-chief of Stroke and neurologist at the University of Western Ontario in Canada, told the group: “These findings suggest that in those who are prone, stroke can precipitate AD.” He continued: “We know that stroke is preventable. In principle, since stroke is treatable, AD too may be treatable.” By Karla Gale Reuters Health 1/15/04

Marian S. Ware AD Program Established at PENN Medicine with a $6 Million Gift - The University of Pennsylvania 1/15/04 announced the establishment of the Marian S. Ware AD Program, comprising a set of collaborative initiatives between PENN Medicine and the University of Pennsylvania School of Nursing to advance drug discovery, clinical research, and patient care related to AD. The Program is created through a $6 million gift from Marian S. Ware, a long-time supporter of the University and advocate for progress in medical research and treatment for AD. The Marian S. Ware AD Program will uphold a three-part mission: drug discovery, identifying and evaluating novel therapeutics; clinical research, particularly in developing and testing biomarkers to identify patients with AD; and patient care, formulating best practice models that coordinate the complex care needs of patients and their family members. PR 1/ 5/04

Emory and Harvard Receive First Grants From the Alzheimer Research Consortium - The Alzheimer Research Consortium, a novel public-private consortium designed to combat AD by supporting the development of new research model systems, announced 2/3/94 that its first grants have been awarded to Emory University and Harvard University. At Emory University, Anthony Chan, D.V.M., Ph.D., received funding for his project “Transgenic rat models of AD.” The grant to Harvard will fund the project “Novel fly and mouse models for the p25/Cdk5 kinase” in the laboratory of Li-Huei Tsai, D.V.M., Ph.D., a Howard Hughes Medical Institute investigator. The Consortium seeks to improve the diagnosis, treatment, and cure of AD by promoting the development of new research models that mimic features of the devastating human disease. PR 2/3/04

MetLife Foundation Award for Medical Research Recognizes Strides Made by Scientists in AD Research - MetLife Foundation’s Award for Medical Research in AD was presented 1/13/04 to Roberto Malinow, M.D., Ph.D, and Thomas Sudhof, M.D., in recognition of their efforts and contributions to understanding AD. Drs. Malinow and Sudhof each received a grant of $200,000 to further their work in AD research, as well as a $50,000 personal award. Both of this year’s honorees have advanced our knowledge of how cells in the brain communicate and how diseases of cognition disrupt that communication. Dr. Malinow is Professor of Neuroscience at the Cold Spring Harbor Laboratory, New York. For the past decade, Dr. Malinow and his colleagues have focused their research on how activity in brain cells controls the strength of communication at the synapses between the cells. This process, called synaptic plasticity, is thought to underlie the formation and storage of memories. Dr. Malinow’s research has led to a greater understanding of how synapses function, as well as the role of amyloid beta peptides (viewed as central to the pathogenesis of AD) in normal and disease cells. Dr. Sudhof directs the Center for Basic Neuroscience at the University of Texas Southwestern Medical Center at Dallas and serves as an investigator of the Howard Hughes Medical Institute. Dr. Sudhof believes that understanding synaptic communication is key to understanding how the brain processes information. The work in Dr. Sudhof’s laboratory has made seminal contributions to our understanding of synaptic communication, including the division of the presynaptic process into an intriguing hierarchy of reactions. His research into amyloid precursor protein (APP) serves as a basis for future studies of the underlying cause of AD. The awards program began with a research briefing at which each winner discussed his work and future AD trends. The research briefing was moderated by Donald L. Price, M.D., Director, AD Research Center at John Hopkins University School of Medicine and Professor of Pathology, Neurology and Neuroscience. PR 1/13/04

Ailing Ronald Reagan Celebrates 93rd Birthday - A decade after dropping out of public view, America’s first movie star president, Ronald Reagan, spent his 93rd birthday at his California home, while his wife, Nancy, was to attend a ceremony in his honor. AFP 2/6/04

Japan Man Wanted on Industrial Spy Charge - Prosecutors in Japan detained a Japanese man 2/2/04 in response to an American request that he be handed over to face industrial espionage charges in the United States, an official said. Takashi Okamoto, 43, a former researcher at the Cleveland Clinic in Cleveland, Ohio, was charged in May 2001 with conspiracy, economic espionage and interstate shipment of stolen property related to AD research. Tokyo prosecutors took Okamoto into custody after receiving an order from Justice Minister Daizo Nozawa to launch extradition proceedings, said a Tokyo High Public Prosecutors Office official, who spoke on condition of anonymity. Prosecutors have submitted investigation documents to the Tokyo High Court, which is set to examine the case for extradition. The court’s ruling is expected in two months, the official said. By Kozo Mizoguchi, Associated Press Writer 2/2/04

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