Alzheimer Related News Items

News as of 5/06/01
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AD Linked to Proteins Associated with Aging - The irreversible brain disorder AD may be caused by inflammatory processes associated with aging and not--as generally believed--by plaque-like deposits in the brain, researchers from the University of Southern California in Los Angeles and Northwestern University in Evanston, Ill. reported 4/20/01. Their findings could open new avenues of exploring ways to treat or even cure the disease. Their findings' still lays the blame for AD on a molecule called amyloid beta, but traces the basic cause of the disease to the formation of toxic proteins rather than the build-up of plaque and tangles inside nerve cells in the brain. "We were able to identify in laboratory test tubes a new kind of toxic activity that is implicated as a root cause of AD,'' Dr. Caleb Finch, director of the Neurogerontology Division at the USC Andrus Center's Gerontology Research Institute, told Reuters in an interview. The researchers discovered a novel form of wadded-up amyloid called "amyloid b-derived diffusible ligands"- ADDLs or "addles" for short--that form in the presence of certain inflammatory proteins in the brain. They have chemical and toxicological properties quite different from either single beta-amyloid molecules or clumps of the molecules called fibrils. For nearly two decades, AD research has focused on ways to prevent the formation of fibrils, which coalesce into even larger deposits in the brain known as plaques, which have been shown to kill nerve cells in the brain. "ADDLs come before fibrils," Finch said. ADDLs affect brain cells that atrophy. Also unlike fibrils, ADDLs are highly selective in their toxicity. The researchers found that ADDLs affect only the same types of brain cells that atrophy in AD patients. Fibrils, however, kill a broad range of nerve cells--even destroying cell types that remain healthy right up until patients die. ADDLs are also soluble, which means they are free to diffuse everywhere in the brain. Fibrils are confined to the specific locations where they first form and these locations correspond poorly with the brain areas that wither as AD progresses, according to the researchers. "These soluble forms may be the answer to the riddle as to why fibrils don't correlate with areas of that brain that are damaged by AD," Finch said. The researchers also suggest that ADDLs begin to interfere with the brain's basic mechanism of long-term memory well before they reach levels high enough to kill brain cells. "ADDLs result from certain types of inflammatory proteins. If we can interfere with this process, we can affect the progress of the disease," Finch said. Given this, the concept of developing an antibody-based vaccine to treat or even prevent AD makes sense, the researcher said. "A couple of years ago, people thought the vaccination approach was the craziest idea. But if the real target is the soluble molecule and not the fibrils, it is a consistent approach," Finch said. By Deena Beasley Reuters 4/23/01 Trends in Neurosciences, 2001, 24:4:219-224

Drugs
Statin Drug Shows Anti-AD Effect - Researchers in Germany have discovered that the cholesterol-lowering drug simvastatin slows production of a key protein associated with AD. Despite the fact that the experiments were conducted in guinea pigs, the results may have treatment implications for humans. AD is characterized by the build-up of plaques that gradually distort the architecture of the brain. A naturally occurring protein called amyloid has been implicated as a key player in this destructive process. "Simvastatin lowered the production (of the beta-amyloid protein) Ab42, decreasing the likelihood of AD," said co-author Dr. Tobias Hartmann of the University of Heidelberg. Hartmann noted the amount of simvastatin given to the guinea pigs was, relative to body size, 100 to 400 times the amount normally taken by humans, and that it is unknown if lower doses of the drug would lower amyloid levels in people. Guinea pigs are good models for humans in studying AD, Dr. Benjamin Wolozin of Loyola University Medical Center in Maywood, Illinois, told Reuters Health. The animals produce amyloid proteins very similar to human ones, he explained, and their reaction to statins is similar to that shown by humans. "This opens up new therapeutic approaches to AD," Wolozin writes in an editorial accompanying the study. "The ability of statins to reduce amyloid beta production offers the exciting prospect that an existing medicine might be effective in delaying the onset or progression of AD." By Keith Mulvihill Reuters Health 4/9/01 Proceedings of the National Academy of Sciences 2001 published online before print 4/10/2001 (10.1073/pnas.081620098)

US Judge Backs Drug Settlement Reimbursement Plan - A federal judge has approved plans to reimburse consumers and taxpayers $100 million from a price-fixing settlement with Mylan Laboratories Inc. and three other drug companies. The states will distribute money from the settlement to consumers who were overcharged for two Mylan anti-anxiety drugs lorazepam and clorazepate. The drugs are both used to treat victims of AD. In the lawsuit, authorities said Mylan had raised prices for the drugs by about 20- to 30-fold. Under terms of the settlement, $72 million of the settlement money will be distributed to individual consumers who overpaid, according to a statement by Connecticut Attorney General Richard Blumenthal. People who bought lorazepam or clorazepate from Jan. 1, 1998 through Dec. Reuters 4/30/01

Researchers Link Failed Cell Division and AD - Researchers at Case Western Reserve University's School of Medicine and University Hospitals of Cleveland (CWRU/UHC) have uncovered a key piece of missing evidence in the proof that nerve cell death in AD is caused by a failed attempt at cell division. They have found a significant number of brain cells in AD patients with extra copies of chromosomes, showing attempts at cell division in cells that are not supposed to divide. This effort to divide is the likely cause of the nerve degeneration and dementia in AD, say the researchers. "It's almost as if AD were a novel form of cancer" says Karl Herrup, senior author of the findings published by the researchers. Cancer is characterized by uncontrolled cell division. In this study, scientists found uncontrolled cell division, arrested in the midst of the process, is the likely cause of the nerve cell destruction. According to Herrup, memory loss in AD is always associated with the accumulation of strange deposits in the brain known as plaques and tangles. Most investigators agree that these deposits are central to the disease, but are not in and of themselves the cause of memory loss. The clinical symptoms are more closely tied to the nerve cell death, but the links between plaques and death were unclear. "The simplest view is that plaques are directly toxic to neurons. The cell division hypothesis puts a different spin on this idea," he says. The researchers do not know what triggers the cells to begin a cycle for which they are not programmed, but a theory they put forth with other CWRU/UHC colleagues hypothesizes that the plaques which are a hallmark of AD brain cells trigger an inflammatory response in the brain, and that this response brings with it proteins that trigger cell division. Herrup said the findings of the paper open new doors to develop therapeutics that could prevent signals for the inflammatory response from reaching the cells or to prevent the cells from responding to the signals to divide. PR 4/17/01 The Journal of Neuroscience, April 15, 2001, 21(8):2661-2668

Adult Stem Cell with Astounding Potential Found - An adult stem cell that may be able to create any organ in the body has been discovered in bone marrow, offering wide-ranging promise for curing disease similar to that of embryonic stem cells, but without the ethics debate researchers said on 5/3/01. Dr. Neil Theise of the NYU School of Medicine made the discovery along with Dr. Diane Krause of Yale University School of Medicine. Their study involving mice provides the strongest evidence to date that the adult body harbors stem cells that are as flexible as embryonic stem cells. Theise said that in theory any organ in the body could be repaired using cells generated from this stem cell, and bone marrow-derived cells could be used to target gene therapy to a specific organ. "This would appear to be the ultimate stem cell -- or the closest we've gotten to it," Theise said. But Theise and Krause said their study should not be used to justify squelching research into embryonic stem cells. We're really at the beginning of this field of understanding stem cells, stem cell plasticity, all these potentials and which cells have it. And if we discontinue embryonic research and fetal tissue research, we'll slow the field down," Krause added. "To close down those options prematurely, I think, is to close down the possibility of curing people. There's a long way to go between what the potential of something is and what its actual practicality is," Theise added in an interview with Reuters. By Will Dunham Reuters. 5/3/01 Cell, vol. 105, 369-377, May 2001

Scientists Isolate, Grow Brain Cells From Corpses - Researchers have isolated and cultivated brain cells from human corpses in a scientific feat that could provide a new source of stem cells for research and developing medical treatments. Professor Fred Gage and his colleagues at the Salk Institute in California obtained the brain cells that can grow, divide and form specialized brain cells from tissue samples of people shortly after their deaths. Their achievement, reported 5/21/01 could overcome the ethical obstacles of using stem cells derived from embryos. "I find it remarkable that we have pockets of cells in our brain that can grow and differentiate throughout our lives and even after death," Gage said in a statement. The scientists used special growth factors to obtain cells from the tissue, which they said was a crucial element to their success. "Cells recovered from healthy individuals could provide a model for understanding how to stimulate and guide the normal processes of brain cell growth and differentiation, lending insight to how growth might be stimulated in people suffering from neurodegenerative diseases such as AD or Parkinson's," said Gage. The scientists are also planning to transplant the brain cells into animals to see if they survive and differentiate. "Testing in whole animals is the only way to know if adult tissue can be a source of stem or progenitor cells for transplant purposes to treat neurodegenerative disease," Gage added. Reuters 5/2/01 Nature 411:6833; 42 (2001)

Study: Fat May Be Stem Cells Source - Researchers at the University of California at Los Angeles and the University of Pittsburgh isolated the stem cells - immature cells that can be coaxed into maturing into specific types of tissue - from ordinary fat removed by liposuction. They then grew the cells into bone, cartilage, muscle and fat. Researchers predict the first practical use of laboratory-engineered tissue could come within five years. Eventually, scientists hope to use a patient's own fat to supply the tissue required to treat disease or repair injuries. By Andrew Bridges, AP Science Writer 4/10/01 Tissue Engineering 7:(2);211-228 (4/10/01)

Company Says It Can Derive Stem Cells From the Placenta - Anthrogenesis Corporation of Cedar Knolls New Jersey said 4/11/01 it had developed a method to extract a novel kind of stem cell from the placenta and that the cells were the equivalent of human embryonic stem cells, which can transform into every tissue of the adult body. "This will make obsolete the need to use human fetuses or blastocysts as sources of stem cells," said John Haines, chief executive of the company. But the articles describing the research have not yet been accepted for publication, an important step in the validation of scientific claims. The Anthrogenesis scientists believe that some inner-cell mass cells also migrate to the placenta and are held there as a reserve in case the fetus needs them. If so, this would be a third source of embryonic-like cells. Other experts said that this was a novel and interesting idea, but that they knew of no evidence to support it, and Dr. Joseph Cioffi, the company's director of research and development, agreed there was no animal data bearing on the issue. By Nicholas Wade NY Times 4/12/01

Scientists Debate Cloning Policy - Scientists, ethicists and philosophers faced off 5/3/01 at a Senate hearing over legislation that would ban not only the cloning of humans for reproductive purposes, but also the cloning of human embryos for research into treatments for a wide variety of conditions and diseases. Backers of the "Human Cloning Prohibition Act" told the Senate Commerce Subcommittee on Science, Technology and Space that in order to truly preclude the cloning intended to produce a live birth, it is necessary to outlaw all forms of embryo cloning. But scientists told the subcommittee that such a broad ban could threaten potentially life-saving research. "Therapeutic cloning techniques are central to the production of breakthrough medicines, diagnostics and vaccines to treat AD, diabetes, Parkinson's, heart attacks, various cancers and hundreds of other genetic diseases," testified Carl Feldbaum, president of the Biotechnology Industry Organization. "We all agree that given the current safety and social factors, human reproductive cloning is repugnant," Feldbaum said. "However, it is critical that in our enthusiasm to prevent reproductive cloning, we not ban vital research, turning wholly legitimate biomedical researchers into outlaws, and thus squelching the hope for relief for millions of suffering individuals." By Julie Rovner Reuters Health 5/3/01

Caregivers
Study Finds Persistent and Severe Pain among Nursing Home Residents - A new nationwide study shows that severe pain among elderly nursing home residents is prevalent, persistent and poorly treated. The authors of the first national look at pain management among this frail population say that the findings underrate the true pain burden experienced by the patients. They call untreated pain in nursing homes "an important national public health problem." The study reports the rate of persistent severe pain, using data gathered through the federally required Minimum Data Set (MDS). The MDS is used to collect details on individuals admitted to U.S. nursing homes, including information on the frequency and severity of pain. "We believe the findings underestimate the actual pain burden," said lead author Joan Teno M.D. "MDS data is collected by nursing home staff. It is based on staff perception, and staff routinely underestimate the pain burden of patients." The authors used the MDS to examine the pain experience of more than 2.2 million people residing in U.S. nursing homes on or about April 1, 1999. They found that 41.2 percent of elderly nursing home residents who were in pain around April 1, 1999, still experienced moderate daily pain or excruciating pain 60 to 180 days later. Of individuals in a nursing home between 2 and 6 months, one in seven had persistent pain. Nationwide, rates of persistent pain varied, with most states between 39.5 percent and 49.5 percent. "Recent media coverage has fed fears about opiate drug prescription abuse," said Teno, "but that should not be a reason for leaving a vulnerable population in persistent severe pain. The focus must be on quality medical care that provides competent, compassionate and coordinated medical care for frail, older Americans residing in nursing homes and treats drug abuse as well." PR 4/24/01 Journal of the American Medical Association April 25, 2001, 285 (16) 2001 Free copy of 1 page letter available at http://jama.ama-assn.org/issues/v285n16/ffull/jlt0425-6.html

Costs of Caring for California's AD Patients will Triple by 2040, say UCSF Researchers - The costs of caring for California community residents with AD will increase 83 percent by 2020 and an additional 59 percent by 2040, according to UCSF researchers from the Institute for Health and Aging. Similarly, costs of caring for AD patients in California institutions will increase 84 percent by 2020 and an additional 61 percent by 2040 - assuming the supply of nursing home beds meets the projected demand. Though state and federal governments will shoulder some of the costs of caring for AD patients (largely through Medicaid and Medicare), the majority of those costs will be borne by family members, said the researchers. "Dementia places substantial medical, social, psychological, and financial burdens on patients, families and communities. People with AD consume both formal medical and social services, those rendered for a price, and informal services, those for which providers, usually family members, are not reimbursed" said Patrick Fox director of the Institute. Projected informal costs of caring for people with AD represent an estimated dollar value of the informal caregiver's labor rather than an actual dollar value, he explained. However, if unpaid caregivers were not available, long-term services would be purchased from paid providers or AD patients now cared for in the community would be placed in institutions. "The changing nature of the family and increasing labor force participation of women may result in fewer available caregivers for elderly people in the future. Therefore, many of the informal care costs borne by family members may become actual expenditures," he said. PR 4/27/01 Journal of Public Health Policy spring 2001 issue.

Testing
Test May Detect AD in Early Stages - A new memory test, the CANTAB Paired Associates Learning Test, developed at Cambridge University can detect early stages of AD in as little as 10 minutes the researchers report 4/24/01. Using images flashed up on a computer screen, the test probes episodic memory, which is lost in the early stages of the degenerative brain disorder. The test can distinguish AD patients from those with depression and others without any brain problems with 98% accuracy, according to the authors. This is a key breakthrough, researcher Dr. Barbara Sahakian told Reuters Health, because it is difficult to tell the difference between AD and depression, especially early in the course of the disease. "The CANTAB-PAL's sensitivity to AD is related to the fact that the areas of the brain first affected in AD are the same areas utilized when performing the test," Sahakian said. She noted that the test may be useful not only in catching AD early, but also in helping doctors measure the effectiveness of current and future drugs for AD patients. "The test will offer a tremendous advantage time-wise," Sahakian said, noting that new drugs that slow the progression of the disease work best if given early on. She added that she hopes the test, which she likens to a computer game, will soon be used by general practitioners. By Stephen Pincock Reuters Health 4/24/01 Dementia and Geriatric Cognitive Disorders 2001; 12(4)

Brain Research Facility To Be Named For Donor W.M. Kreck - A $2 million grant by the W.M. Keck Foundation has determined the name of a San Diego brain research facility expected to be the largest of its kind in the western United States. The facility housing the UCSD Center for Functional Magnetic Resonance Imaging will be named the W.M. Keck Building. The cost of building the 6,500-square-foot facility is estimated at $13.5 million. The center is slated to be complete in October of this year. UCSD officials say the center will be the largest brain imaging facility dedicated to research in this part of the country. UCSD officials explain magnetic resonance imaging, or MRI, as having two capacities in a clinical setting: conventional and functional. Conventional MRI is a noninvasive tool that provides detailed pictures of the anatomy of a brain, while functional MRI expands on that imaging capability to let researchers observe the internal functions of the brain in action. According to Richard Buxton, director of the new center and a UCSD radiology professor, Functional MRI can help researchers look at areas of the brain that aren't working normally in disorders like stroke and epilepsy, and degenerative diseases like AD and Parkinson's. Yahoo News 5/3/01

Prevention
Designer Estrogen Raloxifene May Help Prevent Cognitive Decline in Some Elderly Women but No Benefit for Most, UCSF Study Says - The designer estrogen drug raloxifene, sold as Evista, has been prescribed to millions of postmenopausal women for osteoporosis, but its effects on the aging brain are unclear. A new study led by a University of California, San Francisco researcher shows that although raloxifene does not affect the cognitive performance of most women, it may help prevent decline among women older than 70 and women whose cognitive performance is declining regardless of age. Raloxifene helped these groups of women to sustain better scores on tests of attention and verbal memory, according to Kristine Yaffe, MD. The study suggested that raloxifene did make a difference for women older than 70, and the subgroup of women whose scores were declining substantially. Their scores declined less than the placebo group on two of the tests, which measured attention and verbal memory, suggesting that raloxifene might offer some protection against cognitive decline for these women. Although these results aren't proof of a benefit, Yaffe said, they fit with some of the research on estrogen therapy for post-menopausal women, showing that it gives a small boost on tests of memory and attention. Also, she noted, "typically the first things affected in the early stages of AD are verbal memory and attention." The true test of whether raloxifene or estrogen protects against AD or other types of dementia will be to track the women in the clinical trials for many more years to see whether one group is more likely to develop dementia. Yaffe and her colleagues are planning to do just that. PR 4/18/01 New England Journal of Medicine 2001;344:11207-13

Naturally Occurring Protein Could Slow AD - The amyloid precursor protein (APP) is implicated in AD since a small part of that protein forms a chemical called beta amyloid, which becomes the most important part of the AD plaques that strangle normal brain cells. Using APP in a group of chemicals specifically designed to simulate the human body researchers found it attached another protein called Apolipoprotein A-1. Everyone has some quantity of Apolipoprotein A-1, or Apo-A, in their body, says Dr. Radosveta Koldamova, M.D., Ph.D., a member of the research team at the University of Pittsburgh. It is produced in the small intestine and the liver and is known to help prevent coronary heart disease. At normal levels, the protein clears cholesterol throughout the body, including in the brain. The scientists speculate that boosting Apo-A levels may also help clear beta amyloid. The researchers think that increasing the concentrations of Apo-A in blood might delay the dementia associated with AD. Further testing is needed to confirm their hypothesis, they add. Another such protein, Apolipoprotein E, has been similarly linked with AD and is being studied by other researchers. One way to raise the levels of the protein naturally is through a good diet, according to Professor John S. Lazo, Ph.D., who led the research study. Previous findings indicate that some foods, including fruits, soybeans, coconut oil as well as some wines and teas can stimulate cells to make more Apo-A. Liver diseases or other infections can lower Apo-A levels, he said. In previous clinical studies, AD patients were shown to have lower than normal levels of Apo-A, leading Koldamova to suggest a direct relationship between the two. "We think that if we can increase the concentration of Apo-A in the blood, we might be able to increase the levels of the protein in the brain" Koldamova said. "Our hypothesis is that this might help clear beta amyloid from the brain." Further testing is needed to confirm the role of Apo-A in animals and its relation with AD, she said. Then, new methods to boost the protein's concentrations in the blood would be needed before any human trials could begin, she continued. PR4/2/01 Biochemistry (3/27/01) 40(12):3553-3560

Study: Big-Headed May Keep Brain Power Longer - People with big heads may have reason to rejoice if findings by scientists from Maastricht University in the Netherlands hold true. Individuals with larger brains may be protected from the normal decline in mental abilities that comes with age, researchers report. One explanation for the finding may be the fact that people with bigger brains can afford the natural loss of cells as they age. Dr. Danielle J. Tisserand and her colleagues examined a variety of mental abilities among more than 800 healthy adults between the ages of 50 and 81. They also measured the circumference of each participant's head. It turned out that older people with smaller heads performed worse than those with bigger heads on tests of thinking ability and mental speed, Tisserand explained in an interview with Reuters Health. However, there was no relationship between head size and memory, according to the report. Previous research has identified a relationship between head size and mental ability in individuals with AD, "but studies with healthy subjects are scarce," noted Tisserand. The researchers stress that in their study head size played a larger role in a person's mental ability when compared to educational levels and developmental factors such as socioeconomic level or nutrition. "Hence, it seems that it is really head size which influences the cognitive performance level," Tisserand said. "It is known that after brain lesions, neurons close to the damaged area can take over functions that used to be executed by the lost cells. Bigger brains may therefore offer a better protection against cognitive deterioration: they provide a larger "reserve," explained Tisserand. "However, to be able to test this hypothesis, (more) research is necessary," she added. By Keith Mulvihill Reuters Health 4/24/01 Neurology 2001;56:969-971.

Getting the Goods on Ginkgo - A four-year study to determine whether ginkgo biloba delays or prevents AD is under way at Oregon Health Sciences University. Ginkgo biloba is used around the world by alternative and complementary health providers, who believe it improves a person's memory. It's a huge market: Americans spent $240 million on ginkgo biloba in 1997 alone. But there isn't much scientific evidence to confirm the benefits of this plant extract. Most of the studies on it have been done without rigorous scientific standards. Tracyl Zitelberger, a research assistant in the Dementia Prevention Study, says this study is unique in that it's looking at ginkgo biloba's ability to delay or prevent dementia symptoms, while other studies have focused on whether it could lessen symptoms in people already experiencing dementia. By Robert Preidt HealthScout Reporter 4/18/01

Other Items
Some Rhythmic Clues to AD - It is not always easy for doctors to know whether a patient is suffering from AD or some other form of dementia, a problem that can make choosing appropriate treatments more difficult. But scientists at McLean Hospital, the Harvard psychiatric affiliate, believe the trick may lie in taking a close look at the patient's circadian rhythm, the daily cycle of body temperature change and spontaneous movement. The discovery may lead not only to better diagnosis, but also to better therapy for the devastating sleep disturbances that often accompany dementia, the researchers said. The lead author, Dr. David Harper, and his colleagues came to their conclusions after tracking the circadian rhythms of 38 dementia patients for six years. Some had AD; others had what is known as fronto-temporal degeneration. They found that not only did the patients' rhythms vary from people without dementia, they were quite different in AD than in fronto-temporal degeneration. Their work, the researchers said, may help doctors who have tried to treat insomnia in dementia patients with melatonin and light therapy, in an effort to "reset" their biological clocks. The efforts have partially succeeded, but with a better understanding of how different type of dementia affect the circadian rhythm, the treatments can be tailored to each patient, the researchers said. By Eric Nagourney NY Times 4/17/01 The Archives of General Psychiatry 2001;58:353-360

High Homocysteine Levels Are Associated with Decreased Memory Capability after Age 60 - High circulating levels of homocysteine, especially with increasing age, have been associated with cognitive impairment. In recent studies, AD and dementia after multiple strokes have been linked to extremely high serum homocysteine concentrations. As part of the larger third National Health and Nutrition Examination Survey (NHANES III), 1299 men and women aged 60 and over, none of who had previously had a stroke, participated in the study between 1991 and 1994. Morris et al. assessed the relationship between homocysteine levels and short-term memory recall in this group of older subjects and found an independent relationship between very high homocysteine levels and poor performance on cognitive tests. The folate status of the participants was an important consideration because folate has been shown to significantly modify homocysteine levels. Story recall was worse among subjects with a combination of low folate and high homocysteine than in those whose homocysteine levels were normal or low. Homocysteine levels increased with age and were accompanied by a comparable decline in folate status. The researchers found independent associations between the highest levels of homocysteine and poorer recall. PR 4/26/01 American Journal of Clinical Nutrition 2001; 73:927-33 A free copy of the text of the article is at http://faseb.org/ajcn/May/12098-Morris.pdf

Countering the Body's Own Harmful Response to Stroke - Scientists have found that a compound called Activated Protein C, or APC, holds promise in protecting brain cells from the damage caused by stroke. APC helps snuff out a crucial step in the chain of events that can lead to the death of neurons. While brain damage from stroke initially begins with a lack of blood flow to the brain, the damage is increased by a cascade of reactions, including overzealous attempts by the body's own immune system to "fix" the damage. White blood cells are recruited to the stroke site by chemical messengers and try to clean up the damage - - but the response often magnifies the injury and can cause a patient's condition to worsen. In a study published 4/3/01 scientists from the University of Rochester Medical Center report on work in mice which shows that APC can stem the flood of harmful white blood cells into the brain, one key to reducing the effects of stroke. The lead author Berislav Zlokovic of the U of R did the work in collaboration with John Griffin of Scripps Research Institute in La Jolla, Calif. For more than a decade Griffin and Zlokovic have studied APC together and have discovered how the compound helps prevent blood clots. Zlokovic, and Griffin are continuing their studies to see whether APC might someday become a stroke treatment. "From the time that blood flow stops to the time that brain cells die, there is a series of complex reactions. Understanding those reactions, which involve inflammation, apoptosis, and other processes, is a very hot topic in research," says Griffin, professor of molecular and experimental medicine at Scripps Research Institute. PR 4/23/01 Circulation 2001;103:1799

Scientists Find Way to Block Effects of Marijuana - Chemically blocking receptors in the brain that respond to a key compound in marijuana squelches the "high" caused by the drug, scientists said on Thursday in a finding that could lead to treatment for marijuana abuse and perhaps even for obesity. Cannabinoid receptors are most dense in brain regions involved in thinking and memory, attention and control of movement, the researchers said. Their precise function in people is not well understood, although animal studies have shown compounds that activate the receptor sites impair learning and memory and increase appetite and food intake.  Lead researcher Dr. Marilyn Huestis of U.S. National Institute on Drug Abuse (NIDA), part of the National Institutes of Health, said the findings help point the way toward possible treatment for people addicted to marijuana. Huestis also said the compound, by blocking the brain's cannabinoid receptors, may prove useful in treating obesity and psychotic diseases such as schizophrenia and improving memory. Reuters 4/13/01 Archives of General Psychiatry 2001; 58:322-328

Dementia Survival As Low As 3 Years - Christina Wolfson of the epidemiology and biostatistics department at McGill University's Montreal Neurological Institute looked at  survival time after diagnosis for 821 patients with dementia. The survival time was found to be about 6.6 years. But when the "survivors-only bias" was taken into account, the study found that half of the patients would live less than 3.3 years, and half would live longer. The study also estimated the median life expectancy at 5.7 years for people diagnosed between the ages of 65 and 74; 4.2 years for people diagnosed between 75 and 84; and 2.75 years for those at least 85 when diagnosed. Other experts said Wolfson's overall estimate is so low because the patients were so old - almost 84, on average. "To say your mean life expectancy is 3.3 years at age 84 is not nearly as dramatic as saying it's 3.3 years at age 50," said Dr. Claudia H. Kawas, a neurology professor at the University of California at Irvine. The average number of years left for all 80-year-olds is about seven; for 85-year-olds, it is about five, Kawas said. Bill Thies, vice president for medical and scientific affairs of the Alzheimer's Association, said the study is not especially significant. He, too, noted that the group was old to start with. By Janet McConnaughey, AP Writer 4/11/01 New England Journal of Medicine 2001;344:1111-1116, 1160-

A Host with Infectious Ideas - Paul W. Ewald argues that most cancers, heart disease and other chronic ills stem from infections. If correct, his theory will change the course of medicine. His latest research, outlined in his book Plague Time published last year. The 47-year-old Ewald argued in the book that infection may play a role in cancer, atherosclerosis, AD and other chronic conditions ordinarily thought of as inevitable consequences of genetics, lifestyle or aging. Ewald thinks that more cancers, perhaps the majority, as well as numerous other common, widespread and ancient chronic diseases, will eventually become linked with various infections: for atherosclerosis and AD, he points to studies showing associations with Chlamydia pneumoniae. He even holds that schizophrenia may be related to infection with the protozoan Toxoplasma gondii. Ewald believes that the associations between chronic diseases and infections will be slowly accepted, perhaps in a few decades. By Steve Mirsky Scientific American May 2001

Statement by Richard J. Hodes - On AD before the Senate Appropriations Committee Subcommittee on Labor, Health and Human Services and Education 4/3/01. He is the Director of the National Institute on Aging. He discussed promising news about the progress that has been made in the past year to understand, treat and prevent AD. Topics included preventing AD: the AD Prevention Initiative and ongoing clinical trials. Other topics were from basic science to treatment which relates to developing effective treatments for AD based on advances in basic research which is a major focus of NIA-supported studies. He also discussed drug discovery, development and testing, early AD diagnosis risk and protective factors. He ended up with patient care strategies and caregiver burden. His 11 page statement with charts can be obtained at http://www.nih.gov/nia/about/legislation/fy2002/testimony/ad/ds.htm

Statement by Steven DeKosky - Presented to the Senate Appropriations Committee; Labor, Health and Human Services, Education, and Related Agencies Subcommittee 4/3/01 on behalf of the Alzheimer Association. He said we can now say with confidence that answers are within reach. We are at an unprecedented place in AD research -- facing possibilities that just didn't exist when he first came before this subcommittee in 1998. That is because of the investment the subcommittee had already made, not just in AD research, but in the human genome project, in imaging techniques, and in basic science. He discussed the Prevention Initiative and a few of the far-reaching discoveries that have been reported since the subcommittee met about AD last year. His 9 page statement is at http://www.alz.org/involved/advocacy/record/20010410SK.htm

Testimony by David Hyde Pierce - Presented to the Senate Appropriations Committee; Labor, Health and Human Services, Education, and Related Agencies Subcommittee 4/3/01. He said there are three compelling reasons why Congress must accelerate its investment in AD research now. The first reason is just basic human decency. The second reason is the scientific opportunity that Dr. Hodes and Dr. DeKosky discussed. The third reason, which he focused on is basic economics. When you look at the numbers, it is hard to see how you can protect the Medicare trust fund if we don't find a way to stop AD. Last year, Medicare spent $31.9 billion to care for beneficiaries who had AD. That cost will be $49.3 billion by 2010, an increase of 54.5 percent. His testimony is at http://www.alz.org/involved/advocacy/record/2001403DHP.htm

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