Alzheimer Related News Items
News as of 7/8/01
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Gene Identified That May Indicate AD Risk - The presence of a newly identified gene, in human chromosome 10 in combination with another known gene APOE-E4, signals a 16-fold increase in the risk of developing AD in people whose close relatives have the brain malady, researchers said on 6/18/01. The effect is greater than the increased risk of lung cancer caused by smoking, said Dr. George Zubenko, a professor of psychiatry at the University of Pittsburgh School of Medicine and lead author of the study. These findings may provide new molecular targets for therapeutic drug development and will help researchers design trials involving subjects who have the greatest likelihood of responding to therapy and for whom successful therapy would have the greatest impact. Furthermore, the newly discovered risk locus affects brain levels of dopamine, the neurotransmitter used by neurons that degenerate in Parkinson's disease. As a result, the new findings may have relevance for both of these common neurodegenerative disorders. Reuters 6/18/01 and PR 6/18/01 Molecular Psychiatry 2001 Volume 6, number 4, pages 413-419

Prana's Science Reversed AD in Mice - Harvard based scientist Ashley I. Bush, who is the chief scientific advisor to Prana Biotechnology Ltd., reports that Clioquinol, a copper/zinc-binding drug that is given orally to transgenic mice and Prana's lead compound, markedly reduced their AD brain pathology within nine weeks; decreasing beta-amyloid accumulation by 50 percent during that period. This article comes after years of research conducted by Dr. Bush and his colleagues at Massachusetts General Hospital, Harvard Medical School, and the Mental Health Research Institute of Victoria, University of Melbourne. The focus of their discovery highlights the unique binding attributes of the beta-amyloid protein with zinc and copper. This breakthrough provides a viable explanation for the abnormal binding of these metals with beta-amyloid that is commonplace in AD. This reaction ultimately leads to the corruption of the protein and its ensuing toxicity. Copper and zinc are normally present at high concentrations in the regions of the brain that are most affected by AD damage. Clioquinol is currently in a phase two clinical trials and Prana anticipates results from the double blind study to be available in the early part of 2002. PR 6/21/01 Neuron, Vol. 30, 665-676, and 641-642 June 2001

Study Suggests that Potential AD Drugs Might be Dangerous - Scientists have discovered that gamma-secretase inhibitors, the most promising drugs under development for AD, also prevent certain immune cells from being produced. These drugs are in the early stages of human testing. "Our paper suggests that these drugs could have significant side effects," says Raphael Kopan, an associate professor at Washington University School of Medicine in St. Louis. "By using basic scientific methods such as the one we have developed, we hope to improve the ability of the scientific community to evaluate any AD drugs for their potential to cause life-threatening complications. Our system would also help identify drug dosages that might be safe in clinical trials." Researchers recently identified three genes that, when faulty, predispose individuals to this devastating neurological disorder. Two of them, presenilin-1 and presenilin-2, code for parts of a protein complex called gamma-secretase. In AD, this complex generates a protein fragment that accumulates as plaque in the brain. Using drugs, scientists hope to interfere with gamma-secretase production, thereby preventing plaque buildup. Other parts of the body need gamma-secretase, however. Kopan and colleagues previously found that the complex is required for Notch, a receptor protein, to signal. Notch is needed for production of many cell types in our body, including blood cells such as T-cells - - immune cells made and housed in blood. "We don't want to scare the public about these exciting therapeutic advances," says Kopan. "Quite the contrary - - we're offering a way to evaluate potential AD drugs for toxicity before human testing. Doses that reduce gamma-secretase activity without eliminating it might be the safest." PR 6/19/01 Proceedings of the National Academy of Sciences 2001 98:7487-7491 6/19/01

Nicotine in Quit-Smoking Aids May Feed Tumors - Quitting smoking reduces the risk of cancer, but a new study questions whether certain smoking cessation therapies may themselves be carcinogenic. Stanford University researchers led by associate professor Dr. John Cooke describe two disturbing findings about nicotine's effect on human cells and on the growth of blood vessels that feed tumors in mice. Both Cooke and Jack Henningfield, Henningfield, an associate professor of psychiatry at the Johns Hopkins School of Medicine, say nicotine's use against other diseases requires more study, and, again, the risks and benefits must be weighed. "Any new therapy that is useful to help people with AD or Parkinson's should be explored, but I do think our study does raise a question about possible unwanted consequences," Cooke says. He says his findings need further study in humans. By Nicolle Charbonneau HealthScoutNews Reporter 6/29/01 Nature Medicine 2001;7:833-839, 775-777

J&J to File Reminyl for Stroke Dementia Indication - Johnson & Johnson said on 6/21/01 it would file Shire Pharmaceuticals Group Plc's AD drug Reminyl for the new indication of vascular dementia. J&J spokeswoman Pam Rasmussen told Reuters: "Yes, we'll be filing for an indication. However, I can't give you a specific timeline." New 12-month data presented at the World Congress of Neurology in London showed the drug, which is derived from daffodils, improves the memory, orientation and language skills of patients suffering from vascular dementia, a condition often triggered by strokes. Shire's marketing partner, Janssen-Cilag, a unit of Johnson & Johnson, said Reminyl was the first cholinesterase inhibitor "shown to be potentially effective in treating dementia in patients with cerebrovascular disease, such as stroke -- the second most common type of dementia after AD." Reuters 6/21/01

Stock Focus: AD - In this report on stock prices, the following companies and products are discussed.

Forest Laboratories will be marketing Memantine as a treatment for severe stages of AD. Forest Labs expects Memantine could be available in the U.S. by the second half of 2003 if all goes well. NeoTherapeutics is currently in Phase III of trials of Neotrofin as a treatment for AD. This compound has been shown to stimulate the production of neurotrophic factors--substances that promote nerve cell growth, at least in animals. By Fei Mei Chan Forbes.com 6/15/01 Full article at http://www.forbes.com/2001/06/15/0615sf.html

Novartis Sets Trial of Exelon Versus Pzifer Drug - Novartis AG plans a large-scale clinical trial that will pit its Exelon drug against Pfizer Inc's donepezil (Aricept) for effectiveness in treating AD, Novartis announced 6/19/01. The two-year trial of the two most widely prescribed cholinesterase inhibitors is designed to include 1,000 patients and produce preliminary results in 2003, it said in a statement. It will gauge the drugs' efficacy in routine activity and behavioral and cognitive functions, compare their safety and tolerability profiles and evaluate the potential to reduce the need for psychotropic medication administered to patients. Reuters 6/19/01

Genes & Genetic Issues
Sleep Apnea Linked to AD Gene - A gene already linked to the risk of AD and cardiovascular disease is also closely associated with sleep apnea, scientists report. "It is the first genetic factor ever found to predispose to sleep apnea, a disorder that affects 10% of the population," Dr. Emmanuel Mignot of the Stanford University School of Medicine in California told Reuters Health in an interview. "Also, ApoE-4 predisposes people to high cholesterol and cardiovascular problems. Since sleep apnea is a major predisposing factor for high blood pressure, stroke and other cardiovascular events, these findings may have important effects on general health for the general population," he added. Mignot noted that about 28% of the population carries ApoE-4. The study found participants who carried the ApoE-4 gene were twice as likely to suffer from sleep apnea compared with those who did not have the variant. Those with two copies of the gene had an even higher risk of sleep apnea. "Our results indicate that ApoE-4 is associated with sleep apnea,'' the researchers write. Based on the study findings, Mignot said, his team estimates that about 8% of sleep apnea in the general population may be linked to ApoE-4. "It is a lot of people, but I am not sure if it is enough for suggesting genetic testing," he noted. "I would, however, say that if you have a family member with AD, plus you have obstructive sleep apnea, it may be important to watch more carefully for signs of AD," Mignot said. By Keith Mulvihill Reuters Health 6/12/01 The Journal of the American Medical Association 2001;285:2888-2890

Bush Proposes Ban on "Genetic Discrimination" - President George W. Bush on 6/23/01 in his weekly radio address proposed forbidding employers, insurance companies and others from denying jobs or health coverage to people based on their genetic makeup. "Genetic discriminat-ion is unfair to workers and their families," Bush said in the address. "It is unjustified, among other reasons, because it involves little more than medical speculation." The White House said Bush had signed legislation while he was governor of Texas to outlaw genetic discrimination in employment and group health plans. Genetic variations have been linked to up to 4,000 diseases, including cystic fibrosis, cancer, AD, diabetes, schizophrenia and heart disease, the White House said. However, said Bush: "A genetic predisposition toward cancer or heart disease does not mean the condition will develop. To deny employment or insurance to a healthy person based only on a predisposition violates our country's belief in equal treatment and individual merit. Just as we have addressed discrimination based on race, gender and age, we must now prevent discrimination based on genetic information," he said. By Randall Mikkelsen Reuters 6/25/01

Gene Linked with Verbal Memory Decline - Middle-aged and older people who have a gene variation associated with AD show a greater decline in verbal memory than do those without the gene, researchers reported at the Sixth Annual UCLA Research Conference on Aging in Los Angles 5/22/01. The gene, known as apolipoprotein E, codes for a cholesterol-carrying molecule and comes in three versions--e2, e3 and e4. The e4 version, found in about 28% of the population, has been linked to an increased risk of AD. In a new study, Dr. Helen Lavretsky and colleagues at the University of California, Los Angeles (UCLA) tried to determine if the gene influenced memory in people without dementia, the deterioration of mental faculties seen in people with full-blown AD. The investigators looked at ApoE-e4 status, symptoms of depression and a decline in mental abilities in 49 people without dementia. The researchers found that the gene did influence memory even without a diagnosis of AD. "ApoE-e4 status was predictive of verbal memory decline," Lavretsky told Reuters Health. Both groups of people showed a decline in visual-spatial memory when tested 26 months into the study, however, ApoE-e4 carriers had a greater decline in verbal memory scores compared with those who did not have that gene version, she said. "Because major depression has been found to be a risk factor for AD, we also wanted to investigate the impact of mild depression on cognitive decline," Lavretsky explained. Although mild depressive symptoms were twice as common in ApoE-e4 carriers than in noncarriers at the start of the study, these symptoms were not associated with subsequent loss of mental abilities, she added. Reuters Health 6/22/01

AD Protein Found to Activate Genes - Researchers say the function of a snippet of protein linked to AD may have implications for the treatment of the memory-robbing ailment. The protein fragment appears to be responsible for turning on genes inside a cell, causing genetic information to be translated into functioning proteins. The mental deterioration that is so devastating to patients with is thought to be caused by deposits in the brain that are made up of a protein called beta amyloid. The deposits are formed when enzymes cut a larger protein, known as amyloid beta precursor protein (APP), into smaller fragments. One fragment, beta amyloid, leaves the cell and can build up in plaques that can be found in the brains of patients with AD. A second fragment, called the tail, remains inside the cell but until now has had an unknown function. In a new study, Dr. Thomas C. Sudhof, of the University of Texas Southwestern Medical Center in Dallas, Texas and colleague Dr. Xinwei Cao performed a series of experiments in laboratory-grown human cells. They found that the APP tail remains inside cells and can turn genes on--a process known as transcription--when it comes into contact with two other proteins, Tip60 and Fe65. Their preliminary findings in cells in test tubes might help researchers better understand the disease and could have implications for treatment. "A possible negative implication is that treatments designed to inhibit APP cleavage will also inhibit they type of gene regulation that we describe in the study," Sudhof told Reuters Health. "A possible positive implication is that our results provide a molecular handle to study the regulation of APP cleavage directly," Sudhof told Reuters Health. Because AD may be caused by an overproduction of amyloid beta caused by too much cleavage of APP, slowing the process may be a way to prevent the disease, he said. In the meantime, scientists will need to figure out exactly how APP cleavage is regulated, which genes are activated and how they relate to AD, if at all. By Suzanne Rostler Reuters Health 7/5/01 Science 2001;293:115-120

UCSD Biologists Identify 548 Genes in the Fruit Fly Likely to Play a Role in Human Genetic Diseases - Biologists at the University of California, San Diego have identified genes in the common fruit fly, Drosophila melanogaster, that appear to be counterparts of genes responsible for more than 700 different genetic diseases in humans. Their discovery provides medical geneticists with a powerful new tool to identify the many genes that may be responsible for a particular human genetic disease and to understand its underlying biochemical mechanisms so that effective treatments can be developed. "Scientists have long known that humans share many similar genes with fruit flies," says Ethan Bier, a professor of biology at UCSD who headed the research." The surprise is how deep these similarities really are. Basically, every category of human genetic disease is well represented with a counterpart in the fly." Knowing which genes in fruit flies are the ancestral counterparts to genes that cause genetic diseases in humans is important to medical researchers for a variety of reasons. "The fly offers an ideal model system in which these genes can be studied," explains Lawrence T. Reiter, a UCSD researcher and the lead author of the paper. "It's a simple genetic system that's well understood, and flies are inexpensive to rear and have a short generation time, enabling us to screen through thousands of individuals to identify mutations in new candidate genes that may have human counterparts that cause disease. All of these things make Drosophila a superior model genetic organism compared to the laboratory mouse." Since genes causing human disease are also likely to function in similar pathways, the fly studies should provide invaluable clues to narrow down the search for genes causing similar disease conditions such as the many inherited forms of AD. PR 6/15/01 Genome Research vol. 11, 6, 1114-1125, June 2001

ReNeuron Delays Cell Transplantation Study - British biotechnology firm ReNeuron Holdings Plc has delayed a clinical study of stem cell transplantation, aimed at developing treatments for diseases like AD, because of problems with recreating cells. A spokeswoman said the firm was looking at a delay of around six months to the Phase I trial, which had been due to start in the third quarter of this year. Stem cells are master cells that, with chemical prompting, can develop into different types of cells such as blood, brain and bone cells and hold promise for treating degenerative diseases like AD and Parkinsons. ReNeuron said in a statement cell lines had not shown "sufficient stability," after the very large numbers of doublings needed for a commercial product. "A number of alternative lines are being developed and evaluated to ensure that the product chosen for Phase I and subsequent clinical trials is sufficiently stable to be used in clinical practice," the company said. Reuters 6/20/01

Caregivers
Stroke's "Other" Victims - The trauma of a stroke can be devastating not only for the patient, but also for the caregiver. Studies have shown that one-third of the caregivers wind up suffering from depression. The stress of having to contend with a new and difficult set of behavior characteristics displayed by the patient and with so much effort rightfully devoted to rehabilitating the patient, the caregiver's needs are often neglected. Tammy Bakas, an assistant professor at the Indiana University School of Nursing who interviewed 32 caregivers of stroke victims, says, "People weren't having too much trouble with the tasks of providing personal care. But dealing with the behavioral and emotional issues were what was difficult for them." It's not uncommon for stroke survivors to experience moodiness, irritability, confusion and memory loss. Danny Chun, a spokesman for the Alzheimer's Association, says the toll of caring for a stricken loved one can also be lethal. "A study in the Journal of the American Medical Association last year found that elderly spouses strained by caregiving are 63 percent more likely to die during a four-year period than others their age," Chun says. "In addition, older caregivers of AD patients are three times more likely to be clinically depressed than others in their age group," he says. Acknowledging and dealing with the problems confronting a caregiver is a major role of the Alzheimer's Association, Chun adds. "One of our key services is providing support groups. In fact, our slogan is, 'Someone to stand by you.' People find great relief in support groups. They share coping strategies and common problems. But it's just the connecting to other people and seeing that they're not alone that is so important." Bakas agrees that support and education are both crucial for all caregivers. To help caregivers of stroke victims, Bakas is involved with Operation Stroke. It's an initiative of the American Stroke Association to develop informational materials for distribution to stroke survivors and their caregivers upon discharge from the hospital. By Nancy A. Melville HealthScoutNews Reporter 7/7/01

UF Researchers: Rural Residents less Apt to Seek AD Care from Family Doctors - People who live in rural areas rely on their family doctors for everything from delivering babies to dealing with heart trouble and fixing broken bones. But when faced with the kind of memory difficulties associated with AD, just a third of older rural residents with problems ask their primary-care health provider for help, compared with half of their urban counterparts, according to a University of Florida researcher. In a new study evaluating patterns of health-care use in six Southeastern states, scientists also found that more than 40 percent of people -- urban and rural -- whose forgetfulness and difficulties with ordinary daily tasks could be signs of AD were not receiving care for such problems. The study results underscore the need for better screening of symptoms, which in turn could lead to improved quality of life for the many currently going without treatment. "The big take-home message of this is that rural people are less likely to use a primary-care physician for memory-related problems although those doctors are going to increasingly be seeing these patients because of the reorganization of health care and managed care," said Neale Chumbler a faculty member in UF's Institute on Aging who is the lead author of the journal article. "It concerns me that primary-care doctors may not be screening in the community or picking up on the early signs or markers of older adults who have memory-related impairments. The fact that 41 percent of those with memory impairments did not seek services is particularly alarming and suggests that a significant proportion of people have unmet needs in terms of detection, diagnosis and management of AD and related dementias," said Chumbler. PR 6/13/01 Journal of Behavioral Health Services and Research 28(2) May 2001

Testing
Study: Forgetfulness May Indicate AD - Depression and repeated forgetfulness may be very early signs of AD and other forms of dementia and could help identify people most likely to develop the illness two studies reported at the World Congress of Neurology in London 6/19/01. Researchers said detecting warning signs of dementia could lead to earlier diagnosis and treatment of the incurable degenerative brain disease that affects 18 million people worldwide. Dr. Ronald Peterson of the Mayo Clinic in Minnesota said forgetting meaningful events, or what is known as mild cognitive impairment, could be one of the very earliest stages of AD. The disease begins years or decades before the clinical process," he told a news conference. "It may be a useful time when we can intervene and keep these people functional." Peterson described mild cognitive impairment as memory loss beyond what would be expected for people of that age and education, but without the confusion of AD. Peterson said several clinical trials involving up to 5,000 people with cognitive impairment are currently under way to determine if drug treatments can improve memory loss and delay the onset of AD. In a separate study, Dr. John Meyer of the Baylor College of Medicine in Houston, Texas, discovered that a certain type of depression in the elderly can be an important early indicator of AD and vascular dementia caused by strokes. Meyer said such depression did not respond to treatment with antidepressants. "People with depressive symptoms show a lack of motivation rather than suicidal intent or depressed thinking. We should consider these signs as an early risk factor for stroke dementia and also for AD,'' he added. Meyer found treatment with a class of drugs called cholinesterase inhibitors improved the memory and behavior of people suffering from depression. By Patricia Reaney Reuters 6/19/01

Axis-shield Says Data Positive for AD Test - British-Norwegian Axis-Shield Plc, which makes diagnostic kits to predict disease, said on 7/5/01 its test for part of the vitamin B12 molecule had shown results which could help in identifying AD. A joint study by Oxford and Bergen universities showed that low blood levels of Holo-TC, the firm's patented test for the biologically active part of the vitamin B12 molecule, were associated with AD, Axis-Shield said in a statement. The study found Holo-TC appeared to be a more effective marker than the vitamin molecule as a whole in assessing the status of B12 in AD. "Low levels of vitamin B12 are believed to be connected with loss of brain and nerve function, dementia and AD, particularly in (the) elderly," the company said. "This is significant news, as it demonstrates that not only is Holo-TC a better parameter of identification of vitamin B12 deficiency than measurement of the whole B12 molecule, but also that poor systemic absorption of the vitamin is associated with AD,'' said Axis-Shield chief executive Svein Lien. Reuters 7/5/01

Nymox's AlzheimAlert Test Featured In Current Issue Of Lab Magazine - Nymox Pharmaceutical Corporation announced 6/21/01 that AlzheimAlert(TM), its clinical laboratory test that aids physicians in the diagnosis of AD, is featured in a new article in ADVANCE for Administrators of the Laboratory. The article, "Shining Light into the Dark," written by Pamela Tarapchak, reviews the current state of laboratory diagnostic tests for AD and emphasizes the need for early and accurate non-invasive tests. One of the laboratory tests highlighted is AlzheimAlert(TM), Nymox's state of the art urine test that aids physicians in the diagnosis of AD. The article quotes Michael Munzar, MD, Medical Director of Nymox, about the need for early diagnosis for AD. Dr. Munzar is quoted as saying that he believes that where AlzheimAlert(TM) is "going to have a tremendous impact is really with the physician because of the length of time that it takes to come up with a proper diagnosis. It can take up to three years from the onset of symptoms for a diagnosis to be made. I think in that time frame, you're probably losing a great window of opportunity to intervene with the patient and treat him or her early. This test can be used as a tool to streamline the physician's approach to AD or to any kind of subjective or objective memory loss." AlzheimAlert uses urine samples to detect the levels of a brain protein called neural thread protein known to be elevated in patients with AD. Nymox offers AlzheimAlert(TM) as laboratory test service for physicians at a cost of $295 through its certified Clinical Reference Laboratory in Maywood, New Jersey. PR 6/21/01

Prevention
High Cholesterol, Hypertension Up AD Risk - Middle-aged individuals with high blood pressure (hypertension) and elevated cholesterol may be at increased risk of developing AD later in life, researchers report. The finding indicates that treating these conditions early could reduce the risk of AD, a form of dementia that is expected to become increasingly common as the population ages, according to Dr. Miia Kivipelto, a research fellow at the University of Kuopio in Finland, and colleagues. "Now we have one more reason to pay attention to proper treatment of hypertension and hypercholesterolemia (elevated cholesterol)," Kivipelto said in an interview with Reuters Health. "Not only do you reduce your chances of, say, heart attack, but you also can reduce your chances of getting AD." "The observed relation between midlife vascular risk factors and AD later in life may have implications for the prevention of dementia as both hypertension and hypercholesterolemia can be treated," Kivipelto and colleagues conclude. By Suzanne Rostler Reuters Health 6/15/01 British Medical Journal 2001;322:1447-1451

Other Items
Penn Study Findings Reverse Key Chronology for Development of AD - It is known that amyloid plaques develop while AD is taking over the brain but still not clinically evident. The most common scientific belief holds that those plaques contribute to or cause the oxidative damage and inflammation that occur and, ultimately, destroy brain cells. Now, a mouse-model study at the University of Pennsylvania School of Medicine has demonstrated that oxidative damage precedes the plaques -- a reversal of existing theory that opens new paths of inquiry in combatting AD. "AD is a very complex disease that does not appear to have a single cause, but our research indicates that oxidative stress is probably a primary event in the course of the illness," said Dr. Domenico Pratico. The primary target of AD is the hippocampus, followed by the frontal and temporal lobes of the brain, all of which can lose between 30 and 40 percent of their neurons as the disease progresses. Pratico and his colleagues studied mice that had been engineered to produce amyloid-beta plaque at a rapid rate. They studied the brains of the engineered animals and a control group at six developmental milestones: four weeks, four months, eight months, 12 months, 15 months, and 18 months. "At seven months, there is 25 percent more oxidative damage in the AD mice than is present in normal mice, and this differential keeps increasing until it is 100 percent higher at 10 or 11 months," Pratico said. "At 12 months, oxidative damage is 200 percent higher" than in the normal mice. In the engineered mice, the plaques were still undetectable at eight months. This opens a lot of interesting hypotheses for therapeutics," Pratico said. "If you reduce oxidative stress in these animals very early, when they are very young, can you prevent the formation of amyloid? And by how much? We know Vitamin E, which is an anti-oxidant, can temporarily slow the progression of AD for some patients. What we don't yet know is what will happen if we suppress, reduce or delay oxidative stress over the long run." PR6/15/01 The Journal of Neuroscience. June 15, 2001, 21(12):4183-4187

AD May Affect Sexual Desire Brain Area - AD may affect a part of the brain that plays a key role in sexual desire, according to findings presented at the World Congress of Neurology in London. W. D. Moller and colleagues, from Nervenheilkunde University, Kiel, Germany, carried out a series of interviews with 38 patients suffering from different types of dementia to find out how their condition affected their sexual desires. They found that 76% of patients with vascular dementia--a decline in mental ability due to blood vessel problems--reported feelings of desire, compared with only 14% of AD patients. Fifty-nine percent of men with vascular dementia said they had had sex in the past 14 days compared with only 29% of men with AD. "This finding suggests that in AD-type dementia, the access to memory which is necessary for initiating sexual desire is specifically disturbed," the researchers concluded. By Richard Woodman Reuters Health 6/19/01

Maintaining Memory - The most important first step is to maintain overall good health. Hypertension, or high blood pressure, and other risk factors for cardiovascular disease-such as diabetes mellitus, smoking, and high cholesterol-threaten brain blood vessels as well. So see your doctor and get treatment for high blood pressure, diabetes, and high cholesterol, if needed. A prudent diet will go a long way to improving cholesterol levels and assuring that you get adequate vitamins and minerals to preserve overall brain function. This means a diet low enough in calories to maintain your ideal body weight, which includes low fat (less than 60 gm. per day, less than 20 gm. saturated fat), 2-4 servings of fruit, three to five servings of vegetables, six servings of bread or grain, and 3 servings of dairy per day, fish twice a week, and red meat limited to once a week. If you need assistance with a diet plan, ask for help from your doctor or a nutritionist. Other advice includes don't smoke, take an aspirin a day..., use alcohol in moderation, take note of medication reactions when taking new drugs, maintain psychological health (see your doctor or a therapist if mental and emotional problems trouble you), talk to your doctor about vitamin/herbal supplements, and stimulate your brain. For brain stimulation you need to actively pursue stimulating your brain throughout your older years. This should be fun and enjoyable, too. All the senses should be stimulated:
Hearing: stimulate your hearing by listening to music and talking with friends.
Vision: stimulate your vision by reading, enjoying art or new sights.
Touch: stimulate your touch sensation by working with your hands at arts and crafts, or in the garden or workshop.
Smell and taste: stimulate your smell and taste sensations by spicing your foods and appreciating the smells of nature.
Motor senses: stimulate your motor senses by physical activity. By Patricia Bloom, MD, St. Luke's-Roosevelt Hospital Center Healthology, Special to ABCNEWS.com 6/21/01 See full article at http://abcnews.go.com/sections/living/Healthology/memory_maintaining.html 

Dementia Among Older Blacks May Be Overestimated - Elderly African Americans may suffer slightly higher rates of dementia than whites, but these estimations may be flawed because past research has failed to take patients' education levels into account when diagnosing them with dementia, Yale researchers report. Tests that determine dementia have often failed to factor in education levels, possibly diagnosing African Americans as having dementia who in reality may simply be severely undereducated, the report indicates. Co-author Dr. Sidney Bogardus, assistant professor of geriatrics at Yale University School of Medicine, New Haven, Connecticut, told Reuters Health, "A lot of the strands of evidence point to differences in education, not just the amount, but also the quality. You can't take two people with different education levels and give them a test and have the test mean the same things." There is evidence that, overall, blacks were more likely to suffer dementia caused by tiny strokes accumulating over time, also known as vascular dementia. Whites were more likely to suffer dementia as a result of diseases such as AD and Parkinson's. By Melissa Schorr Reuters Health 6/6/01 Journal of the American Geriatrics Society 2001;49:477-484.

U.S. Deaths From Heart Disease, Cancer Fall - Fewer Americans are dying from heart disease and cancer, the two leading causes of death in the US, according to figures released on 6/26/01 by the Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia. Based upon a methodological change in the way several diseases were classified, federal officials also expressed concern about several other conditions, such as AD. This is because a new classification system resulted in a significant shift in the ranking of AD. The CDC adopted the 10^th International Classification of Diseases (ICD) which caused a number of AD-type dementias to be listed as AD. In 1998, AD ranked 12th among the leading causes of death, but jumped to 9th due to the inclusion of patients suffering from "presenile dementia." "The new data on AD mortality adds to our understanding of the magnitude of this serious problem," Edward Sondik, director of the CDC's National Center for Health Statistics, said in a statement. "It is through improvements in our system that we're able to more accurately measure the impact of this disease and others on our citizens." As a result of the new classification, the 44,507 deaths attributed to AD in 1999 (up from 22,000 in 1998) actually surpassed the totals of other major causes of death, including motor vehicle accidents and breast cancer, the report revealed. Reuters Health 6/26/01 National Vital Statistics Reports Vol. 49, No. 3, 6/26/2001 A full copy of the CDC report is available on the agency's Web site at www.cdc.gov/nchs in the form of 49 page Pdf file

Painter's Artwork Charts AD's Decline - The initial symptoms of AD come on slowly, making it hard to look back and know just when an individual's mental decline began. In the case of an artist, though, the course of AD can be documented in the art itself. UK doctors report on the case of 66-year-old William Utermohlen, an American artist who moved to England in the 1950s. At the age of 61, he was diagnosed with probable AD. To see how the artist's medical condition could have influenced his work, Dr. Martin N. Rossor and his colleagues at London's Institute of Neurology examined paintings and drawings he created from age 60 on. Utermohlen's work at this time centered on self-portraits, and his doctors were able to chart changes in his style that reflect changes in his mental functioning due to AD. For example, they write, a portrait done at age 62 reveals the earliest signs of difficulty in creating individual facial features and spacing them accurately. By age 64, Utermohlen was producing facial features that were "blurred together or strangely disjointed"--changes he and his wife told the doctors were not a shift in artistic style. At age 65, the authors write, their patient's work had grown more abstract because the realism of his earlier art was "no longer attainable." Besides these changes in skill, Rossor's team notes, "the themes of depression or anxiety are apparent particularly in the later self-portraits." Yet despite these artistic changes, the fact that Utermohlen continued to work suggests AD spared his artistic drive, according to the authors. This shows that creativity and technical skills may not be equally affected by brain disease, the report indicates. "This example of continued artistic endeavour at a stage when AD has blunted the craftsman's most precious tools offers a testament to the resilience of human creativity," Rossor and colleagues conclude. Reuters Health 7/3/01The Lancet 2001;357:2129-2133 6/30/01

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