Alzheimer Related News Items

News as of 11/09/02

For more info on these abstracts write/call Ed Cabic (edcabic@comcast.net or 410-992-7197)

NOTE - e-mail address change to new address as of 2/02

For more AD information, see Alzheimer Information athttp://www.connext.net/~seniors/infoad.htm

Copies of these reports are posted there

This web page was started at the Florence Bain Senior Center in Columbia MD

Top Items

Researchers Still Hopeful for AD Vaccine - Progress toward an vaccine suffered a major setback earlier this year when a clinical trial was halted after some patients developed brain inflammation, but a follow-up report indicates that the vaccine was in fact targeting the brain-clogging plaques involved in the disease. And another new study found that a modified form of the vaccine having just residues 4-10 of amyloid β42 worked in mice without causing the worrisome brain inflammation, raising hopes that a safe, effective vaccine for people could still be on the horizon. Both vaccines stimulate the immune system to produce antibodies against the beta-amyloid protein found in the plaques. But the modified vaccine relies on a smaller portion of the beta-amyloid protein than was used in the original vaccine. The modified vaccine was designed with the intent of avoiding the inflam-mation seen in 15 of 360 patients with mild to moderate AD who received the original vaccine. In their research, Dr. JoAnne McLaurin, an assistant professor at the Centre for Research in Neurodegenerative Diseases at the University of Toronto in Ontario, Canada, and colleagues found that mice given the modified vaccine developed antibodies that helped fight plaque, and no brain inflammation occurred. Besides leading to a potential vaccine for people, the researchers said the findings could potentially be used to develop a drug that would mimic the effects of the vaccine but would not require immunization. It is not clear why some of the patients in the first human trial developed brain inflammation, but the investigators of that study are trying to determine the explanation and make modifications to render the vaccine safe. In the new analysis of two dozen patients who received the vaccine in Switzerland, the researchers found that the vaccine was working against beta-amyloid but was not attacking normal brain cells. By Jacqueline Stenson Reuters Health 10/14/02 Nature Medicine Nov. 2002, vol. 8, No. 11, pp 1263-1269, 1270-1275

For more on this story see http://www.alzforum.org/new/detail.asp?id=679 for “The Alzheimer's Vaccination Story, Continued” at the Alzheimer Research Forum web page.

First Long-Term Head to Head Study Shows Superiority of Reminyl(TM) Over Donepezil in Patients With AD - At the 6th Congress of the European Federation of Neurological Societies in Vienna, Shire Pharmaceuticals Group plc 10/29/02 presented data with Janssen-Cilag Ltd which shows that over one year, Reminyl (galantamine) has a superior treatment profile compared to donepezil (Aricept (R)) when treating patients with AD. This is the first one-year head to head study of the two drugs. Results of the long-term, rater-blinded, randomized study conducted in the UK show that in two assessments of AD patients, those treated with Reminyl had statistically superior scores on measures of cognition and attention compared to those treated with donepezil. Reminyl was shown to significantly improve a patient’s attention within six weeks of commencing treatment, using a validated computerized test for assessing cognitive performance. These computerized assessments, by the independent company, Cognitive Drug Research (CDR), measure a patient’s reaction times and showed that patients taking Reminyl significantly improved their choice reaction times (CRT) compared to donepezil patients after only six weeks of treatment. At 52 weeks, Reminyl patients’ CRT had been maintained at baseline levels. Patients treated with donepezil had no significant changes in CRT throughout the study. The improvements in attention, as measured by the computerized tests for patients taking Reminyl, are thought to be due to its action on nicotinic receptors. “Reminyl is different to other acetylcholinesterase inhibitors (AChEIs) because it increases the levels of acetylcholine by two separate mechanisms. As well as inhibiting acetylcholinesterase, it has also been shown to enhance activity of nicotinic receptors,” says Dr Roger Bullock of the Kingshill Research Centre, Swindon. “Nicotinic receptors are known to be important in maintaining attention and concentration. These results demonstrate the importance of Reminyl’s dual mode of action.” PR 10/29/02

Pfizer For Living Share Card Program - Until Congress designs a long-term solution for America’s Medicare patients, the prescription drug industry is working to bridge the gap. For example, Pfizer, a leading pharmaceutical company, has developed the Pfizer for Living Share Card program. It’s a health benefit program that so far has provided more than 242,000 low-income seniors with 795,000 Pfizer prescriptions for a flat fee of $15 per prescription. “The Share Card program is designed to help seniors take charge of their personal health by providing them with access to the medicines and health education information,” said Forest Harper, vice president for Pfizer Share Card. “Through the Share Card program, we are committed to helping seniors lead happier, healthier and longer lives,” he said. Seniors are eligible to receive an up to 30-day supply of each Pfizer prescription medicine for a flat fee of $15. There is no enrollment fee for the Share Card program, and it covers most Pfizer medicines, including some of the most widely prescribed therapies for high blood pressure, high cholesterol, diabetes, AD and depression. To qualify for a Share Card, applicants must: (1) Be enrolled in Medicare and have a gross income of less than $18,000 (for a couple, the total gross income must be less than $24,000) (2) Have no prescription drug coverage and (3) Be ineligible for Medicaid or any other drug benefit plan funded by the state in which the senior lives. In addition, Share Card members have access to a 24-hour, toll-free telephone help line with live operators to assist with enrollment requests and application materials. Callers may also request free, easy-to-read health education information on 16 common medical conditions associated with aging. Those who are eligible to join the Pfizer for Living Share Card Program, or have a family member, friend or neighbor who may be eligible, can call for an application at the toll-free hotline, 800/713-3990. PR 11/8/02

OHSU Takes Part in Unique AD Treatment Trial - Researchers at Oregon Health & Science University are taking part in a multi-center, national clinical trial aimed at preventing the progression of dementia and AD. The trial involves using a drug named LY450139, which in mouse models is shown to inhibit an enzyme implicated in the formation of beta-amyloid deposits in the brain. These deposits, also called plaques, may be responsible for brain cell death and decay, and have been connected to AD. A total of six sites in the United States are taking part in the clinical trial. “If the drug is successful, we expect to see a rise in amyloid levels in the spinal fluid,” said Jeffrey Kaye, M.D., an investigator and director of the Alzheimer’s Research Center at OHSU. “This increase would be due to the breakup of amyloid deposits in the brain. So far, most research has centered on treating the symptoms of AD. This is one of the few trials in the country aimed at stopping the progression of AD by preventing brain cell death. If this approach is successful in people with established AD, then, in the future, this compound may also have the ability to prevent or delay onset of the disease.” PR 10/16/02

Nymox U.S. Patent Issued For Statin Drugs For AD - Nymox Pharmaceutical Corporation announced 11/1/02 its U.S. patent No. 6,472,421 has issued for the use of statin drugs for the treatment and prevention of AD. “This patent gives Nymox an important stake in a potentially very valuable new market for statin drugs. Statins represent an exciting new approach to the prevention and treatment of AD,” said Dr. Michael Munzar, Medical Director of Nymox. “They have a well-established safety record and are widely available.” Claim 1 of the patent reads as follows. “A method for treating, preventing, or reducing the risk of AD in a patient who has one or more risk factors for AD, comprising administering to a patient in need thereof a therapeutically effective amount of one or more inhibitors of the enzyme 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG CoA) reductase, wherein: (a) the HMG CoA reductase inhibitor is not simvastatin, (b) treatment results in a reduction or inhibition of onset of AD, (c) the one or more risk factors are selected from the group consisting of hypercholesterolemia, coronary artery disease, family or previous history of coronary artery disease, hypertension, diabetes, cigarette smoking, cerebrovascular disease, cardiovascular disease, elevated serum cholesterol, heart disease, and male gender, and (d) the patient to be treated does not possess the APOE 4 gene.” PR 11/1/02 Full copy of the patent is available for free at http://164.195.100.11/netahtml/srchnum.htm - just type the patent number in the querry

 window.

Recall Tricks Can Help Memory in AD Patients- Some AD patients can be taught to associate names with faces, suggesting they may be able to improve their memory even as the disease attacks their brain. A new study by British researchers has found that standard face-recognition coaching used to help brain injury patients also works in people with dementia linked to AD. The effects don’t seem to benefit other areas of memory besides the specific task drilled -- in this case, identifying people. Nor are the effects enhanced by drugs that can slow the progression of the disease, a puzzle to the researchers. Still, the scientists say the findings should be encouraging, not only to psychologists but to people who care for AD patients. Linda Clare, a psychologist who led the study, says that while the gains were “quite modest in a way, they could be quite important” for people with early dementia, especially since they become easily discouraged by their worsening memory woes. She and her colleagues studied 12 men and women with early stage dementia consistent with AD. They drilled each volunteer for up to an hour once a week for six weeks, each time showing them a different picture of a famous person or someone from their social circle. To prompt their memory, they used mnemonic devices and other techniques. The researchers then tested the subjects on their recall after a month, and then periodically throughout the following year. At the start of the study, the subjects couldn’t remember even one face. But after the training sessions, they were able to recall an average of about three faces each, the researchers say. Their ability to remember other items was basically unchanged. Ten of the 12 volunteers improved at least somewhat as a result of the coaching. However, those on medication for the dementia did no better than those not taking drugs. Clare calls that “a bit of a surprise,” and adds she would have expected that drugs would augment the drilling. “I think that we need some more research to really see what’s going on there,” she says. By Adam Marcus HealthScoutNews Reporter 10/21/02 latest issue of the journal Neuropsychology, 2002. Vol. 16, No. 4, 538-547

Testing

AD and Cholesterol - Proof of a connection between AD and high cholesterol levels could change the way doctors counsel their older patients, researcher Rudolf Tanzi reported 10/15/02 at the American Association for the Advancement of Science (AAAS). If additional evidence confirms the AD-cholesterol connection, genetic testing of patients with high cholesterol levels may help doctors diagnose AD at earlier stages, said Tanzi, a professor of neurology at Harvard Medical School. “In the past, I would have said no to the test, but if it can be shown that high cholesterol predisposes a person to AD, I’d be willing to suggest testing for AD risk,” Tanzi said during the AAAS Advancing Science seminar. “That’s empowering you to change your lifestyle. If you can’t empower someone, especially with a test for AD, then you might make someone falsely confident or falsely anxious.” PR 10/16/02

Blood Copper Levels Higher in AD -Individuals with AD may have elevated blood levels of copper, a mineral that is necessary for survival but may cause brain cells to "rust" when levels are high. The findings suggest that copper may be a useful measurement in the diagnosis of AD, a neurodegenerative disorder whose symptoms include memory loss and dementia. There is currently no diagnostic laboratory marker for the memory-robbing disease, Dr. Rosanna Squitti from AfaR-Ospedale Fatebenefratelli in Rome, Italy, told Reuters Health. “Such a marker would help with early diagnosis and provide the opportunity to start treatments promptly,” she said. Squitti and colleagues from the University Campus Biomedico measured blood levels of various compounds associated with AD in 79 elderly patients with the disease and 76 healthy adults the same age. The copper levels were 54% higher among patients. Individuals with higher blood levels of copper also performed poorly on tests of immediate and delayed recall. AD patients were also nearly 4 times more likely to have the Apo e4 gene, which was associated with decreased antioxidant capacity. Antioxidants are compounds in the body that neutralize disease-causing substances known as free radicals. While free radicals are normally present in the body, they can contribute to oxidative damage associated with heart disease, some forms of cancer, and possibly AD. The results of the study support the idea that oxidative damage caused by copper may contribute to cell death seen in patients with AD, Squitti said in an interview. They also support previous findings linking Apo e4 with higher blood concentrations of copper. The cause of AD is not known, but deposits of beta-amyloid protein build up inside the brain of people with AD, and the formation of these plaques may somehow be involved in the development of the disease. More and more research suggests that minerals such as copper, iron and zinc may be involved in the formation of these plaques. “Neurodegeneration in AD may stem from copper-mediated toxicity,” the study concludes. By Suzanne Rostler Reuters Health 10/28/02 Neurology 2002;59:1153-1161

Prevention

“Good” Cholesterol Helps Very Old Keep Their Smarts - While it’s well known that high levels of “good” cholesterol reduce a person’s risk of heart disease, experts now report that maintaining high levels of high-density lipoprotein (HDL) may also help the very old stay sharp. “Among the many effects of plasma HDL, it recently became apparent that it protects from decreased cognitive function associated with AD and other forms of dementia,” write lead author Dr. Nir Barzilai and colleagues at the Albert Einstein College of Medicine in New York City. What’s more, the authors point out that people living well into their 90s and beyond age 100 tend to have higher levels of HDL. Children of centenarians also have relatively high HDL levels. In the current study, Barzilai’s team sought to determine whether high HDL levels might be linked to mental ability in the very old. Blood levels of HDL “correlated significantly” with how well a person performed on a test of mental abilities, the authors report. Good cholesterol may help keep the blood vessels functioning properly, reduce inflammation and help support brain cell function in other ways, they note. “Our findings help to emphasize the beneficial and protective effects of increased plasma HDL,” Barzilai said in a prepared statement. “It is clear from the data we collected that increased HDL levels play an important role in maintaining superior cognition in longevity.” Reuters Health 11/6/02 The Journal of Gerontology 2002;57A

Treating High Blood Pressure May Stave Off Dementia - Medications to lower blood pressure may help stave off dementia and AD two new studies show. One, a large European trial, found that anti-hypertensive medications reduced the risk of dementia by 55% among patients who initially had high blood pressure. A second study published in the same journal found that blood-pressure lowering drugs were associated with a decrease in the risk of mental decline in elderly African Americans. “It is important to make the point that, increasingly, the medical-scientific community is recognizing that common cardiovascular risk factors - - such as high blood pressure, high cholesterol and diabetes - - are predictive not only for the development of vascular dementia, but also for AD, the more common form of neurodegenerative dementia,” Dr. Jan Staessen, the European trial’s co-author, said in an interview with Reuters Health. Staessen is a researcher with the University of Leuven in Belgium. Staessen and his colleagues determined that the drugs protected best against AD. “The majority of dementia cases prevented would have been AD,” he noted. While Staessen and his colleagues aren’t yet sure why the blood-pressure lowering drugs help, he’s got some ideas. “Two explanations for our findings are possible,” he said. “A small difference in blood pressure persisted during most of the follow-up between patients initially randomized to placebo and active treatment - - blood pressures were lower in the active treatment group. So lower blood pressure might explain the better outcome.” But not all studies have shown that anti-hypertensive medications reduce the risk of mental decline, he added. An alternative hypothesis, he said, is that one of the medications, a calcium-channel blocker, might offer specific protection against AD. “Laboratory experiments have shown that intracellular calcium plays an important role in causing the death of brain cells,” Staessen added. Studies have also shown that the calcium channel blocker used in the study can enter the brain and “bind to receptors in those areas of the brain affected by AD, and that it can restore the neurotransmitters that become deficient in AD." By Linda Carroll Reuters Health 10/14/02 Archives of Internal Medicine 2002;162: 2046-2052, 2090-2096

Study Ties Fish-Rich Diet to Lower Dementia Risk - French researchers at the Universite Victor Segalen Bordeaux found that among the elderly adults they studied, those who regularly ate fish and other seafood at the study’s start were less likely than others to develop dementia - - including AD - - over the next 7 years. The findings do not prove that fish has a direct effect on dementia risk, and the study authors point out that the fish eaters’ relatively higher education partly explain the connection they found. However, they also note that the healthful fatty acids in fish could have brain-protective effects. Participants who ate fish or seafood at least once a week were found to be 34% less likely than less-frequent fish eaters to develop dementia over 7 years. When the researchers factored in education levels, the fish-dementia association weakened somewhat, however. “The ‘protective’ effect of weekly fish or seafood consumption was partly explained by higher education of regular consumers,” Dr. Pascale Barberger-Gateau’s team writes. A number of studies have suggested that people with higher education may be less vulnerable to memory loss and mental impairment as they age because they have what is called a greater “brain reserve.” However, factors that harm cardiovascular health, such as high cholesterol and high blood pressure, have also been tied to AD risk. And one form of dementia called vascular dementia results from an inadequate blood supply to the brain. The French researchers note that fish fatty acids could be involved in dementia risk by protecting vascular health--or, alternatively, by reducing inflammation in the brain. Reuters Health 10/25/02 British Medical Journal 2002;325:932-933.

A Fitness Guide for the Brain - In a new book “Saving Your Brain,” by Dr. Jeff Victoroff, Bantam Books, $25.95, Dr. Victoroff’s “adventure in neuroprotection” is based on the premise that genes alone are not brain destiny and that billions of external influences and dozens of lifestyle decisions also have profound effects on the health of the brain. Apart from some of the more familiar remedies he offers - - a more natural diet, physical activity, controlling stress and blood pressure - - he advises readers to “avoid head trauma like the bubonic plague,” citing some evidence that has found a high rate of past head trauma in AD patients. Dr. Victoroff’s vision of the future is optimistic: replacement parts for “broken brains” routinely inserted, “smart drugs” and a revolution in the treatment of strokes. But until then, he advises pursuing “the pleasures of the learning-nourished mind,” but not with “dull mental exercises.” By John Langone NY Times 10/8/02

Beer, Wine May Influence Dementia Risk - They say you are what you eat, and new research suggests that how well your mind works into old age could also be influenced by what you drink. Dr. Thomas Truelsen of the Institute of Preventive Medicine in Copenhagen and his colleagues found that people who drank beer--even as infrequently as once per month--were more than twice as likely as non-beer drinkers to experience a deterioration in mental functioning, known as dementia, after age 65. In contrast, people who drank wine weekly were 70% less likely than wine-abstainers to develop dementia after age 65. Regular consumption of spirits appeared to have no effect on dementia risk, the authors report. However, Truelsen explained to Reuters Health that further research is needed before doctors can safely recommend that people drink wine to stave off dementia. The precise amount of alcohol that the study participants consumed throughout their lives is not clear, he noted, and, for some, drinking alcohol can do more harm than good. “I’m not saying that people should drink wine,” Truelsen cautioned. Truelsen and his team found that 83 men and women out of the 15 year study of 2000 people had developed dementia, while another 1,626 remained dementia-free. Comparing mental function to drinking behavior, the researchers found that people who regularly drank beer, at any frequency, were more than twice as likely to develop dementia in old age. However, people who drank wine weekly were 70% less to develop later mental impairments, and monthly wine drinkers saw a 60% drop in dementia risk. Daily wine drinkers were no less likely than non-wine drinkers to develop dementia in old age. The authors presented their findings in New York 10/14/02 at the 127th annual meeting of the American Neurological Association. The study cannot prove that wine intake prevents dementia--some other lifestyle factor could be responsible for the association. However, Truelsen explained in an interview that red wine contains substances known as flavonoids, antioxidants that help protect blood vessels from harmful substances called free radicals. Free radicals are naturally occurring particles that have been linked to AD and vascular dementia, a type of dementia that results from a reduction in the supply of blood to the brain. He emphasized that the present study is not meant to encourage people to drink wine, but rather to help inform the debate regarding the potential health benefits of antioxidants and encourage further studies. By Alison McCook Reuters Health 10/14/02

Ginkgo May Improve Memory of Dementia Patients - Britain’s Alzheimer’s Society said on 10/14/02 that a major review of clinical trials provided “promising evidence” that dietary supplements containing the herbal medicine Ginkgo biloba can improve memory and function in people with dementia. The extract from the leaves of the Chinese ginkgo tree is widely advertised for a variety of conditions including memory loss, but scientific evidence on its effects has often been conflicting. The Society said researchers at the Cochrane Collaboration in Oxford had reviewed 33 clinical trials and concluded that the remedy appeared to be safe with no excessive side effects. “Many of the early trials used unsatisfactory methods, were small, and we cannot exclude publication bias. But overall there is promising evidence of improvement in cognition and function associated with Ginkgo,” it said in a statement. It announced that a large placebo-controlled study on 400 people with dementia would now be carried out by Imperial College and the Royal London Homeopathic Hospital to find out the size and mechanism of the treatment effects. Dr. James Warner, at Imperial College London, said: “The medicinal effects of Ginkgo are believed to be gained by causing blood vessels to dilate, improving blood flow to the brain, and through thinning the blood and making it less likely to clot. Ginkgo probably also has some antioxidant effects, protecting nerve cells against biological ‘rusting.’ All of these effects would suggest that Ginkgo might slow down a degenerative process.” By Richard Woodman Reuters Health 10/14/02

Hormone Replacement/Estrogen

Long-Term Hormone Therapy May Reduce AD Risk for Women - Women who take hormone therapy after menopause and continue with it for 10 years or more may have a reduced risk of AD, researchers report. But scientists, including the study’s lead investigator, caution that the study’s findings are suggestive, not definitive, in part because of the study’s design and because relatively few women who took part developed the disease. For now, medical experts say, there is not enough evidence to tell women, even those at high risk of AD, to take estrogen to lower their risk. The AD study, by Dr. John C. Breitner of the Veterans Affairs Puget Sound Health System and his colleagues, involved 1,357 elderly men and 1,889 elderly women living in Cache County, Utah. The researchers questioned the study participants and gave them memory tests for AD. Three years later, they tested them again. During that time, 35 men and 88 women developed AD. Using statistical modeling, the investigators concluded that estrogen might cut a woman’s risk in half, but only if she took it for 10 years or more. Dr. Breitner emphasized, however, that his study “does not rise to the level of evidence that would warrant physicians prescribing hormone therapy for this indication or for women to start using it for this indication. AD studies, however, have had conflicting results. Animal and laboratory studies indicated that estrogen might protect the brain. But clinical studies have failed so far to make the case. Dr. Breitner said his findings might explain the previous studies by positing that there is a critical period, years before AD symptoms emerge, when a woman must take estrogen if she is to reduce her risk. “What’s new here is that the benefits, if there are any, are delayed a long time after treatment,” Dr. Breitner said in a telephone interview this week. He explained, however, that his study observed whether women who chose to take estrogen were less likely to develop AD disease. One problem is that women who take hormones after menopause are different from those who do not take the drugs. Hormone users tend to be more educated, for example, and healthier. Some of the very features that make them likely to take hormone therapy are also features that, independently, are associated with a lower risk of AD. Scientists use statistical adjustments to try to correct for the differences between hormone users and nonusers, but they can never be sure they have succeeded. “The danger is that it is not the use of hormones that is driving this relationship, but it is being the kind of woman who uses hormone therapy,” Dr. Breitner said. “There is no way you can get around that except by doing a randomized controlled trial,” in which women are randomly assigned to take, or not take, the drugs. Such studies of estrogen and AD risk are now under way. By Gina Kolata NY Times 11/6/02

Animal Studies Prove Hormone Replacement Therapy Improves Memory, Report Pitt Researchers - For estrogen to enhance learning and memory, nerve cells in the brain called cholinergic neurons are essential to the process, suggest animal studies performed by researchers from the University of Pittsburgh School of Pharmacy. “Estrogen replacement in postmenopausal women has important effects on mood and cognition. This research was focused on trying to understand what estrogen does in the brain to reduce the effects on brain aging and cognitive decline,” stated Robert Gibbs, Pharm.D., associate professor of pharmaceutical sciences at the University of Pittsburgh School of Pharmacy. In the study, rats had their ovaries removed and some of the animals had specific cholinergic neurons destroyed. A few weeks after surgery, most of the animals were put on estrogen replacement therapy (ERT), while some were not. Four weeks after ERT, the animals were placed several times in a maze to test their memory and performance. Rats that had their ovaries removed with subsequent ERT outperformed rats on various tasks without ERT. The ability of estrogen to enhance performance was lost in animals that had specific cholinergic neurons removed. “This tells us that the cholinergic neurons are necessary for estrogen to enhance performance in this model,” explained Dr. Gibbs. “We have shown, as in previous studies, that acute and short-term estrogen replacement can significantly enhance the functional status of cholinergic neurons. These results give us hope that estrogen may help to significantly reduce the risk of AD-related dementia in postmenopausal women, possibly by affecting these cholinergic neurons,” added Dr. Gibbs. “The study also suggests why starting estrogen after dementia has developed is ineffective. For estrogen to work, the neurons must be alive and working,” stated Dr. Berga. “I would hesitate to say that these results extend to humans, but the findings are encouraging because they help pinpoint a specific biological effect that may underlie beneficial effects on cognitive performance,” concluded Dr. Gibbs. PR 11/5/02 November 2002 issue of Hormones and Behavior

Rat Study Suggests Estrogen May Worsen AD - The results of a new study in rats suggest that estrogen replacement therapy may hinder - - not help - - memory in older women with AD. In the study, rats had their ovaries removed - - putting them into a low-estrogen state similar to menopause - - and given a drug to stimulate brain inflammation, which occurs in patients with AD. The researchers found that these rats actually fared worse on memory tests when they received steady doses of estrogen. The findings add to a growing body of research demonstrating the potentially negative effects of ERT, long thought to protect women against certain age - related changes. While estrogen may protect certain women from memory loss, it may not be beneficial for those with brain inflammation, which occurs in patients with AD. “Our results suggest that chronic ERT in postmenopausal women may exacerbate the memory impairment induced by the presence of chronic neuro-inflammation associated with AD,” Dr. Gary L. Wenk and colleagues from the University of Arizona in Tucson, conclude. In an interview with Reuters Health, Wenk stressed that future studies will need to investigate whether synthetic estrogen has the same effect when it is given in fluctuating levels, similar to what occurs before menopause. Such a therapy may provide a more effective way to slow the progression of AD and other age-related memory changes. “We want to try to reproduce hormonal fluctuations between estrogen and progesterone as much as possible in rats to try to mimic the conditions that existed previously in rats and in women, he said. By Suzanne Rostler Reuters Health 10/29/02 Behavioral Neuroscience 2002;116:902-911

Other Items

Immune System May Help, Harm AD Patients - Patients with AD accumulate plaques - -clumps of dead cells and a sticky protein called beta-amyloid. “The brain needs to get rid of that stuff,” said Dr. James O. McNamara, chairman of the department of neurobiology at Duke University in Durham, North Carolina, in an interview with Reuters Health. And one of the ways the brain does this is to use “complement” which is a collection of about 30 proteins used by the body to wipe out invaders, such as bacteria. Activating the complement system results in a chain reaction, with the final result being the destruction of cells. Complement normally circulates around the body in the blood and generally doesn’t appear in the brain. But when a person develops the plaques associated with AD, the brain cells start to make complement to mop up the neuronal debris, McNamara said. The problem, McNamara said, is that complement can get out of hand if the AD patient suffers any other kind of damage to the brain--and that damage can include anything from a minor stroke, to a series of seizures or even a head injury. Complement, McNamara explained, does its job in two parts. The first part is good for a brain damaged by AD. The second part is usually shut off by certain defenses mounted by the brain cells. But when the brain suffers an injury, such as a stroke, it releases a substance called glutamate which somehow blocks the natural defenses of the cells to the second part of the complement process and brain cells die. Thus, when the complement goes through both parts of its process, it makes a hole in the membrane of the cell, McNamara said. “It’s a huge one and it allows ions and water to flow into the cell,” he added. “And the cell basically falls apart.” The key, McNamara said, is to remember that the complement is not the primary problem but the way the brain appears to be defending itself against AD. It’s possible that some kind of medication could be devised to block the second part of the complement process from taking place, he added. By Linda Carroll Reuters Health 10/23/02 Neuron 2002;36:363-374
 

Brain Fluid Drain with Shunt Studied as AD Therapy - An investigational treatment designed to improve the circulation of the fluids bathing the brain and spine could be a feasible therapy for AD, results of a pilot study suggest. However, researchers at Stanford University in California caution that it is too early to say whether the therapy - - in which an implanted shunt drains small amounts of cerebrospinal fluid (CSF) from around the brain - - will become a weapon against AD. CSF fills the spaces around the brain and spinal cord, and it is naturally produced, absorbed, then replenished by the body. With age, however, this normal CSF circulation diminishes. The experimental shunt therapy is based on the hypothesis that helping CSF drain from the skull might shuttle away proteins associated with AD brain damage. Dr. Gerald D. Silverberg and his colleagues compared 15 AD patients who had a shunt implanted with 14 who did not have the surgery. They found that over 1 year, mental functioning scores remained fairly stable among the shunt patients, but declined among the other study participants. The investigators point out that the study was too small to conclude that the shunt actually slowed patients’ mental deterioration. However, they did detect changes in the levels of tau and amyloid beta in the CSF drained from patients’ brains--suggesting, Silverberg’s team explains, that improving CSF circulation may help slow the progression of AD by boosting the clearance of substances toxic to the brain. According to Silverberg’s team, a larger clinical trial of the shunt therapy is now under way. Reuters Health 10/25/02 Neurology 2002;59:1126-1127, 1139-1145

Alzheimer’s Association Names Sheldon Goldberg President and CEO - The Alzheimer’s Association has named long-term care advocate Sheldon Goldberg president and chief executive officer. Goldberg, 55, joins the association Dec. 1. “Sheldon Goldberg is an exceptionally dynamic, innovative, charismatic and visionary leader who is passionate about the potential of the Alzheimer’s Association,” said Orien Reid, chair, Alzheimer’s Association’s national board of directors. “He believes consensus is built when all parties are beneficiaries, and he recognizes that it takes creativity to find as many win-wins as possible.” PR 10/22/02

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