Alzheimer Related News Items
News as of 6/09/02
For more info on these abstracts write/call Ed Cabic (edcabic@comcast.net or 410-992-7197)
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Top Items
An Early Sign of AD Brings Fear, and New Insight - Mild cognitive impairment (MCI) is a new term having entered the vocabulary of memory specialists in the late 1990 's. It is usually the first sign of AD. Now more and more doctors, combining tools as sophisticated as brain imaging and as simple as a short test of word recall, are making the diagnosis. Researchers and drug companies say the new category will enable them to track the progression of AD and understand it better. They are already testing a wide array of treatments in these patients - - from vitamins to hormones to new drugs as well as drugs already approved for AD. "If we in fact can intervene at this earlier stage and alter the course of the disease, that would have a big impact on quality of life," said Dr. Ronald Petersen, who directs AD research at the Mayo Clinic in Rochester, Minn. The signs of mild cognitive impairment are an inability to form memories for events that just happened and a slight shrinking of the hippocampus, the area of the brain where these memories are laid down. On a memory test, a patient may be able to repeat a string of unrelated words - -red, Oldsmobile, cabbage -- but then fail to recall even one of them 10 minutes later. Mild cognitive impairment may be caused by other disorders, especially depression. But when no such cause is found, it has been shown in studies to lead to full-blown AD, with its additional impairments in reasoning and thinking, in at least 80 percent of cases. Many with MCI take drugs that have been approved for AD or take substances like vitamin E that researchers hope might help. But for now, Dr. Petersen said, "there have been no clinical trials that demonstrate that anything works or doesn't work -- they are all under way." By Gina Kolata NY Times 6/2/02

Cardiovascular Disease Leads to Higher Risk of Dementia - People with cardiovascular disease have an elevated risk of developing dementia, including both AD and vascular dementia, according to a study by Anne B. Newman, M.D., M.P.D., a geriatrician at the University of Pittsburgh School of Medicine and an associate professor of medicine and epidemiology, which she presented May 9 to the annual meeting of the American Geriatric Society. "We found that those with cardiovascular disease had an increased risk of dementia of about 30 percent, only partially explained by stroke," Dr. Newman said. "Although the relative risk was moderate, the high prevalence of cardiovascular disease coupled with the high risk of dementia in older adults would suggest that prevention of cardiovascular disease may be the most effective preventive measure we have for the prevention of dementia." Dr. Michael Freedman, director of the division of geriatrics at New York University Medical Center commented on the study. "This study is exciting because it's getting closer to the idea of who to treat and what to treat," Freedman said. "I see this in my office every day. A perfectly healthy 75-year-old with high blood pressure and cholesterol walks into my office. Do you treat it?" Freedman asks. "Just thinking logically, they're 75 and perfectly healthy, we'll just leave you alone. But, on the other hand, all the data is beginning to show that if you take a perfectly healthy 75-year-old and don't do anything, they have an increased risk of AD by the time they're 85. If you treat them, you may push off the onset until they're in their 90s, and by then most of us aren't around. This is another bit of evidence that it makes a difference." PR 5/9/02 and Amanda Garder HealthScoutNews 5/9/02

Drugs
New Drug Offers Novel Approach to AD - A new drug that eliminates a natural protein in the body (SAP or serum amyloid P component) could pave the way for better treatments for AD and type II diabetes, scientists said on 5/15/02. Illnesses such as AD develop when normal proteins fold in an unusual way and form clumps called amyloid deposits that damage tissue and organs. After screening 100,000 compounds, Professor Mark Pepys and researchers at University College Medical School in London discovered a drug that removes a protein called SAP in the blood that sticks to the clumps and prevents the body from breaking them down. When they tested it on 19 patients with a disease called systemic amyloidosis, a rare illness in which the clumps form in different organs in the body, it completely removed the protein and reduced the disease-causing amyloid deposits. "We have developed a powerful new drug for which there is much evidence it may be helpful in treating systemic amyloidosis and possibly also AD," Pepys told Reuters. The drug targets SAP and prevents it from attaching to the amyloid deposits, allowing the body to get rid of them. Pepys and his team believe the drug may also be able to help remove amyloid deposits that occur in AD and type II, or adult onset, diabetes. "In AD and type II diabetes there is a universal association of amyloid deposition with progression of the disease, but it is not proven that the amyloid deposits actually cause the disease," Pepys explained. It is also not clear whether the amyloid deposits cause the loss of brain cells and the dementia that AD patients experience. Pepys plans to begin testing the drug on AD patients. "It is a potential treatment for AD because if our idea is right -- that removal of SAP promotes disappearance of the amyloid deposits -- this ought to happen in the patients with AD as well," he said. The drug, which Pepys said produces no side effects, completely removes SAP from the circulation and does not need to get into the brain to work. By Patricia Reaney Reuters 5/15/02 Nature 2002 May 16; 47(6886): 254-9

Drugs Could Be Delivered to Brain via the Nose - Nasal sprays are routinely used to treat conditions that affect the respiratory system such as allergies and nasal congestion, but new research suggests that it may be possible to deliver medication directly to the brain by way of the nose. For the first time in humans, a nasal spray was used to deliver hormones directly to the brain without entering the bloodstream, reports an international team of scientists led by Dr. Jan Born at the University of Lubeck in Germany. Although the technique is in the early stages, eventually it may be possible to treat brain diseases and even obesity with nose sprays that deliver molecules called neuropeptides to the brain, Born told Reuters Health. The study proves "some substances given intranasally can pass directly to the brain" without being absorbed into the blood stream, Born told Reuters Health. Born suggested that the "nasal route" can now be investigated to see whether neuropeptides can be used to treat brain diseases. The next step, according to the German researcher, is to identify which neuropeptides might be therapeutically useful. "Nasal delivery may be useful in the treatment of brain diseases, particularly those involving dysfunction of neuropeptide signaling, such as AD and obesity," according to the report. "Our own research aims at peptides involved in weight regulation, like melanocortins [and] insulin, and in memory function," Born said. The researchers are also working to improve the brains ability to absorb the peptides after they have been delivered through the nose. By Merritt McKinney Reuters Health Nature Neuroscience advance online publication 2002;DOI:10.1038/nn849

'Abortion Pill' Tested for Treating AD - A small, very preliminary study investigating the effects of the medical abortion drug mifepristone, also known as RU-486, on people with mild to moderate AD suggests it might be a promising approach to treatment. According to lead author Dr. Nunzio Pomara of New York University School of Medicine in New York City, the study was intended to be the first controlled "proof of concept" investigation of whether blunting the effects of the stress hormone cortisol in the brain could improve AD symptoms. Previous research in both animals and people, Pomara noted, has found that this hormone can damage nerve cells in parts of the brain associated with memory and learning. "It is well known that large numbers of AD patients show elevations in levels of cortisol," Pomara told Reuters Health. "Mifepristone was the drug tested (in the current study) since it is a known blocker of cortisol receptors in the brain." In the current study, five patients with mild to moderate AD were given mifepristone for 6 weeks. "The study found trends that some patients taking mifepristone may have memory benefits," Pomara said. However, because of the small sample size and short study duration, the researcher cautions that it is premature to draw any conclusions about the effectiveness or safety of the drug. The researchers are calling for more studies. By Keith Mulvihill Reuters Health 5/24/02 Neurology 2002;58:1436-1437

Genes & Genetic Issues
In Folding Proteins, Clues to Many Diseases - In AD, Parkinson's disease and a slew of other neurodegenerative disorders there are problems with the body's cellular machinery for making proteins and recycling misshapen proteins. Misfolded proteins build up, like trash clogging an alleyway. Normally, our cellular machinery identifies misshapen proteins, reduces them to their constituent parts and recycles those parts. But when this process goes awry, small numbers of misfolded proteins accumulate into tiny spherical particles inside cells. These particles are so small and soluble that they had escaped detection until very recently, but many researchers now say they may be what actually harms brain cells in AD and islet cells in Type 2 diabetes and so on. Only later and gradually, however, the spheres stick together, forming tiny rods filaments and much larger fibrils, which in turn accumulate into insoluble deposits of protein called amyloid plaque. Until recently, said Dr. Peter Lansbury, an associate professor of neurology at Harvard Medical School and the Brigham and Women's Hospital in Boston, researchers believed that the fibrils and plaque were themselves the bad actors, and they have been seeking medications and vaccines to remove them or block their formation. But such therapies could make some diseases worse in that plaque removal might alter the kinetics of the system and hasten the rate of production of the toxic spheres. As many as a third of proteins end up misfolded, said Dr. Peter Wolynes, head of the structural biology program at the University of California at San Diego. These are what cells must eliminate and they have an elaborate machinery to do it, said Dr. Fred Cohen, a professor of medicine, pharmacology, biochemistry and biophysics at the University of California in San Francisco. A factor in contracting AD may lie in how fast protofibrils are turned into plaque, Dr. Cohen said. People who make plaque very quickly are protected from disease. Those who make plaque more slowly suffer a greater amount of cell damage. Mutations can slow the process down in many ways. Having two copies of a gene called APOE-4 reduces how quickly a-beta is removed from a cell, Dr. Cohen said. "It's like having a flat tire on your garbage truck," he said. By Sandra Blakeslee NY Times 5/21/02

Former President Ford Supports Cloning - Former President Ford says a proposed ban on cloning research would foreclose "lifesaving cures and treatments merely because they are new." The Senate is expected to begin debate soon on whether to ban cloning. Those pushing to allow cloning for research have argued that it could lead to cures for diseases such as AD and diabetes. Opponents say a cloned embryo is a human even before implantation in a womb, and destroying it for research is immoral. The House passed a bill banning all cloning last year. In an opinion piece in the Washington Post on 6/15/02, Ford argued against a complete cloning ban and cited former President Reagan, who now suffers from AD. "This is not locking the lid on Pandora's box. It is slamming the door to lifesaving cures and treatments merely because they are new," he wrote. "For every Ronald Reagan, so cruelly deprived of the knowledge of his pivotal place in our history, there are millions of elderly, and not so elderly, citizens who will never get there names in history books, although they are similarly imprisoned in memory's darkened rooms," the former Republican president said. "They deserve more than our sympathy. They deserve the finest treatment imaginable by the world's best scientists." By Janelle Carter, Associated Press Writer 5/6/02

Caregivers
At-home Exercise Helps Caregivers Care for Themselves - An estimated 3.5 million American women care for demented spouses or parents at home, putting their own physical and emotional health at risk. New research indicates that a simple, home-based exercise program can reduce the personal toll their caregiving takes. "The negative impact of caregiving … is likely due, at least in part, to the reduced probability that caregivers engage in preventive health behaviors such as regular physical activity," explains Cynthia M. Castro, Ph.D., from the Stanford University School of Medicine. Previous research, Castro notes, has shown that caregivers are unusually prone to such problems as depression, sleep disturbances, compromised immunity, elevated blood pressure and interpersonal strife. What is needed is a program that can successfully encourage a stressed and burdened population to engage in physical activity at levels sufficient to produce health benefits Castro said. A study of 51 women, each caring for a demented relative living in the home with her, were given an in-person counseling session with a health educator, who provided information and instruction on how to work up to a regular schedule of three or four 30- to 40-minute exercise sessions a week at home. Over the following 12 months, each caregiver/counselor team stayed in regular contact via telephone calls and mailed activity logs. By the end of the year, the women were also significantly less depressed and stressed than before starting the exercise program. Although their actual burdens did not decrease, their perception of how burdened they felt markedly improved. PR 5/23/02 Psychosomatic Medicine 64:458-468 (2002)

Testing
MRI Brain Scan May Detect AD Decades Before First Symptoms - MRI scans of the brain may detect AD decades before the first clinical signs of dementia occur, researchers from the University of South Florida (USF) and the University of Kentucky report in the journal Neurology. Because preventive therapies for AD will likely be more effective the earlier they are begun, the ability to identify people at high risk of the disease many years before symptoms are expressed will be important for its eventual prevention, the researchers say. Karen Gosche, PhD, and her colleagues found that shrinkage of the hippocampus, a region of the brain showing some of the first signs of AD, occurs very early in the disease process - - long before the illness spreads to the cerebral cortex and results in cognitive and memory impairment. Dr. Gosche, president of NeuroImaging Research, Inc. in Alachua, FL, conducted the study while she was a doctoral candidate in Aging Studies at USF. "The findings suggest that MRI measures of the hippocampus may help us to identify individuals who will develop AD decades in the future," said James Mortimer, PhD, director of the USF Institute on Aging and one of the co-authors of the study. The volume of the hippocampus was calculated with a new computer program that reduces the time required to compute this volume from more than 30 minutes to a couple of minutes. Previous methods required tracing of this structure by hand, which restricted its application to research studies. The findings suggest hippocampal volume could be valuable in predicting who is likely to develop AD, but the researchers emphasize that applying the technique to MRI brain scans of living people will require further study. PR 5/28/02 Neurology 2002;58:1476-1482

Changes in Retina Linked to Poorer Cognitive Function, Dementia - Abnormalities in tiny branches of retinal blood vessels might serve as an early warning system for dementias associated with AD, stroke, and other diseases, researchers report in the June issue of Stroke: Journal of the American Heart Association. In the study of more than 8,000 middle-aged people who had not suffered a stroke, those with impaired mental function were about three times more likely to have abnormalities in the retinal vessels, called arterioles. "There has been a hypothesis for some time that some vascular cause other than the aging process itself was associated with AD and stroke," says Tien Yin Wong, M.D., M.P.H. "This study shows that people with cognitive dementia are more likely to have pathological changes in the retinal vessels, which may be a reflection of similar pathological changes in the brain." Retinal examination could potentially provide an inexpensive, noninvasive way to diagnose and evaluate vascular dementia in the general population, says Wong, a researcher and professor of ophthalmology at the Singapore National Eye Center and National University of Singapore. PR 6/6/02 Stroke 2002; 33:1487

Improving Accuracy of Cross-cultural Europsychological Testing - To evaluate the elderly for memory loss and dementia, neuropsychologists use a variety of memory, image recognition, and abstract reasoning tests. But African Americans do not perform as well as whites on these tests even if test-takers from both ethnic groups have attained the same number of years of schooling. Because of the lower scores, healthy African Americans may be more likely to be misdiagnosed with AD or other cognitive defects. To make neuropsychological tests more accurate, Columbia Health Sciences researchers decided to study whether quality of education, rather than quantity, could explain the lower test scores among African Americans. The investigators measured quality of schooling by administering a reading test to 192 elderly African Americans and 192 elderly non-Hispanic whites from Northern Manhattan. The participants, who were all 65 years and older, did not have dementia and were functioning normally in their daily lives. The researchers found that they could eliminate most of the racial differences found in the neuropsychological test assessments by factoring in the scores from the reading tests. Both blacks and whites with a poor reading test result achieved similar neuropsychological test scores. "The findings suggest that including an assessment of reading skills will help neuropsychologists know what scores to expect from elders with diverse educational backgrounds," says Dr. Jennifer Manly, lead author of the study and assistant professor of neuropsychology in the Cognitive Neuroscience Division of the Taub Institute for Research on Alzheimer's Disease and the Aging Brain. "Incorporating reading tests into our testing battery could help reduce misdiagnosis of cognitive impairment among people with low reading levels regardless of race." PR 3/18/02 Journal of the International Neuropsychological Society (2002), 8:341-348

Genetic Tests Abound. Why Won't Insurers Pay? - Researchers have already identified genetic links to thousands of diseases like breast and colon cancer, AD, diabetes and heart disease. They have more than 900 tests available, including multiple tests for some diseases. But just because there is a genetic test for a disease does not mean that health insurance will pay for it. How much risk you face depends on factors like family history, sex and age. That makes insurers uncomfortable, particularly if no treatment is currently available. "If they're not sure of the test's outcome, and they don't know what to do with the results, insurers probably won't cover the test," said Susan Levine, vice president of Hayes Inc., a consulting firm in Lansdale, Pa., that helps insurers evaluate new technologies. Although test results may not be definitive, many people still want to know their genetic risk. But for many people, preventing disease is not the only consideration. In preliminary data, one continuing study of 175 adults who have a parent with AD, 23 percent of the participants agreed to be tested for the disease, even though there was no cure. "People have their own reasons for wanting to get a better handle on their risk, reasons that might not make sense to me as a doctor or to an insurer," said Dr. Robert C. Green, associate professor of neurology at the Boston University School of Medicine and director of the study. Asked why they agreed to be tested, 87 percent said they needed to arrange their personal affairs, 82 percent wanted to arrange for long-term care and 78 percent wanted to do things sooner than they had planned. Clinical genetic testing for AD is currently recommended only for people with symptoms of the disease. A lady who watched her father die of AD at the age of 58 has a test done. She found she had two copies of the apoE4 variant of a gene that is associated with AD, increasing her risk 15-fold. But she used that information to take action. She and her husband arranged for three longtime associates - a doctor, a nurse and a nursing home administrator - to collectively make decisions with her husband about her care if that becomes necessary. "Getting tested gave me control and helped me plan for the future," she said. Analysis of a man's genes showed that he had inherited from one parent the apoE4 gene, which is associated with abnormal fat metabolism and the risk of AD. He is now taking fat-lowering drugs to counteract its effects. By Michelle Andrews NY Times 5/19/02

Prevention
Activity Boosts Nerve Cells in Brains of Mice - An active and stimulating life may help elderly adults to maintain and generate higher numbers of nerve cells in the brain linked to memory and learning, research in mice suggests. The results shed light on how physical and intellectual activity might lower the risk of AD and other forms of dementia. However, more research is needed before the findings in mice can be applied to humans, the researchers point out in the May 22nd online edition of the Annals of Neurology. Nonetheless, the study results support a growing body of research demonstrating a link between activity in middle and old age and a lower risk of memory loss. Recent studies have also shown that keeping mice stimulated boosts the production of nerve cells in the hippocampus, an area of the brain that is key to learning and memory and is involved in age-related degenerative disorders. After a 10-month period corresponding to middle to old age in a mouse, one group of rodents living in a more stimulating environment were producing five times as many nerve cells in the hippocampus compared with the other group of mice that lived in a bare cage. They were also more curious when placed in a new environment, adapted faster than their less-stimulated counterparts, and scored higher on learning tests. "Our study suggests that, in mice, we can reduce the effects of aging on the brain with a sustained active and challenging life, even if this stimulation is only begun in middle age," Dr. Gerd Kemperman, from the Max Delbruck Center for Molecular Medicine in Berlin-Buch, Germany, said in a prepared statement. While emphasizing that the results do not automatically apply to humans, Kemperman and colleagues conclude that their data show that the aging brain can produce new cells and that activity influences the rate at which cells are produced. Reuters Health 5/21/02 Annals of Neurology 2002;10.1002/ana.10262

Jog Away From AD - A new animal study has found that exercise-happy rats are more likely to have healthy brains than the rodent equivalents of couch potatoes. Humans are, of course, more complex than rats. However, the two species have enough in common to make biologists at the University of California at Irvine think they may be on to something after observing hundreds of rats go about their daily lives. "The message is that moderate exercise is not only good for your body, it's good for your brain," says Nicole Berchtold, a post-doctoral neurobiology researcher who co-authored the study. Researchers have known for years that elderly people who exercise are more mentally fit than those who don't, Berchtold says. Their reaction times are quicker and their cognitive skills are better, she adds. However, the exact connection between exercise and the brain hasn't been clear. Rats were allowed to run in wheels whenever they wished. Researchers then examined the molecular makeup of the brains of the rats and were surprised to find changes in parts of the brain that control thinking and learning, not just in those that handle decisions about movement. In rats that ran at least 500 meters on a regular basis, exercise appeared to trigger a so-called "growth factor" that plays a role in better brain functioning, Bechtold explains. In turn, the heightened activity of the growth factor may stimulate memory and learning, protecting the brain against deterioration from AD. Berchtold says it's difficult to translate the exercise levels in the rats to equivalents in humans. One expert cautions that while researchers know a healthy lifestyle can prevent cancer and heart disease, no one has proven a direct link between exercise and lower rates of AD. By Randy Dotinga HealthScoutNews Reporter 5/29/02 Trends in Neurosciences, 2002, 25:6:296-301

Homocysteine Related to Brain Atrophy, Vascular Disease - People with elevated blood levels of the amino acid homocysteine are more likely to experience brain atrophy and vascular disease, according to two studies published in the May 28 issue of Neurology. Both brain atrophy and vascular disease are related to the development of dementia, including AD. "This is exciting information, because homocysteine levels can be reduced by taking the vitamins B6, B12 and folic acid," said neurologist James Toole, MD, of Wake Forest University School of Medicine in Winston-Salem, NC, who wrote an editorial accompanying the studies. Mild elevations of homocysteine levels have been reported to occur in five to seven percent of the general population. Toole is leading a study examining whether taking these vitamins to lower these levels can reduce the risk of stroke. "Another area that needs to be studied is whether taking vitamins to lower homocysteine levels can reduce the risk of AD and other dementia," he said. "There's a long way to go before we know the answers to these questions, but it's an exciting possibility." PR 5/27/02 Neurology 2002;58:1449-1450, 1471-1475, 1539-1541

Replacing Hormone Therapy - With Recent Studies Taking Some of the Glow Off HRT, What Other Choices Do Women Have for Symptoms of Menopause? - Recent research has cast critical new light on estrogen replacement therapy, which over the past few decades has been prescribed to one in three menopausal women seeking relief from hot flashes, vaginal dryness and bone loss. Given the treatment's purported extra benefits, ranging from heart health to improved mood, the decision to take estrogen was often easy. But that common practice is now being called into question. First came a study casting doubt on the ability of estrogen to prevent and treat heart disease. Other research questioned whether estrogen helps protect against AD. As continuing research clarifies estrogen's corresponding risks, women and their doctors are looking with new urgency at the question of how -- and whether -- to treat symptoms of menopause. By Sally Squires Washington Post Staff Writer 6/4/02


Other Items
Memory Isn't 'Lost,' Just out of Sync - A study conducted by Dr. John Hart and co-invest- igators at the University of Arkansas for Medical Sciences and at the Johns Hopkins University have developed a novel explanation for how we recall memories for objects that surround us. The medical researchers suggest that objects occur in your memory by uniting together the different brain regions that make up various parts of the object you are trying to remember. For example, the memory of a dog includes uniting smell, sound, appearance and name. By measuring the electrical rhythms that parts of the brain use to communicate with each other, the team of researchers showed that when the memory of a dog occurs, the thalamus, an important region of the brain that connects areas together, actually regulates the rhythms that connect brain regions. "Memory appears to be a constructive process in combining the features of the items to be remembered rather than simply remembering each object as a whole form," Dr. Scott Slotnick explained. "The thalamus seems to direct or modulate the brain's activity so that the regions needed for memory are connected." "It appears that the electrical signals synchronize the brain regions that store each part of an object's memory so that those areas are connected," Dr. Hart, the study's senior author, continued. "This co-activation of brain regions likely represents the memory of the object itself. An important implication of the study's association of the thalamus and rhythms to memory is that patients, including those who suffer from AD, who experience this sort of memory loss may not actually be losing information. Instead, the memory process is being disrupted. Dr. Hart said "We want to try to figure out, based on this approach to memory function, what sort of neurotransmitters and brain regions are being disrupted during the memory process. Then we want to see if we can treat patients by regulating this disrupted memory circuit." PR 5/9/02 Proc. Natl. Acadd. Sci USA vol. 99, Issue 9, 6440-6443 4/30/02

New Drugs Could Markedly Alter AD, but Disease Will Not Go Away - The number of people living with AD will at least double by 2050 even if major treatment breakthroughs should occur over the coming decades, according to a report from the University of North Carolina just released in the Annual Review of Public Health. Dr. Philip D. Sloane, the report's principal author and Professor of Family Medicine in the UNC School of Medicine said the prevalence of AD rises quickly after age 85. Persons beyond that age have 14 times the incidence of the disease compared with those aged 65 to 69. "The U.S. population in the next decades is expected to have so many people over 85 that the growth rate of people with AD will be much greater than that of the population," he said. The management of AD "will undoubtedly be a major and growing public health issue during the first half of the twenty-first century," the new report stated. "The projected increase in AD will need to be paralleled by efforts to assure the availability and quality of care for persons with the disease." Sloane, co-director of the Program on Aging, Disability and Long-term Care at the university's Cecil G. Sheps Center for Health Services Research, said the study was instigated by a widely held view that AD will not be the same threat in twenty years because of advances in science. It occurred to us that people have no guidance to project what will happen in the future regarding AD. Published studies have made no projections based on scientific advances. This study was an attempt to assign some numbers to what would happen in AD if there really are treatment breakthroughs, which we expect there will be." "The lesson we learn from all this is that the disease is not going to go away if we have significant treatment advances," Sloane said, noting that the introduction of significant new therapies would rapidly change the health services needs of people with AD. "And that means that the health system must begin thinking ahead and preparing for these eventualities, particularly as drugs begin to make it through clinical trials." PR 5/29/02 Annu. Rev. Public Health 2002,23:213-231

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