Alzheimer Related News Items

News as of 1/05/04

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

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Top Items

Brain’s Insulation Key to AD - A UCLA neuroscientist, Dr. George Bartzokis, says a possible key to the onset of AD could be the midlife breakdown of myelin, a fatty insulation coating the brain's internal wiring. Myelin is a sheet of lipid, or fat, containing very high cholesterol content. It serves to speed communication through the brain by wrapping tightly around neural “wire” connections called axons. Dr. Bartzokis has determined that myelin degrades over time through a combination of genetic factors and the brain’s own developmental process. His research involves thorough analysis of magnetic resonance images and post-mortem brain tissue. “Close analysis of brain tissue and MRIs clearly shows that the brain’s wiring develops until middle age and then begins to decline as the breakdown of myelin triggers a destructive domino effect,” Bartzokis says. “Our time at the peak is short indeed.” As the brain develops into adulthood, its cholesterol levels grow and eventually promote the production of a toxic protein that attacks the myelin, Bartzokis says. This disrupts message transfer through the axons and eventually leads to the mind-destroying damage visible years later in the cortex of AD patients. Bartzokis suggests preventive therapies worth investigating include medications that lower iron or cholesterol, anti-inflammatory drugs, diet and exercise programs, and hormone replacement therapies. HealthDayNews 12/29/03 Neurobiology of Aging 2004 Jan. 25 (1):49-62



Drugs

Clioquinol May Slow Mental Decline in AD - A drug that binds to metal compounds and clears them from the body may slow cognitive decline in patients severely affected by AD, a new study suggests. The drug, clioquinol, not only promotes the removal of zinc-copper compounds, it also makes beta-amyloid soluble allowing it to be eliminated, Dr. Colin L. Masters, at the University of Melbourne, and associates explain in their article in the Archives of Neurology. Beta-amyloid is the abnormal protein that characteristically accumulates in the brains of patients with AD. Lab studies have shown that decreasing brain amyloid-beta deposits in mice with a form of AD reduces the toxic effect of amyloid on neurons. In a 36-week study, 16 patients with moderately severe AD were given clioquinol and 16 were given an inactive placebo. The drug appeared to slow the worsening of cognitive scores when compared to patients in the placebo group. After 24 weeks, the trend was maintained until the end of the trial but the difference became less pronounced. “The findings support a proof of concept in humans that a drug targeting metal-amyloid beta interactions can have a significant effect on amyloid-beta metabolism and, through this, a beneficial modification on the progression of AD,” Masters’ group concludes. John Q. Trojanowski, co-director of the Center for Neurodegenerative Disease Research at the University of Pennsylvania, says that the results are “encouraging,” even though they have to be confirmed in much larger clinical trials. However, he cautions that this is still an approach to getting rid of the plaque, and that other damage present in the brains of AD patients may be equally important. Moreover, he notes that there is controversy over the role of copper in the disease, as recent studies in mice have actually shown that an increase in copper might help patients. Reuters Health 12/15/03 and Forbes.com 12/16/03 http://www.forbes.com/2003/12/16/cx_mh_1216alzheimers.html Archives of Neurology 2003; 60:1685-1691



Genes & Genetic Issues

AD Signs Found in Young Adults - Young adults who are genetically at risk for AD may show signs of the disease years before the start of memory and thinking problems, a new study suggests. “Patients with AD have progressive reductions in brain glucose metabolism. This is an indicator of brain activity in certain parts of the brain,” says lead researcher Dr. Eric M. Reiman, an associate head of psychiatry at the University of Arizona. Reiman's research team has been investigating whether people with the apolipoprotein (APOE) episilon4 allele, a gene that is associated with an increased risk for AD, show this reduction in glucose metabolism. Almost a quarter of the population carries this allele. In earlier research, Reiman’s group showed people with the APOE episilon4 allele, aged 50 to 65, had reductions in glucose metabolism. In their current study, the researchers used magnetic resonance imaging (MRI) and positron emission tomography (PET) to measure brain structure and function in 12 APOE epsilon4 carriers and 15 non-carriers, aged 20 to 39. The researchers found the patients with the APOE epsilon4 allele had abnormally low glucose metabolism in the same brain areas as patients with AD. “The earlier you can detect changes in the brain, the better the opportunity to intervene -- and the more likely that the treatment would have an effect before the brain is damaged by AD,” Reiman says. Reiman notes that while there were decreases in glucose metabolism, not all patients with the APOE epsilon4 allele go on to develop AD. However, “these early changes are surprising,” he adds. It is possible that decreased glucose metabolism is a very early sign of AD and may provide a target for preventive treatment, Reiman says. “I feel very confident that a prevention therapy of that kind is likely to emerge over time,” Reiman says. “Even if that therapy was only modestly effective, it could have a tremendous public health impact.” By Steven Reinberg HealthDay Reporter 12/15/03 Proceedings of the National Academy of Sciences Jan. 6 2004;101(1):284-289


Genetics Play Smaller Role in Late AD - Genetics play a smaller role in cases of late-onset AD than has been believed. About half of someone’s susceptibility to AD occurring after age 65 can be attributed to environmental factors, according to researchers at the University of Southern California. Earlier studies had suggested genes contribute up to 75 percent of susceptibility in late-onset cases of the brain-wasting disease. “Within an individual there is an unknown mixture of genetic and environmental influences,” says study co-author Margaret Gatz, a professor of psychology at USC. Researchers evaluated 662 pairs of twins between the ages of 52 and 98 -- 265 of them identical and 397 fraternal. The researchers followed them for an average of five years, testing periodically for memory and other cognitive functions to see if they developed AD. Nearly 6 percent of the participants were diagnosed with the disease during the five years. In the identical twin pairs, if one sibling developed AD, the other twin also did 32 percent of the time. In fraternal twins, only about 9 percent of the siblings developed the disease if the twin did. By using statistical modeling techniques, the researchers computed that half or more of an individual’s susceptibility to AD later in life is attributed to environmental, not genetic, factors. “The study confirms the importance of genetics but also points to the limits of only looking to genetic explanations, especially among those who develop AD very late in life,” Gatz says. “This study is special in that it began with twins where neither member of the twin pair had dementia, and it followed the twins to see whether one or both twins later developed AD,” she adds. “What we find is that genetics plays an important role, because we find that nearly 50 percent of the variation in liability to AD could be attributed to genetic variation,” Gatz says. William Thies, a spokesman for the Alzheimer's Association, says, “The most important message of all the twin studies is that at least a portion of our risk is genetic and a portion is environment.” He notes the new study is relatively small, but it does offer some hope. “There are lots of people here [in the study] who didn’t get AD and when they did they were older. It suggests if you are 80 and healthy, you have some risks, but you shouldn’t be worrying every time you forget which cabinet the glasses are in. By Kathleen Doheny HealthDay Reporter 12/15/03 Annals of Neurology published online 12/16/03 10.1002/ana.10999



Caregivers

AD Study Offers Insight into Wandering - More intensive search patterns could be the difference between life and death when an AD patient wanders away from home. That’s the principal finding of a new University of Florida study of U.S. newspaper reports from 1998 to 2002 that described 93 incidents in which people with dementia died as a result of becoming lost. Most of the victims were found dead no farther than a mile from their home or living facility after becoming lost and confused, yet in many cases it took days or weeks to locate them, according to the study. UF nursing researchers have identified distinct patterns in these cases, yielding new insights likely to provide more efficient strategies for rescuers searching for those who wander. “These (dementia-related) searches can vary greatly from a search for a healthy missing adult or even a child because of the dementia patient's tendency to stick close to home in an isolated spot,” said Meredeth Rowe, the study’s principal investigator and an associate professor at UF's College of Nursing. “Thus, law enforcement officers must conduct repeated searches that comb nearby areas thoroughly,” Rowe said. Those who roamed not only stuck surprisingly close to home but also tended to hide and wouldn’t respond when searchers called out for them, Rowe said. Gainesvillesun.com 1/3/04 and U of Florida story at http://news.health.ufl.edu/stories/2003/Dec/Brown_121003.shtm

The Gainesvillesun.com article also has these tips on Wandering and AD

An individual with AD is likely to wander at some point during the disease. Wandering can be caused by several factors, including: Medication side effects. Stress. Confusion related to time.

Restlessness. Agitation. Anxiety. Inability to recognize familiar people, places and objects.

Fear arising from the misinterpretation of sights and sounds. Desire to fulfill former obligations, such as going to work or looking after a child.

Tips for reducing wandering behavior: Encourage movement and exercise to reduce anxiety, agitation and restlessness. Involve the person in productive daily activities, such as folding laundry or preparing dinner. Remind the person that he or she is in the right place. Reassure the person if he or she feels lost, abandoned or disoriented.



Testing

New Method for Detecting AD - Researchers studying Down syndrome patients believe they have found a way to detect AD before symptoms of dementia appear. Brain scans of adults with Down syndrome showed increased metabolic activity in the temporal cortex, the same region of the brain where AD commonly develops. The researchers at the University of California at Irvine School of Medicine speculate AD may begin with a similar metabolic increase, because Down syndrome often leads to dementia during adulthood. If so, early detection of AD could be accomplished through positron imaging tomography (PET), a brain scan that employs radioactively labeled glucose to show the brain at work. In diseased brains, damaged neurons have to work harder to maintain their effectiveness, and those efforts show up in a PET scan, says Dr. Richard Haier, professor of pediatrics and principal researcher. As the disease progresses, the damaged neurons are destroyed and the metabolic rate decreases. “But to confirm this, further imaging tests must be done on the Down syndrome people as dementia progresses,” Haier adds. By Dennis Thompson HealthDay Reporter 12/23/03     

Neurology Dec. 2003;61:1673-1679


Why Memory Fades With Drinking - Deficiencies in the brain’s hippocampus play an important role in the alcoholism-related memory disorder called Korsakoff’s syndrome.

These deficiencies are similar to those fond in the brain’s of people with AD. The study included five men with alcoholic Korsakoff's syndrome, 20 men with AD and 36 healthy men. Their brains were scanned using magnetic resonance imaging (MRI). The brains of the men with Korsakoff's and those with AD were comparable in significant volume loss in the hippocampus, a part of the brain that plays an important role in memory functions. The study found that the greater their hippocampus deterioration, the higher the men with Korsakoff's scored on the memory deterioration index. The researchers found a similar correlation in the men with AD. “Awareness of the clinical and radiological similarities between Korsakoff’s syndrome and AD may help with the detection of each,” study author Edith V. Sullivan, of the Stanford University School of Medicine, says in a prepared statement. “Although controversial, we believe that the nature of the memory impairment in these disorders is the same, while their overall profiles are different,” she says. HealthDayNews 12/22/03 Neurology 2003;61:1716-1719



Prevention

Red Wine Molecule May Battle AD Damage - Studies have shown that having a drink or two a day may be good for the heart, and now new research suggests that a substance in red wine may protect the brain from AD. But it is not a good idea for the elderly to start drinking to stave off the memory robbing disease, cautioned lead investigator Dr. Egemen Savaskan of the University of Basel in Switzerland. While the substance called resveratrol that is abundant in red wine does seem to protect cells in laboratory experiments, Savaskan pointed out to Reuters Health that the alcohol in wine can be toxic to brain cells. Still, the research highlights the possibility that naturally occurring substances may protect against neurological degeneration, according to Savaskan. “We need more research on those substances,” he said. Besides resveratrol, Savaskan's team is also examining the neurological effects of melatonin, estrogen and nerve growth factors. Red wine contains high levels of resveratrol, a naturally occurring substance found in grapes. Resveratrol is an antioxidant, meaning that it targets a process called oxidation in which cell-damaging substances called free radicals accumulate. Oxidation is suspected of increasing the risk of heart disease, stroke and several other diseases. One of the hallmarks of AD is the accumulation of abnormal bits of protein called beta-amyloid. Savaskan’s team set out to see whether resveratrol can counteract some of the oxidative stress caused by beta-amyloid. Resveratrol does indeed protect cells from beta-amyloid induced oxidative damage, the researchers report. Resveratrol seemed to help cells survive by encouraging the mopping of harmful free radicals. Resveratrol “has distinct antioxidative properties,” Savaskan said. But the Swiss scientist stressed that more research is needed to evaluate the long-term effects of resveratrol. By Merritt McKinney Reuters Health 12/31/03 Gerontology, November/December 2003;49:380-383



Other Items

AD Risk Linked with Stroke - Elderly individuals who have had a stroke may have an increased risk of developing AD, according to a study by Dr. Richard Mayeux and colleagues from Columbia University, in New York. They examined the association between a history of stroke and the risk of AD in a long-term study of 1766 Medicare recipients since 1992. The annual rate of AD was 5.2 percent for stroke patients, compared with 4 percent among those without stroke, Mayeux’s group found. They estimate that individuals with a history of stroke had a 60-percent increased risk of developing AD compared with those without a history of stroke. When the investigators considered factors, such as high blood pressure, diabetes and heart disease, they found that only diabetes was related to the risk of AD independent of stroke history. “Stroke remained weakly associated with AD in the absence of these factors,” the authors explain. The risk of AD significantly increased in subjects who also had high blood pressure (28 percent), diabetes (59 percent), or heart disease (95 percent). The association between stroke and AD might be explained by a common vascular disease process, Mayeux and colleagues suggest. Or perhaps the effects of stroke accelerate AD progression, resulting in earlier disease onset. Reuters Health 12/22/03 Archive of Neurology, December 2003;60:1675-1677

 

Psychological Factors May Raise AD Risk - Susceptibility to psychological distress seems to be associated with the risk of AD, researchers in Chicago report 12/9/03. If so, it may be possible that antidepressants or other drugs could reduce the effects of stress on brain structure and function. Because chronic stressful experience is linked to structural changes in the brain and with impaired learning and memory, Dr. Robert S. Wilson and colleagues at Rush-Presbyterian-St. Luke’s Medical Center hypothesized that a propensity to experience psychological distress is related to the risk of AD. To investigate, they analyzed data from the Religious Orders Study, which included 797 individuals, average age 75 years, who were free of dementia at the start of the trial. The subjects underwent complete neurologic examinations and completed a test for signs of neurosis. At annual follow-ups, the subjects also underwent a battery of 19 tests that measured mental functioning. During an average follow-up of about five years, 140 individuals were diagnosed with AD. After adjusting the findings for age, sex, and education, Wilson’s team found that each one-point increase in test score for distress-proneness was associated with a six percent increased risk of AD and a seven percent decline in mental capacity. Compared with people with the lowest scores, the risk was approximately doubled in persons with the highest scores. Wilson notes in a journal press release that antidepressants and other drugs may block the adverse effects of stress. “But much more research is needed before we can determine whether the use of antidepressants could help reduce the risk of AD.” Reuters Health 12/9/03 Neurology 2003;61:1479-1485


THE FORGETTING: A Portrait of Alzheimer’s - This is a two-hour special aimed at helping people better understand and cope with the fearsome disease of Alzheimer's. The cornerstone of the project is a 90-minute documentary based on David Shenk’s best-selling book The Forgetting. Like Shenk’s book, the documentary is a dramatic, compassionate, all-encompassing look at AD that weaves together the history and biology of the disease, the intense real-world experiences of AD patients and caregivers, and the race to find a cure. It is on Wednesday January 21, 2004 on National PBS at 9:00 pm Eastern time . The URL for the program is http://www.pbs.org/theforgetting/ and there they have many links to information on AD.

 

 

 

 

 

 

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