 By LEE BOWMAN Scripps Howard News Service November 16, 2005
The advances, described Tuesday before the annual meeting of the Society for Neuroscience, hinge on a new compound developed at the University of Pittsburgh that binds to beta-amyloid deposits in the brain - the hallmark sign of Alzheimer's disease. "When clinical symptoms start, the disease process has already been at work in the patient for many years, and possibly even decades," said Anne Fagan, a professor of neurology at Washington University School of Medicine in St. Louis, who headed a study of 24 patients using the new techniques.
"Up to 30 percent of neurons in vulnerable areas are already dead, and you can't get them back, so finding markers that can help us identify patients prior to symptoms is really our big push now," Fagan added. Alzheimer's disease currently affects an estimated 4.5 million Americans and is expected to strike some 14 million over the next 50 years if treatments to stop the degenerative brain disease aren't found. Right now, the only definitive diagnosis for Alzheimer's disease relies on autopsy studies of brain tissue to confirm that the deposits and damaged areas fit known patterns for the illness. Researchers from the University of Pittsburgh reported on a series of studies using a brain imaging agent - called Pittsburgh Compound-B or PIB - that helped document the progression of the disease through the brain. "We've had hints about the time course of brain changes in Alzheimer's from autopsy studies, but the current findings in living patients take these observations further,'' said Dr. William Klunk, an associate professor of psychiatry at Pitt and one of the inventors of the compound. "If we can delineate the natural history of brain changes in the disease, we then have a baseline against which to judge the success of therapies designed to prevent those changes,'' he added. PIB adheres to plaque deposits in the brain for 30 to 60 minutes before washing out - long enough for researcher to record where the compound has lodged in the brain using a positron emission tomography (PET) scanning device. Klunk said one study using the imaging method on patients showed that the deposits first pile up in areas of brain related to memory, such as the cingulated and frontal cortex, then to the parietal and temporal cortex and finally to occipital cortex and sensory motor cortex. The progressive damage to these areas matches the functional losses experienced by Alzheimer's patients, who first suffer lapses in memory, reasoning and judgment and eventually lose their ability to move and swallow. The Washington University researchers combined imaging using PIB with a test of spinal fluid to measure levels of a substance called amyloid beta 42, a major ingredient of the plaques that build in Alzheimer's. They tested patients with very mild and mild Alzheimer's symptoms, as well as some subjects whose cognitive tests were normal. The dual tests showed a solid correlation between lower levels of A-beta 42 in spinal fluid and increased buildup of plaque in the brain. Interestingly, they also found that three of the subjects who were considered normal had similar results. Fagan said it's impossible to know whether those patients have latent Alzheimer's disease. "All we can do now is follow the participants closely to see if they eventually develop Alzheimer's dementia,'' she said. The findings are particularly important, because although scientists have known for several years that A-beta 42 can be a marker for Alzheimer's, natural variations of the chemical occur in both healthy people and those with the disease, so it's been difficult to come up with a meaningful scale. "The hope is that 10 to 20 years from now, we'll give people a PIB scan, draw and analyze their cerebrospinal fluid and combine that with other factors to get a global score for their personal risk of Alzheimer's disease,'' Fagan said.
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