A combination of brain scanning with a new imaging agent and cerebrospinal fluid (CSF) analysis has left neuroscientists encouraged that they may finally be moving toward techniques for diagnosing Alzheimers disease before its clinical symptoms become apparent. "When clinical symptoms start, the disease process has already been at work in the patient for many years and possibly even decades," explains Anne Fagan Niven, Ph.D., research associate professor of neurology at Washington University School of Medicine in St. Louis. "Up to 30 percent of neurons in vulnerable areas are already dead, and you cant get them back. So finding markers that can help us identify patients prior to symptoms is really our big push now."
With colleagues Mark Mintun, M.D., professor of radiology, and David Holtzman, M.D., the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology, Fagan studied a group of 24 people that included individuals diagnosed with very mild and mild Alzheimers disease, and cognitively normal subjects. As expected, in patients with cognitive impairments, believed to be attributable to Alzheimers disease, researchers found low CSF levels of amyloid beta 42 (A-beta 42), the principal ingredient of the brain plaques that are characteristic of Alzheimers disease. In the same individuals, brain scans with a new imaging agent that reveals the presence of amyloid plaques in the brain were positive. What scientists didnt anticipate was that three cognitively normal subjects would have both low CSF levels of A-beta 42 and positive results from the brain scans. Fagan stressed that although this aspect of their findings was very intriguing, it doesnt prove that the three normal subjects will one day develop clinical Alzheimers disease.
"For now, definitive diagnosis of Alzheimers disease still cannot be made until autopsy," she says. "Its going to take a number of years for us to fully assess these results, because all we can do now is follow the participants closely to see if they eventually develop Alzheimers dementia." Fagan presents the results of the study at 10:15 a.m. on Nov. 15 at this years annual meeting of the Society for Neuroscience in Washington, D.C. The study will also appear in an upcoming issue of Annals of Neurology. Many prior studies have found that A-beta 42 levels drop in the cerebrospinal fluid of Alzheimers disease patients. A-beta 42 is naturally produced in the brain, and researchers suspect that the creation of amyloid plaques may be linked to breakdowns of the processes that degrade or normally clear A-beta 42 from the brain via the CSF and the bloodstream.
Michael C. Purdy | EurekAlert!
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