December 21, 2005 - The search for new measures, or "biomarkers," to detect Alzheimer's disease (AD) before signs of memory loss appear has advanced an important step in a study by researchers at Washington University in St. Louis, MO, and the University of Pittsburgh.

The researchers combined high-tech brain imaging with measurement of beta-amyloid protein fragments in cerebrospinal fluid (CSF). They found that greater amounts of beta-amyloid containing plaques in the brain were associated with lower levels of a specific protein fragment, amyloid-beta 1-42, in CSF. Prior research indicates that amyloid-beta 1-42 is central to AD development. The fragment is a major component of amyloid plaques in the brain, which are believed to influence cell-to-cell communication and are considered a hallmark of the Alzheimer's brain.

The study, published online December 21, 2005, by the Annals of Neurology, is the first to examine the relationship between levels of amyloid plaque deposits in the brain and different forms of beta-amyloid in CSF in living humans. It was supported by the National Institute on Aging (NIA), a component of the National Institutes of Health (NIH) at the U.S. Department of Health and Human Services, and by the Washington University General Clinical Research Center, funded by the NIH.
The method studied might one day help to more accurately diagnose AD, even before the appearance of cognitive symptoms, and to monitor disease progression. In the near term, the findings could be useful in a research context, allowing scientists to track the effects of potential beta-amyloid lowering treatments in clinical trials.

"We presently don't have fully validated imaging or biomarker measures that can help us monitor the development or progression of Alzheimer's in living people," explains Neil Buckholtz, Ph.D., chief of the Dementias of Aging Branch at the NIA. "This study represents one step in the progress being made toward identifying clinically useful biological measures for AD."

The research was conducted by Anne M. Fagan, Ph.D., and colleagues David M. Holtzman, M.D., Mark A. Mintun, M.D., and John C. Morris, M.D., of the Alzheimer's Disease Research Center (ADRC) at Washington University School of Medicine and used a newly developed imaging tracer for beta-amyloid from investigators at the ADRC at the University of Pittsburgh. Both ADRCs are funded by the NIA.

The study included 24 people ages 48 to 83 years who were cognitively normal or had very mild, mild, or moderate dementia. The researchers used positron emission tomography (PET), a brain imaging technique, with a tracing substance called Pittsburgh Compound B (PIB), to determine the amount of plaques in the participants' brains. PIB travels through the bloodstream into the brain and then binds to beta-amyloid containing plaques in the brain. PIB makes it possible to see on PET images any areas of the brain with high concentrations of plaques.

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