University of Pittsburgh research uncovers new mechanism that may be the cause of mild cognitive ...( Pitt study was conducted in collab...),Health

PITTSBURGH, Jan. 31 A study out of the University of Pittsburgh has uncovered a completely different mechanism behind mild cognitive impairment (MCI), an increasingly common memory problem that is thought to be a precursor to Alzheimers disease (AD). The results are surprising even to the researchers conducting the study and may explain why current medications dont improve memory function effectively. Further, the findings may redirect research into many of the newer treatments designed to prevent memory problems.

The study, published in todays Annals of Neurology, found that in older people with MCI, the brain produces more choline acetyltransferase (ChAT), an enzyme that is important in memory and cognitive functions. The researchers believe this is the brains attempt to maintain normal function as the neurons that form communication lines to the brains memory center die. Strengthening their finding are autopsy results showing more than 60 percent of people who had MCI within a year before they died already had evidence of neurodegeneration that is seen in the early stages of AD.

The results are almost the opposite of what most researchers believed that a decrease in ChAT levels causes MCI the theory behind todays most popular Alzheimers treatments, which include drugs meant to boost levels of the enzymes product, the neurotransmitter acetylcholine (ACh).

Because we thought deficits in ChAT were responsible for memory problems in patients with MCI, the most common treatment we use is a class of drugs called cholinesterase inhibitors that help the brain produce more, said Steven T. DeKosky, M.D., professor of neurology, psychiatry, neurobiology and human genetics at the University of Pittsburgh School of Medicine and principal investigator of the study. These results suggest that the brai
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Contact: Craig Dunhoff
412-624-2607
University of Pittsburgh Medical Center
31-Jan-2002