A research report that appears in the September 2002 issue of the journal Archives of Neurology may improve understanding of the most common form of Alzheimer’s disease. “Our key finding is that beta-secretase activity — the efficiency of how the enzyme works — is increased in Alzheimer’s diseased brains specifically in those areas affected by the disease,” says Michael Irizarry, of the Alzheimer’s Disease Research Unit in the Massachusetts Genearl Hospital Department of Neurology and the paper’s senior author. “The beta-secretase increase persists and even increases throughout the duration of the illness, which may make this enzyme a useful target for treatment, even late in the disease.” In Alzheimer’s, amyloid-beta is released when the large APP molecule is clipped in one location by beta-secretase and in another spot by an enzyme called gamma-secretase. The amyloid-beta fragments collect in plaques — one of the classic brain abnormalities of Alzheimer’s disease — which significant evidence suggests are toxic to brain cells. The research was supported by grants from the National Institutes of Health, the Walters Family Foundation and Takeda Chemical Industries.