Abstract
The personal tragedy of progressive dementia, the emotional distress of family members, and the staggering cost of care to society all challenge the scientific and medical communities to find a cure, or at least an effective treatment, for Alzheimer's disease. The sheer numbers of patients — estimated to be 2 to 4 million persons in the United States — only magnify the urgent need to answer this challenge. In the quest to develop rational pharmacologic treatments, the first step is to identify abnormalities in brain tissue that account for the clinical manifestations of disease.1 The initial reports that mechanisms reflecting . . .