Evidence implicating the beta -amyloid protein (A beta) in the pathogenesis
of Alzheimer's disease has steadily accumulated. However, the mechanism by
which A beta causes dementia is unknown, Here we argue that a more integra
ted, top-down approach to brain function is needed to assess the role of A
beta in Alzheimer's disease, and that more attention should be paid to the
effects of A beta on synaptic function rather than on cell death.