The progressive cognitive and behavioral symptoms which characterize Alzheimer’s disease (AD) derive from profound functional and structural changes observed in neurons, their processes and synapses, and the microgliosis and astrocytosis which accompany these changes. This multicellular dysfunction appears to represent a common cytopathological response to several distinct genetic defects and perhaps also to certain environmental precipitants that remain poorly understood. In short, AD is actually a syndrome in which multiple molecular etiologies can trigger a somewhat varied but largely stereotyped pathogenetic cascade. From this perspective, AD resembles other common, multigenic degenerative pathologies of late life, such as atherosclerosis. Because the AD syndrome has multiple molecular causes and a gradual, chronic evolution, one may anticipate several distinct classes of therapeutic molecules that could interfere with one or another step in the disease cascade.