The effects of a synthetic homolog of beta-amyloid (beta-1-42) on the secretion of interleukin-1 (IL-1) and basic fibroblast growth factor (bFGF) from cultures of microglia and astrocytes, cells that surround beta-amyloid-containing plaques in Alzheimer's disease, were examined. Our results show that beta-amyloid not only enhances glial cell secretion of these factors, it stimulates the proliferation and morphological transformation of microglia. Since IL-1 and bFGF are known to elevate the synthesis of the beta-amyloid precursor protein and other plaque components, it is suggested that in this way, cascades may arise that contribute to the process of plaque development.