A PATHOLOGICAL hallmark of Alzheimer’s disease is the senile plaque, containing beta-amyloid fibrils, microglia and astrocytes(1). beta-amyloid fibrils exert a cytotoxic effect on neurons(2), and stimulate microglia to produce neurotoxins, such as reactive oxygen species(3,4). Mononuclear phagocytes, including microglia, express scavenger receptors that mediate endocytosis of oxidized low-density lipoproteins(5), and adhesion to glucose-modified extracellular matrix proteins(6). Here we report that class A scavenger receptors mediate adhesion of rodent microglia and human monocytes to beta-amyloid fibril-coated surfaces leading to secretion of reactive oxygen species and cell immobilization. Thus, class A scavenger receptors are potential therapeutic targets in Alzheimer’s disease.