Β-Amyloid Peptide Secretion by a Microglial Cell Line is Induced by Β-Amyloid-(25–35) and Lipopolysaccharide

beta-Amyloid protein (beta AP) deposition is a neuropathologic hallmark of Alzheimer's disease (AD). Yet, the source of cerebral beta AP in AD is controversial. We examined the production of beta AP by the BV-2 immortalized microglial cell Line using a sensitive enzyme immunoassay. Constitutive production of beta AP was detected in conditioned media from unstimulated BV-2 cells. Further, production of beta AP was induced by treatment of cultures by lipopolysaccharide (LPS) or beta AP-(25-35) and was inhibited by the calpain protease inhibitor MDL 28170. Treatment of BV-2 cells with LPS or beta AP-(25-35) did not affect cell-associated beta-amyloid precursor protein levels. These findings suggest that microglia may be an important source of beta AP in AD, and that microglial production of beta AP may be augmented by proinflammatory stimuli or by beta AP itself.