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

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