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Volume 271, Number 27, Issue of July 5, 1996 pp. 16084-16089
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.

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

(Received for publication, December 11, 1995, and in revised form, April 23, 1996)

Louise Bitting , Asha Naidu ^§ , Barbara Cordell ^§ and Greer M. Murphy Jr.

From the  Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California 94305 and ^§ Scios, Inc., Mountain View, California 94043

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

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