Journal
NEUROBIOLOGY OF DISEASE
Volume 18, Issue 3, Pages 459-465Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2004.12.013
Keywords
Alzheimer's disease; amyloid-beta(A beta); inflammation; astrocyte; oligomeric A beta 1-42; fibrillar A beta 1-42; interleukin-1 beta (IL-1 beta); inducible intric oxide synthase (iNOS); tumor necrosis factor-alpha (TNF-alpha); nitric oxide (NO)
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Funding
- NIA NIH HHS [P01 AG021184, R01 AG19121, R01 AG20249] Funding Source: Medline
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Activated glia, as a result of chronic inflammation, are associated with amyloid-beta peptide (A beta) deposits in the brain of Alzheimer's disease (AD) patients. In vitro, glia are activated by A beta inducing secretion of pro-inflammatory molecules. Recent studies have focused on soluble oligomers (or protofibrils) of A beta as the toxic species in AD In the present study, using rat astrocyte cultures, oligomeric A beta induced initial high levels of IL-1 beta decreasing over time and, in contrast, fibrillar A beta increased IL-1 beta levels over time. In addition, oligomeric A beta, but not fibrillar A beta, induced high levels of iNOS, NO, and TNF-alpha. Our results suggest that oligomers induced a profound, early inflammatory response, whereas fibrillar A showed less increase of pro-inflammatory molecules, consistent with a more chronic form of inflammation. (c) 2005 Elsevier Inc. All rights reserved.
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