Differential effects of oligomeric and fibrillar amyloid-beta 1-42 on astrocyte-mediated inflammation |
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Authors: | White Jill A Manelli Arlene M Holmberg Kristina H Van Eldik Linda J Ladu Mary Jo |
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Affiliation: | Department of Medicine, Division of Geriatrics, Evanston Northwestern Healthcare Research Institute, Evanston, IL 60201, USA. |
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Abstract: | Activated glia, as a result of chronic inflammation, are associated with amyloid-beta peptide (Abeta) deposits in the brain of Alzheimer's disease (AD) patients. In vitro, glia are activated by Abeta inducing secretion of pro-inflammatory molecules. Recent studies have focused on soluble oligomers (or protofibrils) of Abeta as the toxic species in AD. In the present study, using rat astrocyte cultures, oligomeric Abeta induced initial high levels of IL-1beta decreasing over time and, in contrast, fibrillar Abeta increased IL-1beta levels over time. In addition, oligomeric Abeta, but not fibrillar Abeta, induced high levels of iNOS, NO, and TNF-alpha. Our results suggest that oligomers induced a profound, early inflammatory response, whereas fibrillar Abeta showed less increase of pro-inflammatory molecules, consistent with a more chronic form of inflammation. |
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Keywords: | Alzheimer's disease Amyloid-β (Aβ) Inflammation Astrocyte Oligomeric Aβ1–42 Fibrillar Aβ1–42 Interleukin-1β (IL-1β) Inducible nitric oxide synthase (iNOS) Tumor necrosis factor-α (TNF-α) Nitric oxide (NO) |
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