Abstract
Activated glia, as a result of chronic inflammation, are associated with amyloid-β peptide (Aβ) deposits in the brain of Alzheimer's disease (AD) patients. In vitro, glia are activated by Aβ inducing secretion of pro-inflammatory molecules. Recent studies have focused on soluble oligomers (or protofibrils) of Aβ as the toxic species in AD. In the present study, using rat astrocyte cultures, oligomeric Aβ induced initial high levels of IL-1β decreasing over time and, in contrast, fibrillar Aβ increased IL-1β levels over time. In addition, oligomeric Aβ, but not fibrillar Aβ, induced high levels of iNOS, NO, and TNF-α. Our results suggest that oligomers induced a profound, early inflammatory response, whereas fibrillar Aβ showed less increase of pro-inflammatory molecules, consistent with a more chronic form of inflammation.
| Original language | English |
|---|---|
| Pages (from-to) | 459-465 |
| Number of pages | 7 |
| Journal | Neurobiology of Disease |
| Volume | 18 |
| Issue number | 3 |
| DOIs | |
| State | Published - Apr 2005 |
Bibliographical note
Funding Information:This research was supported by National Institute of Aging RO1 AG19121, RO1 AG20249, PO1 AG021184, and the Charles Walgreen, Jr. Fund (MJLD).
Keywords
- Alzheimer's disease
- Amyloid-β (Aβ)
- Astrocyte
- Fibrillar Aβ1-42
- Inducible nitric oxide synthase (iNOS)
- Inflammation
- Interleukin-1β (IL-1β)
- Nitric oxide (NO)
- Oligomeric Aβ1-42
- Tumor necrosis factor-α (TNF-α)
ASJC Scopus subject areas
- Neurology