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Minocycline inhibits neuronal death and glial activation induced by β-amyloid peptide in rat hippocampus

✍ Scribed by Jae K. Ryu; Sonia Franciosi; Prasongchai Sattayaprasert; Seung U. Kim; James G. McLarnon

Publisher
John Wiley and Sons
Year
2004
Tongue
English
Weight
356 KB
Volume
48
Category
Article
ISSN
0894-1491

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✦ Synopsis

Abstract

Minocycline, a second‐generation tetracycline compound, has been examined as a neuroprotectant in β‐amyloid (Aβ)‐injected rat hippocampus. At 7 days post‐injection, Aβ~1‐42~ caused a significant loss of granule cell layer neurons (28% reduction) compared to control uninjected hippocampus. Hippocampal injection of Aβ peptide also led to marked gliosis with numbers of microglia (increased by 26‐fold) and immunoreactivity of astrocytes (increased by 11‐fold) relative to control, as determined from immunohistochemical analysis. Intraperitoneal administration of minocycline significantly reduced neuronal loss induced by Aβ~1‐42~ (by 80%) and also diminished numbers of microglia (by 69%) and astrocytes (by 36%) relative to peptide alone. Peptide injection increased expression of cyclooxygenase‐2 (COX‐2) in most (about 70%) of granule cells, a subset (about 20%) of microglia, but not in astrocytes; in the presence of minocycline, COX‐2 immunostaining was abolished in microglia. The results from this study suggest that minocycline may have efficacy in the treatment of AD. © 2004 Wiley‐Liss, Inc.

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