期刊
GLIA
卷 48, 期 1, 页码 85-90出版社
WILEY
DOI: 10.1002/glia.20051
关键词
Alzheimer's disease; astrocytes; beta-amyloid peptide; cyclooxygenase-2; hippocampus; microglia; minocycline; neurodegeneration
Minocycline, a second-generation tetracycline compound, has been examined as a neuroprotectant in beta-amyloid (Abeta)-injected rat hippocampus. At 7 days post-injection, Abeta(1-42) caused a significant loss of granule cell layer neurons (28% reduction) compared to control uninjected hippocampus. Hippocampal injection of Abeta 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 Abeta(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. (C) 2004 Wiley-Liss, Inc.
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