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Minocycline inhibits neuronal death and glial activation induced by β‐amyloid peptide in rat hippocampus
Author(s) -
Ryu Jae K.,
Franciosi Sonia,
Sattayaprasert Prasongchai,
Kim Seung U.,
McLar James G.
Publication year - 2004
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.20051
Subject(s) - minocycline , microglia , gliosis , hippocampal formation , biology , hippocampus , neuroglia , intraperitoneal injection , amyloid beta , neurodegeneration , immunostaining , astrocyte , neurotoxicity , endocrinology , medicine , pharmacology , immunohistochemistry , peptide , central nervous system , neuroscience , immunology , inflammation , biochemistry , toxicity , disease , antibiotics
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.