期刊
NEUROBIOLOGY OF AGING
卷 22, 期 6, 页码 823-836出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/S0197-4580(01)00303-7
关键词
Alzheimer's diseased; CNS; hippocampus; human; astrocytes; nonsteroidal anti-inflammatory drugs; prostaglandin-endoperoxide synthase
资金
- NIA NIH HHS [AG08665] Funding Source: Medline
- NINDS NIH HHS [NS33553] Funding Source: Medline
Nonsteroidal anti-inflammatory drugs (NSAIDs) appear to delay the onset of Alzheimer's disease (AD). NSAIDs inhibit cyclooxygenase (COX), of which two isoforms exist. We report decreased neuronal COX-2 expression in AD subjects relative to nondemented controls using qualitative analysis of COX-2 immunoreactivity and quantification of COX-2 positive neurons in different hippocampal subfields. These changes also occurred in subjects with other dementia and thus may not be disease specific. The proportion of COX-2 positive neurons decreased in subjects with clinical dementia rating (CDR) 5 but not CDR 4, suggesting that this was a late event in the course of the disease. Furthermore, COX-2 was not preferentially associated with paired helical filament immunoreactivity, a marker of neuronal pathology. COX-2 immunoreactivity was also observed in astrocytes and cerebrovasculature. Indeed, the density of COX-2 immunopositive astrocytes was increased in AD temporal cortex. Based on our findings, it is unlikely that neuronal COX-2 contributes to pathology in end stage AD; however, COX-2 in other cell types may participate in the inflammation-related response associated with the disease. (C) 2001 Elsevier Science Inc. All rights reserved.
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