Journal
EXPERIMENTAL GERONTOLOGY
Volume 38, Issue 1-2, Pages 101-107Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/S0531-5565(02)00162-6
Keywords
neuroprotection; mitochondria; estrogens; steroids
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Funding
- NIA NIH HHS [AG10485] Funding Source: Medline
- NATIONAL INSTITUTE ON AGING [P01AG010485] Funding Source: NIH RePORTER
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Polycyclic phenols, including the estrogens, have been shown to be potent neuroprotectants in a variety of cellular and animal model systems. Although classical estrogen receptor interactions and consequent responses play a role in certain circumstances, the neuroprotective activity of polycyclic phenols that do not interact with estrogen receptors ERalpha or ERbeta is more likely to be through non-genomic mechanism(s). We propose here that such non-feminizing polycyclic phenols exert their protective effects at least in part by stabilizing mitochondria, preventing apoptotic and/or necrotic forms of cell death that are associated with mitochondrial dysfunction. Consistent with this mitochondrial model and the available data, these compounds protect neurons and other cell types from a wide variety of pathologically relevant stressors. (C) 2002 Elsevier Science Inc. All rights reserved.
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