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29 October 2001. 29 October 2001. Estrogen replacement therapy may protect postmenopausal
women from Alzheimer's disease, according to some epidemiological studies.
For example, a recent short trial of high-dose 17β-estradiol found
significant improvement in cognitive test performance in postmenopausal
women with AD (Asthana et al., 2001). While the role of estrogen in AD is being debated, cell biologists are looking for mechanisms by which the hormone might prevent neurodegeneration. Candidate mechanisms include
transcriptional and post-transcriptional processes, as well as the
hypothesis that estrogen helps prevent programmed
cell death. In the October 15 Journal of Neuroscience, Andrea LeBlanc and
colleagues at McGill University in Montreal report that this
protection could be mediated by the inhibition of caspase-6.
Spurred by disparate bits of evidence that caspase-6 may play a role in the
pathogenesis of AD, LeBlanc's group assessed the effects of several
neuroprotective agents against caspase-6-mediated apoptosis. They found
that 17β-estradiol prevents caspase-6-mediated neuronal death in vitro,
whereas neither the transcriptionally inactive 17α-estradiol nor
testosterone do so. The authors suggest that this is mediated by a
caspase-inhibitory factor (CIF) via the estrogen receptor. Because
17β-estradiol induces CIF activity within minutes, this pathway
apparently does not require new protein synthesis. Junying Yuan, of Harvard
Medical School, is cautious in appraising these results. "There is no
evidence that the CIF in this paper is actually one activity, which may or
may not be relevant to the effect of the hormone on AD," she says.-Hakon Heimer.
Reference:Zhang Y, Tounekti O, Akerman B, Goodyer CG, LeBlanc A. 17b-estradiol induces an inhibitor of active caspases. J Neurosci 2001 October 15;21(20):RC176. Abstract
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17-beta-estradiol induces an inhibitor of active caspases.
