Estrogen AD and Possible Mechanisms of Estrogen Induced Neuroprotection

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Recent evidence indicates that ERT both reduces the risk of AD in women and slows cognitive decline.1-2 The duration of ERT also seems to be important, because women with long-term use of ERT have the lowest risk.2 Gender differences were suggested as a possible explanation for the higher incidence of the familial AD in women that is also linked to the apoE-associated risk factor.5 In addition, Phillips and Sherwin32 showed that exogenous E2 maintains short-term memory in surgically-induced menopausal young women. Several levels of evidence demonstrated multiple sites of estrogen actions in the brain. The specific mechanism/s by which estrogen reduces dementia are unclear, and they might be combined in order to be beneficial in improvement of clinical symptoms. Estrogen and several other estrogenic steroids which are contained in Premarin (the most common ERT drug) were also indicated as potential neurotrophins that increased survival and growth of hippocam-pal and cortical neurons in vitro.33 Direct actions of E2 and other estrogenic steroids on neurons occurred rapidly, suggesting involvement of membrane receptor(s) that mediate estrogen-induced responses.34 Rapid membrane-mediated E2-induced responses are also consistent with E2 induction of cAMP, which was observed in breast cancer cells.35 The colocalization of estrogen receptors in several brain regions (hippocampus, frontal cortex, etc.) with nerve growth factor receptors suggests a possible role of growth factors in mediated estrogen beneficial effects.36

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