Gender is one of the main risk factors for Alzheimers disease (AD). Estrogen signaling has thus been implicated as an important factor in the incidence and development of AD. Decreased expression of estrogen receptor-? (ER?) in female patients with AD has been linked to impaired mitochondrial function and increased markers of oxidative stress. Furthermore, evidence from ER?-knockout mice suggests that ER? deficiency increases mitochondrial vulnerability to amyloid-? toxicity, which may contribute to aggravation of AD pathogenesis. Similarly, overexpression of ER? was shown to protect against A?-induced cytotoxicity via multiple mechanisms, doing so in a ligand-independent manner. The latter finding presents a new strategy in the development of treatments that will selectively agonize ER?, potentially allowing for efficacious neuroprotection while avoiding the side effects associated with estrogen replacement therapy.
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