Abstract
Estrogens, particularly estradiol-beta, constitute a complexity in hormonereceptivity that evolves via the prevention of delayed cell-death pathways. Neurodegeneration, and ischemic injury to neural tissue, represent a panoramic array of effects that are especially linked to physiologic levels of estradiol-beta. The aging brain, in particular, involves the developmental emergence of immediate gene response that is linked to such estrogen-receptor interactions.
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