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.
