Abstract
Clinical studies have shown that estrogen replacement therapy is associated with reduced risk of Alzheimer's disease (AD). We tested whether or not estrogen blocks neurotoxic effects of β-amyloid (1–42) (A β 1–42) on cultured B103 cells. A β 1–42 (1 μM) induced typical necrotic cell death, as revealed by light and electron microscopic examinations. Co-administration of estrogen not only blocked A β 1–42 toxicity to a large degree, but also enhanced neurite extension. Pretreatment with estrogen was even more effective in blocking A β 1–42 toxicity. When added 18 h after the beginning of A β 1–42 treatment, estrogen was still effective in halting the progress of cell death and enhancing neurite extension. The protection against A β 1–42-induced neuronal death by estrogen was unlikely due to a blockade of lipid peroxidation injury, since estrogen completely failed to attenuate ferrous chloride-induced cell death. These results demonstrate that estrogen blocks A β 1–42-induced neurotoxicity and enhances neurite extension on B103 cells, both of which may well be underlying mechanisms of beneficial effects of estrogen in AD.
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