I. Mookjung et al., ESTROGEN BLOCKS NEUROTOXIC EFFECTS OF BETA-AMYLOID(1-42) AND INDUCES NEURITE EXTENSION ON B103 CELLS, Neuroscience letters, 235(3), 1997, pp. 101-104
Clinical studies have shown that estrogen replacement therapy is assoc
iated with reduced risk of Alzheimer's disease (AD). We tested whether
or not estrogen blocks neurotoxic effects of beta-amyloid (1-42) (A b
eta(1-42)) on cultured B103 cells. A beta(1-42) (1 mu M) induced typic
al necrotic cell death, as revealed by light and electron microscopic
examinations. Go-administration of estrogen not only blocked A beta(1-
42) toxicity to a large degree, but also enhanced neurite extension. P
retreatment with estrogen was even more effective in blocking A beta(1
-42) toxicity. When added 18 h after the beginning of A beta(1-42) tre
atment, estrogen was still effective in halting the progress of cell d
eath and enhancing neurite extension. The protection against A beta(1-
42)-induced neuronal death by estrogen was unlikely due to a blockade
of lipid peroxidation injury, since estrogen completely failed to atte
nuate ferrous chloride-induced cell death. These results demonstrate t
hat estrogen blocks A beta(1-42)-induced neurotoxicity and enhances ne
urite extension on B103 cells, both of which may well be underlying me
chanisms of beneficial effects of estrogen in AD. (C) 1997 Elsevier Sc
ience Ireland Ltd.