Estradiol protects against β-amyloid (25–35)-induced toxicity in SK-N-SH human neuroblastoma cells

• Published in: Neuroscience letters Vol. 218; no. 3; pp. 165 - 168
• Main Authors: Green, Pattie S., Gridley, Kelly E., Simpkins, James W.
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 08.11.1996; Elsevier
• Subjects: Alzheimer's disease; Amyloid beta-Peptides - toxicity; Biological and medical sciences; Cell Survival - drug effects; Dose-Response Relationship, Drug; Estradiol; Estradiol - pharmacology; Estrogens; Humans; Medical sciences; Neuroblastoma; Neuropharmacology; Neuroprotective agent; Neuroprotective Agents - pharmacology; Neurotoxins - pharmacology; Peptide Fragments - toxicity; Pharmacology. Drug treatments; SK-N-SH cells; Tumor Cells, Cultured - cytology; Tumor Cells, Cultured - drug effects; β-Amyloid; β-Amyloid; SK-N-SH cells; Estradiol; Alzheimer's disease; Estrogens; Human; Chemotherapy; Cell line; Neuron; Treatment; Cell death; β Amyloid protein; Toxicity; Estrogen; Neuroprotective agent; In vitro
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/S0304-3940(96)13148-7

Estrogen-replacement therapy has been associated with a reduced incidence of Alzheimer's disease (AD) and improved cognition in several small open clinical trials. We assessed the possibility that estrogens may reduce toxicity of β-amyloid (Aβ) by testing the effects of β-estradiol on the toxicity of the neurotoxic fragment of β-amyloid (Aβ 25–35) in SK-N-SH neuroblastoma cells. Aβ 25–35 caused a dose-dependent death in SK-N-SH cells with a LD 50 of 28.9 μM. In cultures simultaneously exposed to 20 μM Aβ and 17 β-estradiol (2 nM), Aβ-induced toxicity was reduced by 83 and 51% in two separate studies. Further studies show that 0.2 nM 17 β-estradiol was as effective as the 2 nM concentration. 17 a-Estradiol (2 nM) conferred neuroprotection equivalent to that of 17 β-estradiol. These data support the hypothesis that estrogens reduce β-amyloid toxicity and this may help explain the beneficial effects of estrogens in AD.