Inhibition of amyloid-β-induced neurotoxicity and apoptosis by moderate ethanol preconditioning
Title
Inhibition of amyloid-β-induced neurotoxicity and apoptosis by moderate ethanol preconditioning
Publication type
Journal Article
Year of Publication
2004
Authors
Journal
NeuroReport
Volume
15
Issue
13
Pagination
2093 - 2096
Date published
2004
ISBN
09594965 (ISSN)
Keywords
alcohol, Alzheimer disease, amyloid beta protein, Amyloid beta-Protein, Amyloid-beta, animal model, animal tissue, Animals, Animals, Newborn, apoptosis, article, Benzimidazoles, brain level, cell protection, Central Nervous System Depressants, chaperone, Dose-Response Relationship, Drug, Drug Interactions, entorhinal cortex, enzyme linked immunosorbent assay, Enzyme-Linked Immunosorbent Assay, Ethanol, glia cell, glycoprotein gp 120, heat shock protein 70, hippocampus, hoe 33342, HSP70 Heat-Shock Proteins, Human immunodeficiency virus 1, Hydro-Lyases, lactate dehydrogenase, nerve degeneration, neuroprotection, neurotoxicity, nonhuman, Organ Culture Techniques, Preconditioning, priority journal, Propidium, propidium iodide, rat, Rats, Rats, Sprague-Dawley, staining, tissue culture cell
Abstract
Consumers of moderate amounts of ethanol have a lower risk of Alzheimer's dementia than do abstainers. In Alzheimer's disease the brain contains many extracellular plaques composed of amyloid-β (Aβ), a neurotoxic protein linked to pathogenesis of the disease. Here we report that moderate ethanol preconditioning (20-30 mM for 6 days) of organotypic hippocampal-entorhinal slice cultures prevents Aβ-induced neurotoxicity and apoptosis as measured by media lactate dehydrogenase levels and staining with propidium iodide and Hoechst 33342. With Aβ, as with our previous studies of the neurotoxic HIV-1 protein gp120, moderate ethanol preconditioning may interfere with various glial-mediated neurotoxic responses in the slices to Aβ. In addition, we found that moderate ethanol preconditioning causes an almost 3-fold increase in brain levels of heat shock protein 70 (hsp70), a protective molecular chaperone. Our results suggest possible molecular mechanisms underlying the protective effect of moderate drinking against Alzheimer's dementia.