Abstract
α-lipoic acid (α-LA) improved longer-term memory of aged female NMRI mice in the habituation in the open field test at a dose of 100 mg/kg body weight for 15 days. In a separate experiment, no such effect could be found for young mice. α-LA alleviated age-related NMDA receptor deficits ( B max) without changing muscarinic, benzodiazepine, and α 2-adrenergic receptor deficits in aged mice. The carbachol-stimulated accumulation of inositol monophosphates was not changed by the treatment with α-LA. These results give tentative support to the hypothesis that α-LA improves memory in aged mice, probably by a partial compensation of NMDA receptor deficits. Possible modes of action of α-LA based on its free radical scavenger properties are discussed in relation to the membrane hypothesis of aging.
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