Cognitive performance declines moderately with normal aging and severely with pathological aging. A similar range of intellectual impairment has been described in association with prolonged alcohol consumption. It is doubtful that all types and degrees of alcohol‐associated impairments of cognitive function are attributable only to thiamin deficiency. Evidence from human and animal data indicates increasingly that alcohol per se has direct CNS toxic effects as well, and it is dangerous to suggest that adequate thiamin consumption alone would prevent all CNS toxic effects of chronic alcohol consumption.If a direct role of ethanol in CNS toxicity is accepted, it becomes important to study the molecular basis of the behavioral impairment caused by both aging and alcohol abuse in order to develop rational treatment and prevention. An entire spectrum of relationships is possible between aging and alcohol‐related CNS changes. At the one end of the spectrum could simply be deficits additive at the behavioral level but caused by different molecular events. Conversely, molecular processes of biological aging could interact with molecular effects of ethanol, potentiating each other and culminating in an accelerated aging process. Many pathological mechanisms could lead to an irreversible loss of neuronal cell bodies. However, changes in peripheral cell processes, including the synapses, may be equally important in limiting interneuronal communications that result in behavioral deficits. Some changes could even be limited to a decrease of numbers or affinity of synaptic receptor molecules of a particular region. From the human and animal data reviewed, chronic ethanol consumption appears to increase some behavioral deficits caused by aging. What the exact interrelationships are at the molecular basis for the behavioral changes is not yet cl