Abstract

Alcohol abuse causes impairment of cognitive function ranging from mild forms to end-stage dementia. Alcohol-related dementia accounts for nearly 20% of all admissions to state mental hospitals and may result from head trauma, thiamine deficiency, Alzheimer's, and other brain diseases that can be diagnosed conclusively only at autopsy. However, we postulate that after all these conditions have been excluded, an "alcohol encephalopathy" remains. This is characterized by impaired synaptic function, which underlies the continuum of impaired intellectual function. We found in 79 histologically normal brains of a nondemented general hospital population a 40% decrease in the density of cholinergic muscarinic receptors in the frontal cortex of alcoholics when compared with matched controls of the same age. Only alcohol abuse and not aging, postmortem changes, medications, clinical (including liver) diseases, or differences in causes of death could account for this loss.

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