Apoptosis, genetically preprogrammed death of scattered cells, leaves
few histological traces and is compatible with autopsy findings in bra
ins of alcoholics. This type of cell death could be triggered by chron
ic exposure to alcohol. Interactions between alcohol and the activatin
g and inhibiting molecular events of the apoptotic cascade could occur
at several different levels. Sites of alcohol action could range from
the transcription of the apoptosis genes to translation and posttrans
lational modifications of their protein products. The recent developme
nts of in situ hybridization technology make it possible to determine
the levels of the neurotoxic actions of ethanol and to detect early st
ages of toxicity where increased mRNA activity may compensate for loss
es of receptors, enzymes, peptide transmitters, or structural proteins
. The potential for treatment with antisense nucleotides is discussed.