ABSTRACT
Alcohol is a neuroactive addictive depressant drug, and chronic ethanol consumption has been associated with pleiotropic effects on cellular function. The mechanism by which it exerts its toxic effects is still unclear. Ethanol is known to elicit neurotoxicity characterized by ataxia, loss of coordination, hyperexcitation, convulsions, and paralysis. Excess alcohol consumption alters neuronal growth and causes striking neuronal degeneration and cell death in several brain regions, resulting in loss of memory and cognitive impairments. Several mechanisms, such as calcium overload, excitotoxicity, free radical injury, and disturbance in protein synthesis have been implicated in chronic ethanol-mediated neuronal cell death. By contrast, the signal transduction pathways that converge in cell death are incompletely defined and briefly reviewed in this chapter in the context of ethanol-induced neurotoxicity. Further, applications and utility of recent advances in microarrays,
gene expression profiles, transgenic knockout technology, and stem cell biology have been considered in alcoholic neuropathology.
