Marked increase in lipid peroxidation product (4-HNE) and decrease of neuron-specific neurofilaments support the notion that the peroxidation process of cellular protein and disruption of neuronal cytoskeleton could be initial steps in alcohol-associated neurodegeneration. Clinical trials for many neurological diseases target the role of antioxidants, and it is imperative to understand the mechanisms leading to induction of oxidative stress and the nature of oxidative damage resulting in progressive neurodegeneration. Thus, our data on how alcohol (drug of abuse and potent stimulant) initiates the activation of biochemical pathways and the cell signaling leading to neuronal injury will serve as the basis for future therapeutic interventions.
