Susan E. Bergeson

TL;DR: The results suggest that drugs that alter neuroimmune pathways may represent a new approach to developing additional therapies to treat alcoholism and suggest that neuroimmune activity of brain glia may have a role in drinking.

TL;DR: expression profiling of the cortex and striatum, hippocampus, cerebellum and the ventral brain region from alcohol‐naïve B6C and B6J mice showed intervals on three chromosomes that are enriched in clusters of coregulated transcripts significantly divergent between the substrains.

TL;DR: It is demonstrated that the PFC is more vulnerable to chronic alcohol-induced oxidative stress and neuronal cell death than the hippocampus, evidenced by elevated oxidative stress-induced DNA damage and enhanced expression of apoptotic markers in PFC neurons.

TL;DR: The role of DNA damage and DNA repair dysfunction in chronic alcohol-induced neurodegeneration is outlined and both DNA repair and DNA methylation are critical for maintaining genomic stability.

TL;DR: The results of this study are a proof of concept that bioinformatics analysis of brain gene expression can lead to the generation of new hypotheses and a positive translational outcome for individualized pharmacotherapeutic treatment of high alcohol consumption.