The specific mechanisms of oligodendrocyte dysfunction have been explored with mixed results. In cortical cultures, both Th1 (pro-inflammatory) and Th2 (anti-inflammatory) cytokines decrease alcohol-induced oligodendrocyte cell death (Benjamins et al. 2011). Furthermore, alcohol downregulates oligodendroglial c-Fos (an immediate early gene) and upregulates myelin basic protein (MBP) in a protein kinase C-dependent manner (Bichenkov et al. 2009). However, myelin gene expression (including MBP) is less disrupted (with decreased concomitant neurodegeneration) in TLR4 knockout mice after chronic ethanol exposure (Alfonso-Loeches et al. 2012).
