dependence (Blednov et al., 2015). Reduced alcohol consumption by tesaglitazar and fenofibrate may be associated with signaling at GABAergic interneurons, neuropeptide systems and dopaminergic signaling pathways which ultimately regulate stress-related neurocircuitry (Ferguson et al., 2014). In sum, an association of SNPs in PECR and alcohol dependence fits with recent literature demonstrating a critical role of peroxisome neurobiology, particularly PPARs, in mediating alcohol-related phenotypes including alcohol consumption and withdrawal. A logical hypothesis may then be that genetic variation in PECR functions to alter the alcohol dependence phenotype in a similar fashion (via neuroinflammatory processes) to that of PPARs, particularly in stress-related neurocircuitry including the extended amygdala.
