chromosome region 2q35 (PECR), see Fig. 1. PECR participates in chain elongation of fatty acids and is an integral component of peroxisomes which play a key role in protection against oxidative stress particularly in glial cells (Di Cesare Mannelli et al., 2014). Peroxisomal neurobiology has previously been implicated in alcohol dependence. Peroxisome proliferator-activated receptors (PPARs) are nuclear transcription factors with well-known roles in lipid metabolism and more recently have been associated with neuroinflammatory processes induced by alcohol (Varga et al., 2011). It is logical to assume that PECR and PPAR are part of the same biological pathway and thus likely have cooperative/complementary functions. PPAR agonists, including tesaglitazar and fenofibrate, reduce voluntary alcohol consumption, withdrawal severity and stress-induced relapse in rodents (Blednov et al., 2015, 2016; Stopponi et al., 2013; Stopponi et al., 2011). Re-analysis of GWAS data focusing only on SNPs within PPAR genes found an association of SNPs in PPARA and PPARG with alcohol withdrawal and PPARGC1A with alcohol 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
