through methyl-malonyl-CoA, an intermediate formed by the essential cofactors methyl-tetrahydrofolate as the methyl-donor, and vitamin B12. Folate deficiency, often observed in alcohol-dependent patients,70 may therefore interfere with this pathway and prevent the availability of a sufficient supply of acetyl-CoA. Expression of PECR is highest in the liver, followed by the kidney, muscle tissue, the lungs and the heart, but barely – if at all – in the brain.71If this gene is involved in alcohol dependence, it must act in the periphery rather than in the CNS. It could therefore be expected that we detected PECR only in our GWAS, which identifies susceptibility genes independent of organ-specific expression, but not in the animal approach, which is brain-specific.
