These results are in line with several studies that reported, in models of depression other than that induced by alcohol, that PPAR-α agonists were able to increase the expression of BDNF (B. Jiang et al., 2015; 2017; Ni et al., 2018; Yang et al., 2017), and that this effect would be directly related to the decrease in neuroinflammation (Yang et al., 2017). The gene discussed is BDNF; the disease is depressive symptom measurement.