However, it is becoming increasingly evident that all cellular and biochemical alterations observed in metabolic syndrome like impairment of endothelial cell function, abnormality in essential fatty acid metabolism and alterations in lipid mediators along with abnormal insulin/leptin signaling may represent a pathological bridge between metabolic syndrome and neurological disorders (Raffaitin et al., 2009; Vanhanen et al., 2006; Yates et al., 2012). This evidence concerns the gene LEP and metabolic syndrome.