Therapeutic strategies aimed at downregulating brain PUFA metabolism, such as the administration of carnitine palmitoyltransferase inhibitors [72,73] or PLA2 inhibitors (e.g. the mood stabilizers, lithium and carbamazepine), might be effective in slowing the progression of brain lipid abnormalities identified in this study, the associated changes in synaptic loss and possibly, cognitive dysfunction in the metabolic syndrome. This evidence concerns the gene PLA2G6 and metabolic syndrome.