The finding that, in animal models of type II diabetes, LSN induced potent glucose and lipid lowering effects comparable to rosiglitazone [25], combined with our demonstration of LSN-induced neuroprotection associated with decreased neuroinflammation in mice models of PD, suggests that pure PPAR-γ activity is not required for metabolic or neuroprotective efficacy. This evidence concerns the gene PPARG and type 2 diabetes mellitus.