Likewise, exercise mimetics such as GW501516 (PPARδ agonist) and thiazolidinedione (PPARγ agonists) activate the PGC-1α–PPAR axis and can indirectly influence the KP; however, despite these mechanistic effects, their clinical use in mood disorders remains experimental, with potential relevance only in depression associated with cardiometabolic conditions [99,100]. The gene discussed is PPARGC1A; the disease is depressive symptom measurement.