PD involves AMPK dysfunction characterized by reduced AMPK phosphorylation in the substantia nigra, impairing cellular stress responses, where AMPK activation exerts neuroprotection through direct phosphorylation of ULK1 and mTORC1 inhibition to enhance autophagy, along with TFEB activation to promote lysosomal biogenesis, facilitating α‐synuclein clearance and improving neuronal survival in MPTP models [92, 93, 94, 95]. This evidence concerns the gene PRKAA2 and Parkinson disease.