PRKAA1 and Parkinson disease: 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].