Figure 1.

Mitochondrial Dysfunction in Parkinson’s Disease (PD). Various factors, including genetic susceptibility, environmental influences, mtDNA mutations and aging, have been implicated in the onset of Parkinson’s disease. Notably, abnormalities in mitochondrial metabolic function, morphology and homeostasis are observed, which contribute to the formation of α-synuclein aggregates and the subsequent death of dopaminergic (DA) neurons, thereby driving the progression of neurodegeneration. SNCA, Synuclein Alpha; LRRK, leucine-rich repeat kinase 2; VSP35, Vacuolar protein sorting ortholog 35; CHCHD2, Coiled-coil-helix-coiled-coil-helix domain containing 2; PINK1, PTEN-induced kinase 1; PARK7, Parkinson disease protein 7; PRKN, parkin RBR E3 ubiquitin protein ligase; ATP13A2, ATPase Cation Transporting 13A2; mtDNA, mitochondrial DNA; Ca²⁺, calcium ions; ROS, Reactive Oxygen Species; ATP, Adenosine triphosphate.