ანოტაცია
Parkinson’s Disease (PD) is a progressive neurodegenerative disorder marked by dopaminergic neuron loss in the substantia nigra pars compacta and α-synuclein aggregation. Growing evidence identifies mitochondrial dysfunction as a central driver of PD pathogenesis (1-3), linking genetic mutations, oxidative stress, environmental toxins, and lysosomal impairment. This review summarizes major mitochondrial abnormalities-complex I deficiency, mtDNA damage, disrupted dynamics, defective mitophagy, and impaired mitochondria - lysosome crosstalk (1,4). The roles of PD-related genes (PINK1, Parkin, LRRK2, GBA1, DJ-1, VPS35) and environmental toxins (MPTP, rotenone, paraquat) (5-7) are discussed, along with therapeutic strategies including antioxidants, mitophagy enhancers, gene therapy, and lifestyle interventions. Understanding mitochondrial mechanisms provides a foundation for precision, disease-modifying therapies.
წყაროები
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