Electron Transport Disturbances and Neurodegeneration: From Albert Szent-Györgyi’s Concept (Szeged) till Novel Approaches to Boost Mitochondrial Bioenergetics

Figure 4

The involvement of mitochondrial dysfunction in Parkinson’s disease. Complex I deficiency, the predominant electron transport disorder in sporadic PD has long been linked to the deleterious effects of α-synuclein aggregation, a pathognomonic alteration in PD, and inhibitors of complex I (such as MPTP, rotenone, and paraquat) are used in experimental modeling of the disease. Since then a number of genes have been associated with familial forms of the disease, many of them having direct implications in mitochondrial dysfunction. Disturbed OXPHOS in the affected cells can lead to the development of a vicious circle, eventually leading to cell death. Novel findings link PGC-1α dysfunction to the pathogenesis of sporadic PD, the restoration of which may hold therapeutic value. (↑ = increased presence/expression/activity; ↓ = decreased presence/expression/activity; arrow = promotion; bulb-headed arrow = inhibition/deterioration.)