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Mitochondria in the context of Parkinson's disease


Parkinson's disease (PD) is the second most common neurodegenerative disease, affecting 1–2% of the population over the age of 65. Rigidity, bradikynesia, postural instability and tremor are the principal clinical characteristics of this disease, caused by the progressive loss and degeneration of dopaminergic neurons in the Substantia nigra pars compacta (SNpc). Tremor and motor impairment appear when approximately 50–60% of these neurons degenerate, causing a 70–80% depletion of striatal dopamine (Lang and Lozano, 1998). The pathogenesis of PD involves a series of characteristics that are commonly observed in the affected brain areas of PD patients, like mitochondrial complex I and global lysosomal dysfunctions. Other features of the disease are increased indices of oxidative stress linked to a dysregulated inflammatory response or the presence of intra-neuronal protein aggregates designated as Lewy bodies (LBs), composed principally of metabolically altered alpha-synuclein. This dopaminergic neurodegeneration is closely related to autophagic degradation and protein aggregation, two especially important processes in the viability of the neuron (Ryan et al., 2015)

© Neural Regeneration Research

Neural Regen Res. 2017 Feb;12(2):214-215. doi: 10.4103/1673-5374.200802.

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