Parkinson’s disease (PD), the second most common neurodegenerative disease after Alzheimer’s disease, affects approximately 1 % of the population over 65 years of age. PD is primarily a sporadic disease and aging is the principal risk factor. Sporadic PD is a complex multifactorial disorder with variable contribution of genetic susceptibility and environmental factors. Several mechanisms are involved in the disease pathogenesis, such as mitochondrial dysfunctions, oxidative damage, autophagic alterations, proteasome impairment and protein aggregation . There are also familial forms of PD, accounting for 5–10 % of all cases, associated with mutations in PARK genes. Interestingly, PARK genes encode for proteins involved in the maintenance of protein homeostasis, mitochondrial integrity and release of neurotransmitter-containing vesicles . One of the major pathological hallmarks of PD is the accumulation of α-synuclein-containing aggregates (Lewy bodies) in neuronal perikarya and processes as a consequence of the proteolytic deficit, typical of the pathology.
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