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Parkinson's disease (PD) is the most common neurodegenerative movement disorder, which affects about 1% of the population over age 60. The pathological hallmark of the disease is the loss of dopaminergic neurons in the substantia nigra leading to the major clinical symptoms, including bradykinesia, rigidity, tremor and postural instability. These symptoms respond well to the dopaminergic therapy, however complications such as dyskinesia and dystonia are often observed after 5-10 years of treatment. The majority of all PD cases are sporadic suggesting a multifactorial etiology based on environmental and genetic factors. However, 5 to 15 % of all PD patients present with a positive family history for the disease. Onset is usually earlier in these forms. The characterization of familial forms of PD allowed the identification of 10 gene loci (PARK1-10) with subsequent characterization of five disease genes: alpha-synuclein, parkin, ubiquitin-C-terminal hydrolase L1, DJ-1 and PINK1. Some of these genes are also suspected to function as susceptibility factors in common sporadic PD. The identification of mutations in additional genes, i.e. NR4A2, neurofilament M and synphilin-1 in familial or apparently sporadic forms of PD provides increasing evidence for genetic heterogeneity of PD and opens new therapeutic perspectives.
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