Abstract
Parkinson's disease (PD) is a common, age-related, neurodegenerative disorder characterized by motor deficits and a cognitive decline. In the large majority of cases, it is associated with cytoplasmic aggregation of α-synuclein/SNCA and the formation of Lewy bodies in the dopamine neurons in the substantia nigra pars compacta. The etiopathogenesis of PD remains poorly understood. The disease results from an interplay of genetic and environmental factors, including pharmacological molecules, which destroy dopaminergic neurons. Recently, several notable data have highlighted various immune alterations underlying that PD is associated to autoimmune features and could be considered as an autoimmune disease. In this short article, we briefly review key elements participating to this emerging viewpoint.
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