title: Alpha-synuclein and intracellular trafficking: impact on the spreading of Parkinson's disease pathology.
abstract: Parkinson's disease is characterized by intracellular proteinaceous depositions known as Lewy bodies. These largely consist of the protein α-synuclein, whose physiological function remains unclear, but mutations and overexpression of the protein have been shown to cause early onset cases of Parkinson's disease. Deregulation of α-synuclein biology causes neurodegeneration and impaired neuronal trafficking, hinting at a possible contribution to the pathological mechanism. Recent studies produced some evidence hinting at the involvement of several regulators of the transport machinery such as Rab GTPases and SNARE proteins, but also shown that α-synuclein can be propagated between cells. Here, we discuss the molecular interplay of α-synuclein with the intracellular transport machinery, its consequences, and the implications for disease mechanisms.
authors.affiliation: Department for Neurodegeneration and Restorative Research, Center for Nanoscale Microscopy and Molecular Physiology of the Brain, University Medical Center Göttingen, Waldweg 33, 37073 Göttingen, Germany.
authors.forename: Sibylle E
authors.initials: SE
authors.lastname: Eisbach
authors.forename: Tiago F
authors.initials: TF
authors.lastname: Outeiro
mesh_terms: D000818:Animals; D001369:Axons / Q000378:metabolism; D001692:Biological Transport; D006801:Humans; D010300:Parkinson Disease / Q000378:metabolism*; D050600:SNARE Proteins / Q000378:metabolism; D013572:Synaptic Vesicles / Q000378:metabolism; D051844:alpha-Synuclein / Q000378:metabolism*; D020691:rab GTP-Binding Proteins / Q000378:metabolism
chemical_list: D050600:SNARE Proteins; D051844:alpha-Synuclein; D020691:rab GTP-Binding Proteins