Browse by author
Lookup NU author(s): Professor Tiago OuteiroORCiD
Full text for this publication is not currently held within this repository. Alternative links are provided below where available.
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. © 2013 Springer-Verlag Berlin Heidelberg.
Author(s): Eisbach SE, Outeiro TF
Publication type: Review
Publication status: Published
Journal: Journal of Molecular Medicine
Print publication date: 01/06/2013
Online publication date: 25/04/2013
ISSN (print): 0946-2716
ISSN (electronic): 1432-1440
PubMed id: 23616088