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Lookup NU author(s): Professor Tiago OuteiroORCiD
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The pathogenesis of many neurodegenerative disorders arises in association with the misfolding and accumulation of a wide variety of proteins. Much emphasis has been placed on understanding the nature of these protein accumulations, including their composition, the process by which they are formed and the physiological impact they impose at cellular and, ultimately, organismal levels. Alpha-synuclein (ASYN) is the major component of protein inclusions known as Lewy bodies and Lewy neurites, which are the typical pathological hallmarks in disorders referred to as synucleinopathies. In addition, mutations or multiplications in the gene encoding for ASYN have also been shown to cause familial cases of PD, the most common synucleinopathy. Although the precise function of ASYN remains unclear, it appears to be involved in a vast array of cellular processes. Here, we review, in depth, a spectrum of cellular and molecular mechanisms that have been implicated in synucleinopathies. Importantly, detailed understanding of the biology/pathobiology of ASYN may enable the development of novel avenues for diagnosis and/or therapeutic intervention in synucleinopathies. © 2013 -IOS Press and the authors.
Author(s): Wales P, Lazaro DF, Pinho R, Outeiro TF
Publication type: Review
Publication status: Published
Journal: Journal of Parkinson's Disease
ISSN (print): 1877-7171
ISSN (electronic): 1877-718X
Publisher: I O S Press
PubMed id: 24270242