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Journal of Biomedicine and Biotechnology
Volume 2006 (2006), Article ID 19365, 4 pages
doi:10.1155/JBB/2006/19365
Mini-Review Article

Mechanisms of Neuronal Death in Synucleinopathy

Atsushi Takeda,1 Takafumi Hasegawa,1 Michiko Matsuzaki-Kobayashi,1 Naoto Sugeno,1 Akio Kikuchi,1 Yasuto Itoyama,1 and Katsutoshi Furukawa2

1Department of Neurology, Center for Asian Traditional Medicine Research, Graduate School of Medicine, Tohoku University, 1-1 Seiryomachi, AobakuSendai 980-8574, Japan
2Department of Geriatric and Complementary Medicine, Center for Asian Traditional Medicine Research, Graduate School of Medicine, Tohoku University, 1-1 Seiryomachi, Aobaku 980-8574, Sendai, Japan

Received 1 December 2005; Accepted 20 March 2006

Copyright © 2006 Atsushi Takeda et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

α-synuclein is a key molecule in the pathogenesis of synucleinopathy including Parkinson's disease and multiple system atrophy. In this mini-review, we mainly focus on recent data obtained from cellular models of synucleinopathy and discuss the possible mechanisms of neurodegeneration. Recent progress suggests that the aggregate formation of α-synuclein is cytoprotective and that its precursor oligomer (protofibril) may be cytotoxic. The catechol-derived quinones are the candidate molecules that facilitate the oligomer formation of α-synuclein. Furthermore, the cellular membranes are shown to be the primary targets injured by mutant α-synucleins, and the mitochondrial dysfunction seems to be an initial step in the neuronal death.