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Neurotherapeutics
Published in: Neurotherapeutics 3/2013

01-07-2013 | Review

α-Synuclein and Mitochondria: Partners in Crime?

Author: Ken Nakamura

Published in: Neurotherapeutics | Issue 3/2013

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Abstract

Increased α-synuclein levels and mutations in mitochondria-associated proteins both cause familial Parkinson’s disease (PD), and synuclein and mitochondria also play central, but poorly understood, roles in the pathogenesis of idiopathic PD. A fraction of synuclein interacts with mitochondria, and synuclein can produce mitochondrial fragmentation and impair mitochondrial complex I activity. However, the consequences of these mitochondrial changes for bioenergetic and other mitochondrial functions remain poorly defined, as does the role of synuclein–mitochondria interactions in the normal and pathologic effects of synuclein. Understanding the functional consequences of synuclein’s interactions with mitochondria is likely to provide important insights into disease pathophysiology, and may also reveal therapeutic strategies.
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Metadata
Title
α-Synuclein and Mitochondria: Partners in Crime?
Author
Ken Nakamura
Publication date
01-07-2013
Publisher
Springer US
Published in
Neurotherapeutics / Issue 3/2013
Print ISSN: 1933-7213
Electronic ISSN: 1878-7479
DOI
https://doi.org/10.1007/s13311-013-0182-9

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