| Literature DB >> 26526613 |
Dominik Haddad1, Ken Nakamura2.
Abstract
Mitochondria are undoubtedly changed in Parkinson's disease (PD), and mitochondrial functions are disrupted in genetic and pharmacologic models of PD. However, many of these changes might not truly drive neurodegeneration. PD is defined by the particular susceptibility of nigrostriatal dopamine (DA) neurons, but little is understood about the mitochondria in these cells. Here, we critically review the evidence that mitochondrial stressors cause PD. We then consider how changes in the intrinsic function of mitochondria and in their mass, distribution, and dynamics might synergize with an increased need for mitochondria and produce PD, and the importance of understanding how mitochondria contribute to its pathogenesis.Entities:
Keywords: Bioenergetics; Dopamine; Mitochondria; Neurodegeneration; Parkinson’s disease
Mesh:
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Year: 2015 PMID: 26526613 PMCID: PMC4679488 DOI: 10.1016/j.febslet.2015.10.021
Source DB: PubMed Journal: FEBS Lett ISSN: 0014-5793 Impact factor: 4.124