Mitochondrial alpha-synuclein accumulation impairs complex I function in dopaminergic neurons and results in increased mitophagy in vivo
Research highlights
▶ α-Syn physically localizes to dopaminergic mitochondria in vivo and impacts on mitochondrial function. ▶ Localization coincides with a selective age-related mitochondrial complex I inhibition and decreased substrate-specific respiration. ▶ Also observed an increase in lysosome-mediated mitochondrial autophagy (mitophagy) in A53T overexpressing midbrain dopaminergic neurons, likely a compensatory attempt to remove defective mitochondria.
Section snippets
Conflict of interest
The authors report no conflicts of interest.
Acknowledgements
We would like to thank Daniel Crippen for technical assistance with EM studies and Dr. Bharat Srinivas for early discussions on this project. This work was financially supported by NIH R01 AG12141 to JKA and American Parkinson's Disease Association to SJC.
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