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Alpha‐synuclein N‐ and C‐terminal regions have distinct in vivo roles in mitochondrial fragmentation and oxidation: Implications for a pathogenic mitochondrial pathway for Parkinson’s disease (PD)

Mitochondrial health depends on a critical balance between fission via dynamin‐related protein 1 (DRP1) and fusion via mitofusin (MFN) in concert to mitochondrial motility, and defects in fission‐fusion and motility are linked to neuronal dysfunction. In Parkinson’s disease (PD) which is characterized by progressive neuronal loss and α‐syn‐rich Lewy bodies, the presence of impaired mitochondrial function, fragmentation, and high oxidative stress are also seen.