Journal
NATURE REVIEWS NEUROSCIENCE
Volume 9, Issue 7, Pages 505-518Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrn2417
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Funding
- NCRR NIH HHS [P41 RR004050-208517, P41 RR004050] Funding Source: Medline
- NEI NIH HHS [R01 EY016164-03, R01 EY016164-04, R01 EY016164, R01 EY016164-05, R01 EY016164-02, R01 EY016164-01] Funding Source: Medline
- NIEHS NIH HHS [P42 ES010337, P42 ES010337-09] Funding Source: Medline
- NINDS NIH HHS [R01 NS047456-01S1, R01 NS055193-02, R01 NS047456-04, R01 NS055193, R01 NS047456-01, R01 NS047456-05, R01 NS047456-03S1, R01 NS055193-01A2, R01 NS047456-02, R01 NS047456, R01 NS047456-03] Funding Source: Medline
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Mitochondria are remarkably dynamic organelles that migrate, divide and fuse. Cycles of mitochondrial fission and fusion ensure metabolite and mitochondrial DNA mixing and dictate organelle shape, number and bioenergetic functionality. There is mounting evidence that mitochondrial dysfunction is an early and causal event in neurodegeneration. Mutations in the mitochondrial fusion GTPases mitofusin 2 and optic atrophy 1, neurotoxins and oxidative stress all disrupt the cable-like morphology of functional mitochondria. This results in impaired bioenergetics and mitochondrial migration, and can trigger neurodegeneration. These findings suggest potential new treatment avenues for neurodegenerative diseases.
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