Abstract

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.

Author affiliations

1. Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, 4000 Central Florida Boulevard, Orlando, Florida 32816, USA.
2. National Center for Microscopy and Imaging Research, School of Medicine, University of California, San Diego, La Jolla, California 92093, USA.
3. Department of Molecular Biology, University of Salzburg, 5020 Salzburg, Austria.

Correspondence to: Ella Bossy-Wetzel¹ Email: ebossywe@mail.ucf.edu

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