Mitochondrial dynamics in neurodegeneration

Trends Cell Biol. 2013 Feb;23(2):64-71. doi: 10.1016/j.tcb.2012.10.006. Epub 2012 Nov 16.

Abstract

It has been only 15 years since studies began on the molecular mechanisms underlying mitochondrial fission and fusion using simple model organisms such as Drosophila, yeast, and Caenorhabditis elegans. Beyond the primary functions of mitochondrial fission and fusion in controlling organelle shape, size, and number, it became clear that these dynamic processes are also critical to regulating cell death, mitophagy, and organelle distribution. Now, studies suggest that prominent changes occur in mitochondrial dynamics in a broad array of neurodegenerative diseases, and there is substantial evidence suggesting a key role in disease pathogenesis because neurons are among the most energy-consuming cell types and have a highly developed cell shape. Here, we review the recent findings on mitochondrial dynamics in neurodegeneration.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Alzheimer Disease / metabolism
  • Alzheimer Disease / pathology
  • Animals
  • Biological Transport
  • Cell Death
  • Dynamins
  • GTP Phosphohydrolases / genetics
  • GTP Phosphohydrolases / metabolism
  • Humans
  • Mammals / metabolism
  • Mammals / physiology
  • Microtubule-Associated Proteins / genetics
  • Microtubule-Associated Proteins / metabolism
  • Mitochondria / metabolism
  • Mitochondria / pathology*
  • Mitochondrial Dynamics*
  • Mitochondrial Proteins / genetics
  • Mitochondrial Proteins / metabolism
  • Mitophagy*
  • Mutation
  • Neurodegenerative Diseases / metabolism*
  • Neurodegenerative Diseases / pathology
  • Optic Atrophy, Autosomal Dominant / metabolism
  • Optic Atrophy, Autosomal Dominant / pathology
  • Oxidative Stress

Substances

  • Microtubule-Associated Proteins
  • Mitochondrial Proteins
  • GTP Phosphohydrolases
  • DNM1L protein, human
  • Dynamins