Title

Mitochondrial fragmentation in neurodegeneration

Authors

Authors

A. B. Knott; G. Perkins; R. Schwarzenbacher;E. Bossy-Wetzel

Comments

Authors: contact us about adding a copy of your work at STARS@ucf.edu

Abbreviated Journal Title

Nat. Rev. Neurosci.

Keywords

DIFFERENTIATION-ASSOCIATED PROTEIN-1; DYNAMIN-RELATED GTPASE; HUMAN; SKELETAL-MUSCLE; MARIE-TOOTH-DISEASE; CYCLIN-DEPENDENT KINASES; CELL-DEATH; ALZHEIMERS-DISEASE; OPTIC ATROPHY; OXIDATIVE DAMAGE; DNA; MUTATIONS; Neurosciences

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.

Journal Title

Nature Reviews Neuroscience

Volume

9

Issue/Number

7

Publication Date

1-1-2008

Document Type

Review

Language

English

First Page

505

Last Page

518

WOS Identifier

WOS:000256929300011

ISSN

1471-003X

Share

COinS