Mitochondrial DNA damage and reactive oxygen species in neurodegenerative disease

Mitochondria are essential organelles within the cell where most ATP is produced through oxidative phosphorylation (OXPHOS). A subset of the genes needed for this process are encoded by the mitochondrial DNA (mtDNA). One consequence of OXPHOS is the production of mitochondrial reactive oxygen specie...

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Bibliographic Details
Published in:FEBS letters 2018-03, Vol.592 (5), p.728-742
Main Authors: Nissanka, Nadee, Moraes, Carlos T.
Format: Article
Language:English
Subjects:
Animals
DNA Damage
DNA, Mitochondrial - genetics
DNA, Mitochondrial - metabolism
Humans
mitochondrial DNA
neurodegeneration
Neurodegenerative Diseases - genetics
Neurodegenerative Diseases - metabolism
Neurodegenerative Diseases - pathology
Oxidative Phosphorylation
reactive oxygen species
Reactive Oxygen Species - metabolism
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Summary:Mitochondria are essential organelles within the cell where most ATP is produced through oxidative phosphorylation (OXPHOS). A subset of the genes needed for this process are encoded by the mitochondrial DNA (mtDNA). One consequence of OXPHOS is the production of mitochondrial reactive oxygen species (ROS), whose role in mediating cellular damage, particularly in damaging mtDNA during ageing, has been controversial. There are subsets of neurons that appear to be more sensitive to ROS‐induced damage, and mitochondrial dysfunction has been associated with several neurodegenerative disorders. In this review, we will discuss the current knowledge in the field of mtDNA and neurodegeneration, the debate about ROS as a pathological or beneficial contributor to neuronal function, bona fide mtDNA diseases, and insights from mouse models of mtDNA defects affecting the central nervous system.
ISSN:0014-5793
1873-3468
DOI:10.1002/1873-3468.12956