Journal
BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS
Volume 1847, Issue 11, Pages 1401-1411Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbabio.2015.05.015
Keywords
DNA; Mitochondrial; Aging; Parkinson disease; Alzheimer disease; Lewy body disease
Categories
Funding
- Wellcome Trust [103396/Z/13/Z, 101876/Z/13/Z, 096919Z/11/Z]
- Medical Research Council (UK) Centre for Translational Muscle Disease research [G0601943]
- EU FP7 TIRCON
- National Institute for Health Research (NIHR) Newcastle Biomedical Research Centre based at Newcastle upon Tyne Hospitals NHS Foundation Trust and Newcastle University
- Wellcome Trust [103396/Z/13/Z] Funding Source: Wellcome Trust
- MRC [G0601943] Funding Source: UKRI
- Medical Research Council [G0601943] Funding Source: researchfish
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Mitochondrial dysfunction is observed in both the aging brain, and as a core feature of several neurodegenerative diseases. A central mechanism mediating this dysfunction is acquired molecular damage to mitochondrial DNA (mtDNA). In addition, inherited stable mtDNA variation (mitochondrial haplogroups), and inherited low level variants (heteroplasmy) have also been associated with the development of neurodegenerative disease and premature neural aging respectively. Herein we review the evidence for both inherited and acquired mtDNA mutations contributing to neural aging and neurodegenerative disease. This article is part of a Special Issue entitled: Mitochondrial Dysfunction in Aging. (c) 2015 Elsevier B.V. All rights reserved.
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