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Mitochondria take center stage in aging and neurodegeneration.
Ann Neurol. 2005 Oct; 58(4):495-505.AN

Abstract

A critical role of mitochondrial dysfunction and oxidative damage has been hypothesized in both aging and neurodegenerative diseases. Much of the evidence has been correlative, but recent evidence has shown that the accumulation of mitochondrial DNA mutations accelerates normal aging, leads to oxidative damage to nuclear DNA, and impairs gene transcription. Furthermore, overexpression of the antioxidant enzyme catalase in mitochondria increases murine life span. There is strong evidence from genetics and transgenic mouse models that mitochondrial dysfunction results in neurodegeneration and may contribute to the pathogenesis of Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, hereditary spastic paraplegia, and cerebellar degenerations. Therapeutic approaches targeting mitochondrial dysfunction and oxidative damage in these diseases therefore have great promise.

Authors+Show Affiliations

Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York-Presbyterian Hospital, New York, NY 10021, USA. fbeal@med.cornell.edu

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review

Language

eng

PubMed ID

16178023

Citation

Beal, M Flint. "Mitochondria Take Center Stage in Aging and Neurodegeneration." Annals of Neurology, vol. 58, no. 4, 2005, pp. 495-505.
Beal MF. Mitochondria take center stage in aging and neurodegeneration. Ann Neurol. 2005;58(4):495-505.
Beal, M. F. (2005). Mitochondria take center stage in aging and neurodegeneration. Annals of Neurology, 58(4), 495-505.
Beal MF. Mitochondria Take Center Stage in Aging and Neurodegeneration. Ann Neurol. 2005;58(4):495-505. PubMed PMID: 16178023.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mitochondria take center stage in aging and neurodegeneration. A1 - Beal,M Flint, PY - 2005/9/24/pubmed PY - 2005/12/16/medline PY - 2005/9/24/entrez SP - 495 EP - 505 JF - Annals of neurology JO - Ann Neurol VL - 58 IS - 4 N2 - A critical role of mitochondrial dysfunction and oxidative damage has been hypothesized in both aging and neurodegenerative diseases. Much of the evidence has been correlative, but recent evidence has shown that the accumulation of mitochondrial DNA mutations accelerates normal aging, leads to oxidative damage to nuclear DNA, and impairs gene transcription. Furthermore, overexpression of the antioxidant enzyme catalase in mitochondria increases murine life span. There is strong evidence from genetics and transgenic mouse models that mitochondrial dysfunction results in neurodegeneration and may contribute to the pathogenesis of Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, hereditary spastic paraplegia, and cerebellar degenerations. Therapeutic approaches targeting mitochondrial dysfunction and oxidative damage in these diseases therefore have great promise. SN - 0364-5134 UR - https://www.unboundmedicine.com/medline/citation/16178023/Mitochondria_take_center_stage_in_aging_and_neurodegeneration_ L2 - https://doi.org/10.1002/ana.20624 DB - PRIME DP - Unbound Medicine ER -