Mitochondrial Dysfunction in Mammalian Ageing

  1. Derek J. Chadwick Organizer and
  2. Jamie Goode
  1. Mügen Terzioglu and
  2. Nils-Göran Larsson

Published Online: 20 MAY 2008

DOI: 10.1002/9780470725207.ch14

Mitochondrial Biology: New Perspectives: Novartis Foundation Symposium 287

Mitochondrial Biology: New Perspectives: Novartis Foundation Symposium 287

How to Cite

Terzioglu, M. and Larsson, N.-G. (2007) Mitochondrial Dysfunction in Mammalian Ageing, in Mitochondrial Biology: New Perspectives: Novartis Foundation Symposium 287 (eds D. J. Chadwick and J. Goode), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/9780470725207.ch14

Author Information

  1. Karolinska Institutet, Department of Laboratory Medicine, Division of Metabolic Diseases, Novum, S-14186 Stockholm, Sweden

  1. This paper was presented at the symposium by Nils-Göran Larsson to whom correspondence should be addressed.

Publication History

  1. Published Online: 20 MAY 2008
  2. Published Print: 5 OCT 2007

Book Series:

  1. Novartis Foundation Symposia

Book Series Editors:

  1. Novartis Foundation

ISBN Information

Print ISBN: 9780470066577

Online ISBN: 9780470725207



  • mitochondria;
  • ageing;
  • mtDNA;
  • respiratory chain;
  • Parkinson's disease;
  • life span;
  • mitochondrial dysfunction;
  • mitochondrial disease


Ageing is likely a multifactorial process caused by accumulated damage to a variety of cellular components. Increasing age in mammals correlates with increased levels of mitochondrial DNA (mtDNA) mutations and deteriorating respiratory chain function. Mosaic respiratory chain deficiency in a subset of cells in various tissues, such as heart, skeletal muscle, colonic crypts and neurons, is typically found in aged humans. Experimental evidence in the mouse has linked increased levels of somatic mtDNA mutations to a variety of ageing phenotypes, such as osteoporosis, hair loss, greying of the hair, weight reduction and decreased fertility. It has been known for a long time that respiratory chain-deficient cells are more prone to undergo apoptosis and increased cell loss is therefore likely of importance in age-associated mitochondrial dysfunction. There is a tendency to automatically link mitochondrial dysfunction to increased production of reactive oxygen species (ROS). However, the experimental support for this concept is rather weak. Mouse models with respiratory chain deficiency induced by tissue-specific mtDNA depletion or by massive increase of point mutations in mtDNA have very minor or no increase of oxidative stress. Future studies are needed to address the relative importance of mitochondrial dysfunction and ROS in mammalian ageing.