Journal
TRENDS IN NEUROSCIENCES
Volume 31, Issue 5, Pages 251-256Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tins.2008.02.008
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Funding
- NCI NIH HHS [R01 CA085700-08, R01 CA085700, CA085700, R01 CA085700-07] Funding Source: Medline
- NEI NIH HHS [EY10804, R01 EY010804-14A1, R01 EY010804-13, R01 EY010804] Funding Source: Medline
- NINDS NIH HHS [NS41777, R01 NS041777-08, R56 NS041777, R01 NS041777, R01 NS041777-07] Funding Source: Medline
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Aging is the most important risk factor for common neurodegenerative disorders such as Parkinson's and Alzheimer's diseases. Aging in the central nervous system has been associated with elevated mutation load in mitochondrial DNA, defects in mitochondrial respiration and increased oxidative damage. These observations support a 'vicious cycle' theory which states that there is a feedback mechanism connecting these events in aging and age-associated neurodegeneration. Despite being an extremely attractive hypothesis, the bulk of the evidence supporting the mitochondrial vicious cycle model comes from pharmacological experiments in which the modes of mitochondrial enzyme inhibition are far from those observed in real life. Furthermore, recent in vivo evidence does not support this model. In this review, we focus on the relationship among the components of the putative vicious cycle, with particular emphasis on the role of mitochondrial defects on oxidative stress.
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