The Scientist reports on new support for the mitochondrial DNA mutational theory of aging: "Pigmented neurons in aged human substantia nigra -- the main site of neurodegeneration in Parkinson disease -- contain very high levels of mitochondrial DNA (mtDNA) deletions ... Neurons with the most mtDNA deletions showed defects in cellular respiration, which the authors say may lead to common symptoms of aging, such as the mild Parkinson-like symptoms often observed in older people. ... I think our result in nigra is the most convincing case so far. ... These aged cells often possessed extremely high levels of deletions -- many showed more than 60% deleted mtDNA, which is considered the phenotypic threshold above which respiratory function of the cell becomes impaired." A good job that researchers are already working on ways to replace age-damaged mitochondrial DNA.
10
Apr
2006
Mitochondrial DNA and Aging
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First Steps
The Causes of Aging
- Accumulating AGEs
- Buildup of Amyloid Between Cells
- The Failing Adaptive Immune System
- The Failing Innate Immune System
- Declining Lysosomal Function
- Mitochondrial DNA Damage
- Nuclear DNA Damage
- Buildup of Senescent Cells
- Other Causes of Aging
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Required Reading
- Calorie Restriction
- The Community, Visualized
- Cryonics
- Engineered Negligible Senescence
- Envisaging a World Without the FDA
- How to Argue for Longevity Science
- Introductory Articles
- The Odds of Human Longevity Mutations
- The Need For Activism and Advocacy
- Stem Cells, Regenerative Medicine
- Twelve Ways to Extend Mouse Life Span
- Transhumanism and Human Longevity
- The Vital Debate in Aging Research
- What is Anti-Aging?
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