Another longevity mutation is shown to work by reducing the all-important emmission of free radicals from the mitochondria: "first discovered in 2000 [a] mutation in the Indy ('I'm Not Dead Yet') gene [extends] the life span of fruit flies .. Subsequent studies of the Indy flies have led to the new finding that a mechanism in those genetically altered fruit flies appears to reduce significantly the production of free radicals, a cellular byproduct that can contribute to the aging process. This intervention takes place with few or no side effects on the quality of life for the fruit fly. The discovery could lead to the development of new anti-aging treatments. ... There are very few, if any, interventions that are known to dramatically extend healthy lifespan. Understanding how [the] Indy mutation alters the metabolic state of the fruit fly would allow someone to come up with pharmacological interventions that could mimic it and give you the benefit of genetic manipulation without having to do genetics."
23
Jan
2009
Indy Longevity Mutation Works Through Mitochondria
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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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- Engineered Negligible Senescence
- Envisaging a World Without the FDA
- How to Argue for Longevity Science
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- The Odds of Human Longevity Mutations
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- 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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