Never a straight road in the life sciences. The extension of mouse life span by genetic modification to target the antioxidant catalase to the mitochondria is a result I've considered important for years, but another study finds no benefit to life span: "We evaluated the effect of overexpressing antioxidant enzymes on the lifespans of transgenic mice that overexpress CuZnSOD, catalase, or combinations of either CuZnSOD and catalase or CuZnSOD and MnSOD. Our results show that the overexpression of these major antioxidant enzymes, which are known to scavenge superoxide and hydrogen peroxide in the cytosolic and mitochondrial compartments, is insufficient to extend lifespan in mice." So something more complex is going on here; back to square one, and more studies to try and understand how it is that earlier results of extended healthy life were in fact produced.
25
Dec
2008
Catalase-Based Longevity Not Replicated In Mice
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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
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- 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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