You might recall the demonstration of extended healthy longevity in mice by localizing the antioxidant catalase to the mitochondria - a strategy replicated by other researchers to some success. Here is an update on that work: "We describe the effects of mitochondrially targeted catalase (MCAT) expression on end-of-life pathology in mice using detailed semiquantitative histopathological evaluation. We previously reported that the median and maximum life spans of MCAT mice were extended relative to those of wild-type littermates. We now report that MCAT expression is associated with reduced malignant [tumor] burden, reduced cardiac lesions, and a trend toward reduced systemic inflammation ... Combined disease burden and comorbidity are also reduced, and MCAT expression is not associated with any detrimental clinical effects. The results suggest that oxidative damage is involved in aging of [mice] via modulation of a subset of age-associated lesions. Antioxidant interventions targeting mitochondria may therefore be a viable strategy for prevention or postponement of some age-associated diseases."
08
Sep
2008
An Update on Catalase in the 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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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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