From ScienceWeek, a grab bag of mainstream scientific thoughts on the mechanisms of aging; Klotho, oxidative damage, and senescence. "A defect in Klotho gene expression in mice accelerates the degeneration of multiple age-sensitive traits. The authors demonstrate that overexpression of Klotho in mice extends life span. ... overexpression of human catalase in the mitochondria of mice extends median and maximal lifespan by about 20%. Catalase prevents the formation of reactive oxygen species (ROS) that can damage cellular constituents. ... Cellular senescence is also thought to contribute to aging, although how it does so is poorly understood. In addition to arresting growth, senescent cells show changes in function. Because senescent cells accumulate with age, they may contribute to age-related declines in tissue function."
12
Nov
2005
Scientific Thoughts on 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
Archives and Feeds
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- Using the Fight Aging! Content Feeds
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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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