Good news from Betterhumans: scientists have found that another longevity gene exists in mice as well as nematode worms. The more mechanisms of aging are similar between species, the more rapidly basic aging research can proceed - this is because it is much cheaper and faster to work with worms, flies and yeast than with mice or other mammals. If work in lesser organisms has greater value, then this is good news for us. From the article: "the longevity-promoting effect of reducing clk-1/mclk1 activity that was initially observed in C. elegans is conserved in mice, supporting the idea that some molecular mechanisms of aging are shared throughout the animal kingdom."
04
Oct
2005
Similar Mechanisms Mean Faster Research
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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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