Model organism lifespan research

Assembled from 17 blocks · 2 evidence · 16 related

1. Story
2. The body of work in which lifespan is manipulated in short-lived laboratory species — chiefly the nematode Caenorhabditis elegans, the fruit fly Drosophila melanogaster, and laboratory mice — and from which almost every mechanistic claim about ageing originates. The results are genuinely dramatic: single-gene mutations in the insulin/IGF-1 signalling pathway more than double nematode lifespan, and dietary or pharmacological interventions extend mouse lifespan by measurable percentages. The translation record is the problem. Effects shrink monotonically with organism complexity and lifespan — a doubling in a worm becomes tens of percent in a fly, ten to twenty percent in a mouse, and nothing demonstrated in a human. Laboratory rodents are inbred, live in pathogen-free cages on ad libitum diets, and die predominantly of cancer, so a compound that extends their lifespan may be doing something about their specific failure mode rather than about ageing. Reading a mouse result as a human one is the single most common error in this field.
3. Knowledge
4. Model organism lifespan research
5. Caenorhabditis elegans
6. Connections
7. The hallmarks of ageing
8. Caenorhabditis elegans
9. Caloric restriction
10. NIA Interventions Testing Program
11. A single-gene mutation doubles nematode lifespan
12. The NIA Interventions Testing Program begins
13. Model organism lifespan research
14. A single-gene mutation doubles nematode lifespan
15. Evidence
16. Supports the daf-2 lifespan doubling and its dependence on daf-16. V55 verification basis: not retrieved in this session.
17. Supports the late-life lifespan extension by rapamycin replicated across the Interventions Testing Program's three sites. V55 verification basis: not retrieved; the specific percentage extensions and the sex difference are unchecked and are therefore not quoted numerically in the objects citing this record.