Aging
We explain the patterns of aging using a stochastic ODE for damage production and removal, called the saturated removal model, deduced from experiments on damage dynamics in mice and in individual bacteria, the latter done by us. This simple model explains a wide range of phenomena in human aging and age-related diseases, as well as in model organisms. It pinpoint core molecular and cellular drivers of aging, specific to each organism, and suggests interventions that can compress the relative sickspan (fraction of lifespan that an individual is disabled).
- Senescent cell turnover slows with age providing an explanation for the Gompertz law
- Senescent Cells and the Incidence of Age-Related Diseases
- Senescent cell accumulation mechanisms inferred from parabiosis
- Principles of Aging, Institute of Advanced Studies, Princeton
- Damage dynamics in single E. coli and the role of chance in the timing of cell death
- Compression of sickspan by interventions that steepen the survival curve
- Heritability of intrinsic human life span is about 50% when confounding factors are addressed
- A damage accumulation model identifies distinct aging regimes across
- A unified framework links infant vulnerability with aging-related mortality dynamics
- Maximal human lifespan in light of a mechanistic model of aging