.Aging shows nearly universal quantitative patterns
We approach aging research by combining physics-style theory, experiment, large scale medical datasets and 'connecting the dots' between the massive amount of published research across organisms. 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).
Reference:
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
A theory for aging :