Aging is a process of damage accumulation in cells and tissue structures, followed by reactions to that damage, some of which are compensatory and some of which make matters worse, and lastly the consequent failure of biological systems necessary to support health and life. Age-related diseases are names we give to some of the aspects of system failure, but they are not distinct from aging. One cannot draw a line between aging and age-related disease; it is a futile endeavor, and that the medical industry and regulatory bodies are set up to do so is one of the major challenges facing those who want to develop commercial rejuvenation therapies based on clearance of senescent cells or other recent scientific advances.
This point about aging and age-related disease is somewhat reinforced by the genetic analysis noted here, though I'm yet to be convinced of the utility of this sort of research beyond gaining a purely curiosity-driven scientific understanding of how aging progresses in detail. Since we all age for the same reasons, the same underlying damage, and since rejuvenation therapies will repair that damage in the same way in all patients, and since we have a good list of that damage, there are certainly days when it seems to me that anything other than just building the repair therapies and testing their effects is something of a sideline.
"According to Gompertz mortality law, the risk of death from all causes increases exponentially after the age of 40 and doubles approximately every 8 years. By analyzing the dynamics of disease incidence in the clinical data available from the UK Biobank, we observed that the risks of age-related diseases grow exponentially with age and double at a rate compatible with the Gompertz mortality law. This close relation between the most prevalent chronic diseases and mortality suggests that their risks could be driven by the same process, that is aging. This is why healthspan can be used as a natural proxy for investigation of the genetic factors controlling the rate of aging, the 'holy grail' target for anti-aging interventions."
To find genetic factors associated with human healthspan, the researchers studied the genomes of 300,477 British individuals. Overall, 12 genetic loci affecting healthy life expectancy were discovered. To confirm that these results hold true for other ethnicities, they used genetic data of UK Biobank participants with self-reported European, African, South Asian, Chinese and Caribbean ancestry. Of the 12 single nucleotide polymorphisms (SNPs), 11 increased risk both in discovery and in replication groups. Three of the genes affecting healthspan, HLA-DQB, LPA, and CDKN2B, were previously associated with parental longevity, a proxy for overall life expectancy.
At least three genetic loci were associated with risk of multiple diseases and healthspan at the same time and therefore could form the genetic signature of aging. HLA-DQB1 was significantly associated with COPD, diabetes, cancer, and dementia in this study and was demonstrated to be associated with parental survival earlier. The genetic variants near TYR predict death in the prospective UKB cohort and are involved in the earlier onset of macular degeneration. The chromosome 20 locus containing C20orf112 was not associated with the incidence of any of the diseases at the full-genome level, and yet was affecting the healthspan of studied individuals.