Building Biological Age Clocks from Immune and Redox Markers
Any sufficiently large set of biological data can be used to produce clocks that measure biological age, where a clock is some weighted combination of measurements that produces age as an output. At this point novel clocks are much less interesting than standardizing on one clock and working towards a better understanding of how exactly the clock measurements relate to underlying processes of aging. Without that understanding it is impossible to use clock assessments of biological age to accelerate research and development of therapies to treat aging as a medical condition. One has to know that they clock does in fact correctly assess the burden of damage that is targeted specifically by the therapy, whether it is senescent cells, or mitochondrial dysfunction, or any of the many other options, or the clock results are simply not actionable. Nonetheless, researchers continue to produce new clocks at a fair pace these days, with this paper being an example of the type.
Immune function and redox markers are used for estimating the aging rate, namely biological age (BA). However, it is unknown if this BA and its changes can be reflected in longevity. Thus, we must quantify BA in experimental animals. In peritoneal immune cells of 202 female mice (ICR/CD1) in different ages, 10 immune and 6 redox parameters were evaluated to construct two mathematical models for BA quantification in mice by multiple linear regression. Immune and redox parameters were selected as independent variables and chronological age as dependent, developing two models: the Immunity and the Redox Clocks, reaching both an adjusted coefficient of determination of 80.9% and a standard error of 6.38 and 8.57 weeks, respectively.
Both models were validated in a different group of healthy mice obtaining a Pearson's correlation coefficient of 0.844 and 0.800 between chronological age and BA. Furthermore, they were applied to adult prematurely aging mice, which showed a higher BA than non-prematurely aging mice. Moreover, after positive and negative lifestyle interventions, mice showed a lower and higher BA, respectively, than their age-matched controls. In conclusion, the Immunity and Redox Clocks allow BA quantification in mice and both the ImmunolAge and RedoxAge in mice relate to lifespan.