GERO



In this work we introduce a novel blood-based biomarker of aging, the dynamic morbidity index (DMI), that is complementary to frailty indices and biological clocks. DMI increases with age in the UK Biobank and NHANES cohorts, is associated with frailty, and predicts the prospective incidence of age-related diseases and death.

We observed population DMI distribution broadening associated with a progressive loss of physiological resilience. Extrapolation of this data suggested that DMI recovery time and variance would simultaneously diverge at a critical point of 120 – 150 years of age corresponding to a complete loss of resilience. We conclude that the criticality resulting in the end of life is an intrinsic biological property of an organism that is independent of stress factors and signifies a fundamental or absolute limit of human lifespan.
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T. Pyrkov, K. Avchaciov, A. Tarkhov, L. Menshikov, A. Gudkov, P. Fedichev
In this research, we carried out a systematic investigation of supervised learning techniques for biological age modeling. We demonstrated that biological age is a universal biomarker of age, frailty and stress suitable for applications involving large scale studies of the effects of longevity drugs on risks of diseases and quality of life.

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Using the sub-population of 300,447 British individuals as a discovery cohort, we identify 12 loci associated with healthspan and find strong genetic correlations between healthspan and all-cause mortality, life-history, and lifestyle traits. We observe that the risks of major chronic diseases increased exponentially and double every eight years. The rate is compatible with the Gompertz mortality law.

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In this study, we evaluated various indicators of age and frailty using a highly accessible measurement of human physiological state: the time series representing the accelerometer records of physical activity.

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March 14, 2019
BIOLOGICAL AGE
IS A UNIVERSAL MARKER
OF AGING, STRESS AND FRAILTY

T. Pyrkov, P. Fedichev
January 30, 2019
IDENTIFICATION OF 12 GENETIC LOCI ASSOCIATED WITH HUMAN HEALTHSPAN
A. Zenin, Y. Tsepilov, S. Sharapov, E. Getmantsev, L.I. Menshikov, P. Fedichev
    October 26, 2018
    QUANTITATIVE CHARACTERIZATION OF BIOLOGICAL AGE AND FRAILTY BASED ON LOCOMOTOR ACTIVITY RECORDS
    T. Pyrkov, E. Getmantsev, B. Zhurov, K. Avchaciov, M. Pyatnitskiy, L. Menshikov, K. Khodova, A. V. Gudkov, P. Fedichev
    In this article, we follow how big data from large human medical studies, and analytical approaches borrowed from physics of complex dynamic systems can help to reverse engineer the underlying biology behind aging.

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    October 23, 2018
    HACKING AGING: A STRATEGY TO USE BIG DATA FROM MEDICAL STUDIES TO EXTEND HUMAN LIFE

    Peter O. Fedichev
    We used physical activity records from NHANES to compare three increasingly accurate biological age models: the unsupervised PCA score, a multivariate linear regression, and a state-of-the-art deep CNN.
    We introduced a novel way to train parametric proportional hazards models and produced a deep CNN for mortality risks prediction that outperformed any of the biological age or a simple linear proportional hazards model.

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    In this study, we tested the robustness of determination of frequently used mortality curves parameters: the initial mortality rate, the rate of aging, and lifespan. We showed that for typical experimental cohorts only lifespan is a well-defined quantity, whereas the other two are spuriously correlated.

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    In this study, we relate lifelong instability of gene networks to aging and the Gompertz law of mortality. Stability of gene regulatory networks may be a key determinant of longevity. Be the repair systems sufficiently effective, the gene network can stabilize gene damage along with mortality of the organism. An example of this is negligible senescent species that do not alter their gene-expression profiles with age as much as other organisms do, and have age-independent mortality.

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    March 26, 2018
    EXTRACTING BIOLOGICAL AGE FROM BIOMEDICAL DATA VIA DEEP LEARNING: TOO MUCH OF A GOOD THING?
    T. Pyrkov, K. Slipensky, M. Barg, A. Kondrashin, B. Zhurov, A. Zenin, M. Pyatnitskiy, L. Menshikov, S. Markov, P. Fedichev
      March 7, 2017
      STREHLER-MILDVAN CORRELATION IS A DEGENERATE MANIFOLD OF GOMPERTZ FIT
      A. Tarkhov, L. Menshikov, P. Fedichev
      STABILITY ANALYSIS OF A MODEL GENE NETWORK LINKS AGING, STRESS RESISTANCE, AND NEGLIGIBLE SENESCENCE
      V. Kogan, I. Molodtsov, L. Menshikov, R. J. Shmookler Reis, P. Fedichev
      August 28, 2015
      Accumulation of molecular damage is suggested to be an important molecular mechanism of aging. And yet a quantitative link between the dynamics of damage accumulation and mortality of species has so far remained elusive. We examined stability properties of a generic gene regulatory network (GRN) and demonstrated that many characteristics of aging and the associated population mortality rate emerge as inherent properties of the critical dynamics of gene regulation and metabolic levels.

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      CRITICAL DYNAMICS OF GENE NETWORKS IS A MECHANISM BEHIND AGING AND GOMPERTZ LAW
      D. Podolskiy, I. Molodtcov, A. Zenin, V. Kogan, L. I. Menshikov, V. Gladyshev, R. J. Shmookler Reis, P. Fedichev
      February 15, 2015