I’ll curate this 2019 German review through its figures: “With the discovery of beneficial aspects of cellular senescence and evidence of senescence being not limited to replicative cellular states, a redefinition of our comprehension of aging and senescence appears scientifically overdue. Figure 1. Current determinants and relevant open questions, marking the processes of aging and … Continue reading Organismal aging and cellular senescence
This 2018 Baltimore cell study found: “Based on similarities in overall methylation patterns in replicative senescence and cancers, it is hypothesized that tumor-promoting DNA methylation in cancers derives from cells escaping senescence. We show that the tumor-associated methylation changes evolve independently of senescence and are pro-survival events with functional implications contrasting that in senescence. In … Continue reading Cell senescence and DNA methylation
The 2016 UK/UCLA human study found: “Induction of replicative senescence (RS) and oncogene-induced senescence (OIS) are accompanied by ageing of the cell. However, senescence induced by DNA damage is not, even though RS and OIS activate the cellular DNA damage response pathway, highlighting the independence of senescence from cellular ageing. We used primary endothelial cells … Continue reading Using an epigenetic clock to distinguish cellular aging from senescence
This 2020 interview was with UC Berkeley researchers: “Lack of cure goes hand in hand with inability to accept that this [aging] is disease. For example, there was some resistance to accept tuberculosis as the actual disease. When there was no antibiotics or cure against it, people tended to discard it and said, oh, it’s … Continue reading Aging as a disease
The founder of the PhenoAge epigenetic clock methodology authored this 2020 article: “The Ge[r]oscience paradigm suggests that targeting the aging process could delay or prevent the risk of multiple major age-related diseases. We need clinically valid measures of the underlying biological process and/or classification criteria for what it means to be biologically, rather than chronologically, … Continue reading Do epigenetic clocks measure causes or effects?
This 2019 Stanford human study developed an aging clock using blood plasma proteins: “We measured 2,925 plasma proteins from 4,331 young adults to nonagenarians [18 – 95] and developed a novel bioinformatics approach which uncovered profound non-linear alterations in the human plasma proteome with age. Waves of changes in the proteome in the fourth, seventh, … Continue reading A blood plasma aging clock
This 2019 US human clinical trial reported preliminary results: “Senescent cells, which can release factors that cause inflammation and dysfunction, the senescence-associated secretory phenotype (SASP), accumulate with ageing and at etiological sites in multiple chronic diseases. Senolytics, including the combination of Dasatinib and Quercetin (D + Q), selectively eliminate senescent cells by transiently disabling pro-survival networks that … Continue reading Preliminary findings from a senolytics clinical trial
The title of this post is essentially the same as the 2019 human clinical trial: “Epigenetic aging can be reversed in humans. Using a protocol intended to regenerate the thymus, we observed protective immunological changes, improved risk indices for many age‐related diseases, and a mean epigenetic age approximately 1.5 years less than baseline after 1 … Continue reading Reversal of aging and immunosenescent trends
This 2019 US/UK human cell study by the founder of the epigenetic clock method investigated epigenetic aging: “It is widely assumed that extension of lifespan is a result of retardation of ageing. While there is no counter-evidence to challenge this highly intuitive association, supporting empirical evidence to confirm it is not easy to acquire. The … Continue reading What drives cellular aging?
This 2018 Chinese study was a series of statistical and methodological counter-arguments to a previous epigenetic clock study finding that: “Only [CpG] sites mapping to the ELOVL2 promoter constitute cell and tissue-type independent aDMPs [age-associated differentially methylated positions].” The study used external data sets and the newer epigenetic clock’s fibroblast data in its analyses to … Continue reading Epigenetic clock statistics and methods