Epigenetic Age Tests and Centenarians

I wonder how centenarians show up on epigenetic age Tests. Would they show up as the same age, younger or older due to their high incidence of age related disease? If their ages were older, I think it would call into question the validity of these types of tests. Is there any data available?

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Uh younger simply bc changes in epigenetic aging decelerate over time. See Morgan Levine tweet

The reason why I was interested is that my son told me that when his teacher asked in class if anyone had a relative who lived over the age of 100, 33% of the class raised their hands. That’s a lot of centenarians here! (11,575 in one city to be exact!)

Among the elderly population aged 65 or above, the proportion aged 85 or over has risen from 5 per cent in 1981 to 16 per cent in 2021. This is expected to surpass 30 per cent by 2066, which means one in every three elderly people will be 85 or above.
Furthermore, the number of people aged 100 or above has increased from 289 in 1981 to 11,575 in 2021, which is an alarming rise over the past 40 years. The number of centenarians in Hong Kong is expected to continue increasing.

Coudl you share the tweet here?

Related, as to whether current “age” testing is useful:

The article here notes that researchers find cognitively healthy centenarians exhibit levels of protein aggregation and other brain lesions typical of people showing symptoms of neurodegenerative diseases. They are in some way more resistant, but why this is the case is a continuing research project. It is possible to identify specific gene variants and more youthful gene expression for some genes in cognitively healthy older individuals, but it is long trek from that data to an understanding of the mechanisms involved.
… (continued)

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https://www.researchgate.net/publication/333406987_Rate_of_brain_aging_and_APOE_e4_are_synergistic_risk_factors_for_Alzheimer’s_disease

A proxy for the rates of brain aging was obtained as the dif-

ference between molecular age and chronological age for each

brain, termed Δage (see Fig 1). We, thus, calculated Δage for each

brain as the difference between each individual data point and the

regression line in all cohorts. Consistent with a survivor effect, the

oldest subjects in CM (age > 60 yr) show a significant inverse re-

lationship between Δage and chronological age (Fig S1A), which is

not present in subjects younger than 60 yr (Fig S1B). This is con-

sistent with the reported prediction of all-cause mortality by

methylation-based transcriptional age in blood (Marioni et al, 2015).

Centenarians consistently present a younger epigenetic age than their chronological age with four epigenetic clocks based on a small number of CpG sites
(Oct 2022) Centenarians consistently present a younger epigenetic age than their chronological age with four epigenetic clocks based on a small number of CpG sites | Aging
Aging is a progressive time-dependent biological process affecting differentially individuals, who can sometimes present exceptional longevity. Epigenetic alterations are one of the hallmarks of aging, which comprise the epigenetic drift and clock at DNA methylation level. In the present study, we estimated the DNA methylation-based age (DNAmage) using four epigenetic clocks based on a small number of CpGs in French centenarians and semi-supercentenarians (CSSC, n=214) as well as nonagenarians’ and centenarians’ offspring (NCO, n=143) compared to individuals from the French general population (CG, n=149). DNA methylation analysis of the nine CpGs included in the epigenetic clocks showed high correlation with chronological age (-0.66>R>0.54) and also the presence of an epigenetic drift for four CpGs that was only visible in CSSC. DNAmage analysis showed that CSSC and to a lesser extend NCO present a younger DNAmage than their chronological age (15-28.5 years for CSSC, 4.4-11.5 years for NCO and 4.2-8.2 years for CG), which were strongly significant in CSSC compared to CG (p-values<2.2e-16). These differences suggest that epigenetic aging and potentially biological aging are slowed in exceptionally long-lived individuals and that epigenetic clocks based on a small number of CpGs are sufficient to reveal alterations of the global epigenetic clock.

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