DNA methylation entropy is a biomarker for aging
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ABSTRACT:
PROVIDER: PRJNA1216266 | ENA |
REPOSITORIES: ENA
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Project description:The dynamic nature of epigenetic modifications has been leveraged to construct epigenetic clocks that accurately predict an individual’s age based on DNA methylation levels. Here we explore whether the accumulation of epimutations, which can be quantified by Shannon’s entropy, changes reproducibly with age. Using targeted bisulfite sequencing, we analyzed the associations between age, entropy, and methylation levels in human buccal swab samples. We find that epigenetic clocks based on the entropy of methylation states predict chronological age with similar accuracy as common approaches that are based on methylation levels of individual cytosines. Our approach suggests that across many genomic loci, methylation entropy changes reproducibly with age.
2025-01-27 | GSE288139 | GEO
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2022-09-30 | GSE213628 | GEO
Project description:Background: Liquid biopsies analyzing cell-free DNA methylation in plasma offer a non-invasive diagnostic for diseases, with aging biomarker potential underexplored. Methods: Utilizing enzymatic methyl-seq (EM-seq), this study assessed cfDNA methylation patterns in aging with blood from 35 healthy individuals. Results: It found aging signatures, including higher cfDNA levels and variations in fragment sizes, plus over 2 million age-related differentially methylated CpG sites. A biological age predictive model based on 41 CpG sites showed a strong correlation with chronological age, verified by two datasets. Age-specific epigenetic shifts linked to inflammation were revealed through differentially methylated regions profiling and Olink proteomics. Conclusion: These findings indicate cfDNA methylation as a potential biomarker for aging, and it might exacerbate immunoinflammatory reactivity in older individuals.
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Project description:DNA methylation entropy as a measure of stem cell replication and aging
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Project description:Long-term culture associated changes need to be considered for quality control of cell preparations – especially in cellular therapy. Here we describe a simple method to track cellular aging based on continuous DNA-methylation changes at six specific CpG sites. This epigenetic signature can be used as a biomarker for various cell types to predict the state of cellular aging with regard to the number of passages or days of in vitro culture. 8 samples of human dermal fibroblasts. 4 samples of mesenchymal stem cells (MSC) from human adipose tissue.
2012-05-21 | E-GEOD-29661 | biostudies-arrayexpress
Project description:As epigenetic clocks have evolved from powerful estimators of chronological aging to predictors of mortality and disease risk, it begs the question of what role DNA methylation plays in the aging process. We hypothesize that while it has the potential to serve as an informative biomarker, DNA methylation could also be a key to understanding the biology entangled between aging, (de)differentiation, and epigenetic reprogramming. Here we use an unsupervised approach to analyze time associated DNA methylation from both in vivo and in vitro samples to measure an underlying signal that ties these phenomena together. We identify a methylation pattern shared across all three, as well as a signal that tracks aging in tissues but appears refractory to reprogramming, suggesting that aging and reprogramming may not be fully mirrored processes.
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Project description:DNA methylation in aging BXD mouse strains
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Project description:DNA methylation (DNAm) is one of the most reliable biomarkers of aging across many mammalian tissues. While the age-dependent global loss of DNAm has been well characterized, age-dependent DNAm gain is less specified. Multiple studies have demonstrated that polycomb repressive complex 2 (PRC2) targets are enriched among the CpG sites which gain methylation with age. However, systematic whole-genome examination of all PRC2 targets in the context of aging methylome as well as determination of the pan-tissue or tissue-specific nature of these associations is lacking. Here, by analyzing DNAm data from different assays and from multiple young and old human and mouse tissues, we found that low-methylated regions (LMRs) which are highly bound by PRC2 in embryonic stem cells (PRC2 LMRs) gain methylation with age in all examined somatic mitotic cells. We also estimated that this epigenetic change represents around 90% of the age-dependent DNAm gain genome-wide. Therefore, we propose the “PRC2-AgeIndex,” defined as the average DNAm in PRC2 LMRs, as a universal biomarker of cellular aging in somatic cells. In addition, we demonstrate the application of this biomarker in the evaluation of different anti-aging interventions, including dietary restriction and partial epigenetic reprogramming.
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Project description:Although DNA methylation data yields highly accurate age predictors, little is known about the dynamics of this quintessential epigenomic biomarker during lifespan. To narrow the gap, we investigated the methylation trajectories in DNA from 82 male mouse (C57BL/6J/Ukj) colons at five different time points (3, 9, 15, 24, 28 months). Our study indicates the existence of linear and nonlinear DNA methylation changes during aging. Precisely, we identify two epigenomic switches during early-to-midlife (3-9 mo) and mid-to-late-life (15-24 mo) transitions, separating the rodents' life into three major stages. The results were validated with samples from an independent mouse cohort of 20 male C57BL6/J mice at four different ages (3, 7, 12, 27 months).
2023-05-31 | GSE233734 | GEO
Project description:Long-term culture associated changes need to be considered for quality control of cell preparations – especially in cellular therapy. Here we describe a simple method to track cellular aging based on continuous DNA-methylation changes at six specific CpG sites. This epigenetic signature can be used as a biomarker for various cell types to predict the state of cellular aging with regard to the number of passages or days of in vitro culture.
2012-05-22 | GSE29661 | GEO