scholarly journals Corrigendum: Simplified Assay for Epigenetic Age Estimation in Whole Blood of Adults

2017 ◽  
Vol 8 ◽  
Author(s):  
Laura Vidal-Bralo
2016 ◽  
Vol 7 ◽  
Author(s):  
Laura Vidal-Bralo ◽  
Yolanda Lopez-Golan ◽  
Antonio Gonzalez

2020 ◽  
Vol 47 ◽  
pp. 101763
Author(s):  
Helena Correia Dias ◽  
Eugénia Cunha ◽  
Francisco Corte Real ◽  
Licínio Manco

Author(s):  
Pavanello ◽  
Campisi ◽  
Tona ◽  
Lin ◽  
Iliceto

DNA methylation (DNAm) is an emerging estimator of biological aging, i.e., the often-defined “epigenetic clock”, with a unique accuracy for chronological age estimation (DNAmAge). In this pilot longitudinal study, we examine the hypothesis that intensive relaxing training of 60 days in patients after myocardial infarction and in healthy subjects may influence leucocyte DNAmAge by turning back the epigenetic clock. Moreover, we compare DNAmAge with another mechanism of biological age, leucocyte telomere length (LTL) and telomerase. DNAmAge is reduced after training in healthy subjects (p = 0.053), but not in patients. LTL is preserved after intervention in healthy subjects, while it continues to decrease in patients (p = 0.051). The conventional negative correlation between LTL and chronological age becomes positive after training in both patients (p < 0.01) and healthy subjects (p < 0.05). In our subjects, DNAmAge is not associated with LTL. Our findings would suggest that intensive relaxing practices influence different aging molecular mechanisms, i.e., DNAmAge and LTL, with a rejuvenating effect. Our study reveals that DNAmAge may represent an accurate tool to measure the effectiveness of lifestyle-based interventions in the prevention of age-related diseases.


2020 ◽  
Vol 135 (1) ◽  
pp. 167-173 ◽  
Author(s):  
Barbara Elisabeth Koop ◽  
Felix Mayer ◽  
Tanju Gündüz ◽  
Jacqueline Blum ◽  
Julia Becker ◽  
...  

AbstractAge estimation based on the analysis of DNA methylation patterns has become a focus of forensic research within the past few years. However, there is little data available regarding postmortem DNA methylation analysis yet, and literature mainly encompasses analysis of blood from corpses without any signs of decomposition. It is not entirely clear yet which other types of specimen are suitable for postmortem epigenetic age estimation, and if advanced decomposition may affect methylation patterns of CpG sites. In living persons, buccal swabs are an easily accessible source of DNA for epigenetic age estimation. In this work, the applicability of this approach (buccal swabs as source of DNA) under different postmortem conditions was tested. Methylation levels of PDE4C were investigated in buccal swab samples collected from 73 corpses (0–90 years old; mean: 51.2) in different stages of decomposition. Moreover, buccal swab samples from 142 living individuals (0–89 years old; mean 41.2) were analysed. As expected, methylation levels exhibited a high correlation with age in living individuals (training set: r2 = 0.87, validation set: r2 = 0.85). This was also the case in postmortem samples (r2 = 0.90), independent of the state of decomposition. Only in advanced putrified cases with extremely low DNA amounts, epigenetic age estimation was not possible. In conclusion, buccal swabs are a suitable and easy to collect source for DNA methylation analysis as long as sufficient amounts of DNA are present.


Author(s):  
D. Nick Weber ◽  
Andrew T. Fields ◽  
William F. Patterson ◽  
Beverly K. Barnett ◽  
Christopher M. Hollenbeck ◽  
...  

Cutting-edge DNA methylation-based epigenetic aging techniques were applied to Gulf of Mexico northern red snapper (Lutjanus campechanus; n = 10; 1–26 years old) and red grouper (Epinephelus morio; n = 10; 2–14 years old). Bisulfite-converted restriction site-associated DNA sequencing was used to identify CpG sites (cytosines followed by guanines) that exhibit age-correlated DNA methylation, and species-specific epigenetic clocks developed from 100s of CpG sites in each species showed strong agreements between predicted and otolith-derived ages (r2 > 0.99 for both species). Results suggest epigenetic age estimation could provide an accurate and efficient approach to mass-aging fishes in a non-invasive manner.


Aging ◽  
2021 ◽  
Author(s):  
Anna Woźniak ◽  
Antonia Heidegger ◽  
Danuta Piniewska-Róg ◽  
Ewelina Pośpiech ◽  
Catarina Xavier ◽  
...  

Author(s):  
Danuta Piniewska-Róg ◽  
Antonia Heidegger ◽  
Ewelina Pośpiech ◽  
Catarina Xavier ◽  
Aleksandra Pisarek ◽  
...  

AbstractDNA methylation-based clocks provide the most accurate age estimates with practical implications for clinical and forensic genetics. However, the effects of external factors that may influence the estimates are poorly studied. Here, we evaluated the effect of alcohol consumption on epigenetic age prediction in a cohort of extreme alcohol abusers. Blood samples from deceased alcohol abusers and age- and sex-matched controls were analyzed using the VISAGE enhanced tool for age prediction from somatic tissues that enables examination of 44 CpGs within eight age markers. Significantly altered DNA methylation was recorded for alcohol abusers in MIR29B2CHG. This resulted in a mean predicted age of 1.4 years higher compared to the controls and this trend increased in older individuals. The association of alcohol abuse with epigenetic age acceleration, as determined by the prediction analysis performed based on MIR29B2CHG, was small but significant (β = 0.190; P-value = 0.007). However, the observed alteration in DNA methylation of MIR29B2CHG had a non-significant effect on age estimation with the VISAGE age prediction model. The mean absolute error in the alcohol-abusing cohort was 3.1 years, compared to 3.3 years in the control group. At the same time, upregulation of MIR29B2CHG expression may have a biological function, which merits further studies.


Author(s):  
Xiaohui Wu ◽  
Junping Ye ◽  
Zhongju Wang ◽  
Cunyou Zhao

Abstract Schizophrenia is a serious neuropsychiatric disorder with abnormal age-related neurodevelopmental (or neurodegenerative) trajectories. Although an accelerated aging hypothesis of schizophrenia has been proposed, the quantitative study of the disruption of the physiological trajectory caused by schizophrenia is inconclusive. In this study, we employed 3 “epigenetic clock” methods to quantify the epigenetic age of a large sample size of whole blood (1069 samples from patients with schizophrenia vs 1264 samples from unaffected controls) and brain tissues (500 samples from patients with schizophrenia vs 711 samples from unaffected controls). We observed significant positive correlations between epigenetic age and chronological age in both blood and brain tissues from unaffected controls and patients with schizophrenia, as estimated by 3 methods. Furthermore, we observed that epigenetic age acceleration was significantly delayed in schizophrenia from the whole blood samples (aged 20–90 years) and brain frontal cortex tissues (aged 20–39 years). Intriguingly, the genes regulated by the epigenetic clock also contained schizophrenia-associated genes, displaying differential expression and methylation in patients with schizophrenia and involving in the regulation of cell activation and development. These findings were further supported by the dysregulated leukocyte composition in patients with schizophrenia. Our study presents quantitative evidence for a neurodevelopmental model of schizophrenia from the perspective of a skewed “epigenetic clock.” Moreover, landmark changes in an easily accessible biological sample, blood, reveal the value of these epigenetic clock genes as peripheral biomarkers for schizophrenia.


2018 ◽  
Vol 34 (7) ◽  
pp. 489-491 ◽  
Author(s):  
Mahsa Shabani ◽  
Pascal Borry ◽  
Inge Smeers ◽  
Bram Bekaert

2018 ◽  
Author(s):  
Dhingra Radhika ◽  
Lydia Coulter Kwee ◽  
David Diaz-Sanchez ◽  
Robert B. Devlin ◽  
Wayne Cascio ◽  
...  

AbstractDNA methylation age (DNAm age) has become a widely utilized epigenetic biomarker for the aging process. The Horvath method for determining DNAm age is perhaps the most widely utilized and validated DNA methylation age assessment measure. Horvath DNAm age is calculated based on methylation measurements at 353 loci which were present on Illumina’s 450k and 27k DNA methylation microarrays. With the increasing use of the more recently developed Illumina MethylationEPIC (850k) microarray, it is worth revisiting this widely used aging measure to evaluate differences in DNA methylation age estimation based on array design. Of the requisite 353 loci, 17 are missing from the current 850k microarray. Using 17 datasets with 27k, 450k, and/or 850k methylation data, we calculated and compared each sample’s epigenetic age estimated from all 353 loci required from the Horvath DNAm age calculator (full), and using only the 336 loci present on the 27k, 450k, and 850k arrays (reduced). In 450k/27k data, missing loci caused underestimation of epigenetic age when compared with the full clock. Underestimation of full epigenetic age grew from ages 0 to ~20, remaining stable thereafter (mean= −3.46 y, SD=1.13) years for individuals ≥20 years. Underestimation of DNAm age by the reduced 450k/27k data was similar to the underestimation observed in the 850k data indicating that array differences in DNAm age estimation are primarily driven by missing probes. Correlations between age and DNAm age were not dependent on missing probes or on array designs and consequently associations between DNAm age and outcomes such as sex remained the same independent of missing probes and probe design. In conclusion, DNAm age estimations are array dependent driven by missing probes between arrays. Though correlations and associations with DNAm age may remain the same, researchers should exercise caution when interpreting results based on absolute differences in DNAm age or when mixing samples assayed on different arrays.DisclaimerThis paper has been reviewed by the National Health and Environmental Effects Research Laboratory, U.S. EPA, and is approved for publication. Approval does not signify that the contents necessarily reflect the views and policies of the agency, nor does mention of trade names or commercial products constitute endorsement or recommendation for use. The authors declare they have no competing financial interests.


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