Epigenetic age prediction

Advanced age is the main common risk factor for cancer, cardiovascular disease and neurodegeneration. Yet, more is known about the molecular basis of any of these groups of diseases than the changes that accompany ageing itself. Progress in molecular ageing research was slow because the tools predic...

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Published in:Aging cell Vol. 20; no. 9; pp. e13452 - n/a
Main Authors: Simpson, Daniel J., Chandra, Tamir
Format: Journal Article
Language:English
Published: England John Wiley & Sons, Inc 01.09.2021
John Wiley and Sons Inc
Subjects:
Age
ageing
Aging
Aging - genetics
Animals
Biomarkers
Cardiovascular diseases
Cognitive ability
composite predictors
Datasets
Disease
DNA methylation
Epigenesis, Genetic - genetics
epigenetic clocks
Epigenetic inheritance
Epigenetics
Fibroblasts
Forensic science
Health aspects
Humans
Methylation
minimised clocks
mortality
Neurodegeneration
Review
Reviews
Risk factors
mortality
epigenetic clocks
ageing
minimised clocks
composite predictors
ISSN:1474-9718, 1474-9726, 1474-9726
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Abstract Advanced age is the main common risk factor for cancer, cardiovascular disease and neurodegeneration. Yet, more is known about the molecular basis of any of these groups of diseases than the changes that accompany ageing itself. Progress in molecular ageing research was slow because the tools predicting whether someone aged slowly or fast (biological age) were unreliable. To understand ageing as a risk factor for disease and to develop interventions, the molecular ageing field needed a quantitative measure; a clock for biological age. Over the past decade, a number of age predictors utilising DNA methylation have been developed, referred to as epigenetic clocks. While they appear to estimate biological age, it remains unclear whether the methylation changes used to train the clocks are a reflection of other underlying cellular or molecular processes, or whether methylation itself is involved in the ageing process. The precise aspects of ageing that the epigenetic clocks capture remain hidden and seem to vary between predictors. Nonetheless, the use of epigenetic clocks has opened the door towards studying biological ageing quantitatively, and new clocks and applications, such as forensics, appear frequently. In this review, we will discuss the range of epigenetic clocks available, their strengths and weaknesses, and their applicability to various scientific queries. Over the past decade, the repertoire of DNA methylation‐based age predictors, known as epigenetic clocks, has grown. Here, we review four main types of epigenetic clocks that have been developed; human‐array based, reduced, composite and non‐human.
AbstractList Advanced age is the main common risk factor for cancer, cardiovascular disease and neurodegeneration. Yet, more is known about the molecular basis of any of these groups of diseases than the changes that accompany ageing itself. Progress in molecular ageing research was slow because the tools predicting whether someone aged slowly or fast (biological age) were unreliable. To understand ageing as a risk factor for disease and to develop interventions, the molecular ageing field needed a quantitative measure; a clock for biological age. Over the past decade, a number of age predictors utilising DNA methylation have been developed, referred to as epigenetic clocks. While they appear to estimate biological age, it remains unclear whether the methylation changes used to train the clocks are a reflection of other underlying cellular or molecular processes, or whether methylation itself is involved in the ageing process. The precise aspects of ageing that the epigenetic clocks capture remain hidden and seem to vary between predictors. Nonetheless, the use of epigenetic clocks has opened the door towards studying biological ageing quantitatively, and new clocks and applications, such as forensics, appear frequently. In this review, we will discuss the range of epigenetic clocks available, their strengths and weaknesses, and their applicability to various scientific queries.
Advanced age is the main common risk factor for cancer, cardiovascular disease and neurodegeneration. Yet, more is known about the molecular basis of any of these groups of diseases than the changes that accompany ageing itself. Progress in molecular ageing research was slow because the tools predicting whether someone aged slowly or fast (biological age) were unreliable. To understand ageing as a risk factor for disease and to develop interventions, the molecular ageing field needed a quantitative measure; a clock for biological age. Over the past decade, a number of age predictors utilising DNA methylation have been developed, referred to as epigenetic clocks. While they appear to estimate biological age, it remains unclear whether the methylation changes used to train the clocks are a reflection of other underlying cellular or molecular processes, or whether methylation itself is involved in the ageing process. The precise aspects of ageing that the epigenetic clocks capture remain hidden and seem to vary between predictors. Nonetheless, the use of epigenetic clocks has opened the door towards studying biological ageing quantitatively, and new clocks and applications, such as forensics, appear frequently. In this review, we will discuss the range of epigenetic clocks available, their strengths and weaknesses, and their applicability to various scientific queries.Advanced age is the main common risk factor for cancer, cardiovascular disease and neurodegeneration. Yet, more is known about the molecular basis of any of these groups of diseases than the changes that accompany ageing itself. Progress in molecular ageing research was slow because the tools predicting whether someone aged slowly or fast (biological age) were unreliable. To understand ageing as a risk factor for disease and to develop interventions, the molecular ageing field needed a quantitative measure; a clock for biological age. Over the past decade, a number of age predictors utilising DNA methylation have been developed, referred to as epigenetic clocks. While they appear to estimate biological age, it remains unclear whether the methylation changes used to train the clocks are a reflection of other underlying cellular or molecular processes, or whether methylation itself is involved in the ageing process. The precise aspects of ageing that the epigenetic clocks capture remain hidden and seem to vary between predictors. Nonetheless, the use of epigenetic clocks has opened the door towards studying biological ageing quantitatively, and new clocks and applications, such as forensics, appear frequently. In this review, we will discuss the range of epigenetic clocks available, their strengths and weaknesses, and their applicability to various scientific queries.
Advanced age is the main common risk factor for cancer, cardiovascular disease and neurodegeneration. Yet, more is known about the molecular basis of any of these groups of diseases than the changes that accompany ageing itself. Progress in molecular ageing research was slow because the tools predicting whether someone aged slowly or fast (biological age) were unreliable. To understand ageing as a risk factor for disease and to develop interventions, the molecular ageing field needed a quantitative measure; a clock for biological age. Over the past decade, a number of age predictors utilising DNA methylation have been developed, referred to as epigenetic clocks. While they appear to estimate biological age, it remains unclear whether the methylation changes used to train the clocks are a reflection of other underlying cellular or molecular processes, or whether methylation itself is involved in the ageing process. The precise aspects of ageing that the epigenetic clocks capture remain hidden and seem to vary between predictors. Nonetheless, the use of epigenetic clocks has opened the door towards studying biological ageing quantitatively, and new clocks and applications, such as forensics, appear frequently. In this review, we will discuss the range of epigenetic clocks available, their strengths and weaknesses, and their applicability to various scientific queries. Over the past decade, the repertoire of DNA methylation‐based age predictors, known as epigenetic clocks, has grown. Here, we review four main types of epigenetic clocks that have been developed; human‐array based, reduced, composite and non‐human.
Advanced age is the main common risk factor for cancer, cardiovascular disease and neurodegeneration. Yet, more is known about the molecular basis of any of these groups of diseases than the changes that accompany ageing itself. Progress in molecular ageing research was slow because the tools predicting whether someone aged slowly or fast (biological age) were unreliable. To understand ageing as a risk factor for disease and to develop interventions, the molecular ageing field needed a quantitative measure; a clock for biological age. Over the past decade, a number of age predictors utilising DNA methylation have been developed, referred to as epigenetic clocks. While they appear to estimate biological age, it remains unclear whether the methylation changes used to train the clocks are a reflection of other underlying cellular or molecular processes, or whether methylation itself is involved in the ageing process. The precise aspects of ageing that the epigenetic clocks capture remain hidden and seem to vary between predictors. Nonetheless, the use of epigenetic clocks has opened the door towards studying biological ageing quantitatively, and new clocks and applications, such as forensics, appear frequently. In this review, we will discuss the range of epigenetic clocks available, their strengths and weaknesses, and their applicability to various scientific queries. Over the past decade, the repertoire of DNA methylation‐based age predictors, known as epigenetic clocks, has grown. Here, we review four main types of epigenetic clocks that have been developed; human‐array based, reduced, composite and non‐human.
Audience Academic
Author Simpson, Daniel J.
Chandra, Tamir
AuthorAffiliation 1 MRC Human Genetics Unit MRC Institute of Genetics and Molecular Medicine University of Edinburgh Edinburgh UK
AuthorAffiliation_xml – name: 1 MRC Human Genetics Unit MRC Institute of Genetics and Molecular Medicine University of Edinburgh Edinburgh UK
Author_xml – sequence: 1
  givenname: Daniel J.
  orcidid: 0000-0002-8431-7384
  surname: Simpson
  fullname: Simpson, Daniel J.
  email: s1684303@sms.ed.ac.uk
  organization: University of Edinburgh
– sequence: 2
  givenname: Tamir
  orcidid: 0000-0002-7935-317X
  surname: Chandra
  fullname: Chandra, Tamir
  email: tamir.chandra@igmm.ed.ac.uk
  organization: University of Edinburgh
BackLink https://www.ncbi.nlm.nih.gov/pubmed/34415665$$D View this record in MEDLINE/PubMed
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IsDoiOpenAccess true
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Issue 9
Keywords mortality
epigenetic clocks
ageing
minimised clocks
composite predictors
Language English
License Attribution
2021 The Authors. Aging Cell published by Anatomical Society and John Wiley & Sons Ltd.
This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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Snippet Advanced age is the main common risk factor for cancer, cardiovascular disease and neurodegeneration. Yet, more is known about the molecular basis of any of...
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StartPage e13452
SubjectTerms Age
ageing
Aging
Aging - genetics
Animals
Biomarkers
Cardiovascular diseases
Cognitive ability
composite predictors
Datasets
Disease
DNA methylation
Epigenesis, Genetic - genetics
epigenetic clocks
Epigenetic inheritance
Epigenetics
Fibroblasts
Forensic science
Health aspects
Humans
Methylation
minimised clocks
mortality
Neurodegeneration
Review
Reviews
Risk factors
Title Epigenetic age prediction
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Facel.13452
https://www.ncbi.nlm.nih.gov/pubmed/34415665
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https://pubmed.ncbi.nlm.nih.gov/PMC8441394
Volume 20
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