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      Utility of DNA Methylation as a Biomarker in Aging and Alzheimer’s Disease

      review-article
      Author(s): a , b , c , a , b , c , d , a , e , a , b , c , d , *
      Publication date (Electronic, preprint):
      Publication date (Electronic, pub):
      Publication date (Electronic, collection):
      Journal: Journal of Alzheimer's Disease Reports
      Publisher: IOS Press
      Keywords: Aging, Alzheimer’s disease, dementia, DNA methylation, epigenetics

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          Abstract

          Epigenetic mechanisms such as DNA methylation have been implicated in a number of diseases including cancer, heart disease, autoimmune disorders, and neurodegenerative diseases. While it is recognized that DNA methylation is tissue-specific, a limitation for many studies is the ability to sample the tissue of interest, which is why there is a need for a proxy tissue such as blood, that is reflective of the methylation state of the target tissue. In the last decade, DNA methylation has been utilized in the design of epigenetic clocks, which aim to predict an individual’s biological age based on an algorithmically defined set of CpGs. A number of studies have found associations between disease and/or disease risk with increased biological age, adding weight to the theory of increased biological age being linked with disease processes. Hence, this review takes a closer look at the utility of DNA methylation as a biomarker in aging and disease, with a particular focus on Alzheimer’s disease.

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          The Hallmarks of Aging

          Carlos López-Otín, Maria Blasco, Linda Partridge … (2014)
          Aging is characterized by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death. This deterioration is the primary risk factor for major human pathologies, including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. Aging research has experienced an unprecedented advance over recent years, particularly with the discovery that the rate of aging is controlled, at least to some extent, by genetic pathways and biochemical processes conserved in evolution. This Review enumerates nine tentative hallmarks that represent common denominators of aging in different organisms, with special emphasis on mammalian aging. These hallmarks are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. A major challenge is to dissect the interconnectedness between the candidate hallmarks and their relative contributions to aging, with the final goal of identifying pharmaceutical targets to improve human health during aging, with minimal side effects. Copyright © 2013 Elsevier Inc. All rights reserved.
          Article 0 comments Cited 3621 times – based on 0 reviews     Review now
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            The diagnosis of dementia due to Alzheimer's disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease

            Guy M McKhann, David S. Knopman, Howard Chertkow … (2011)
            The National Institute on Aging and the Alzheimer's Association charged a workgroup with the task of revising the 1984 criteria for Alzheimer's disease (AD) dementia. The workgroup sought to ensure that the revised criteria would be flexible enough to be used by both general healthcare providers without access to neuropsychological testing, advanced imaging, and cerebrospinal fluid measures, and specialized investigators involved in research or in clinical trial studies who would have these tools available. We present criteria for all-cause dementia and for AD dementia. We retained the general framework of probable AD dementia from the 1984 criteria. On the basis of the past 27 years of experience, we made several changes in the clinical criteria for the diagnosis. We also retained the term possible AD dementia, but redefined it in a manner more focused than before. Biomarker evidence was also integrated into the diagnostic formulations for probable and possible AD dementia for use in research settings. The core clinical criteria for AD dementia will continue to be the cornerstone of the diagnosis in clinical practice, but biomarker evidence is expected to enhance the pathophysiological specificity of the diagnosis of AD dementia. Much work lies ahead for validating the biomarker diagnosis of AD dementia. Copyright © 2011. Published by Elsevier Inc.
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              DNA methylation age of human tissues and cell types

              Steve Horvath, Ilias Lagkouvardos (2014)
              Background It is not yet known whether DNA methylation levels can be used to accurately predict age across a broad spectrum of human tissues and cell types, nor whether the resulting age prediction is a biologically meaningful measure. Results I developed a multi-tissue predictor of age that allows one to estimate the DNA methylation age of most tissues and cell types. The predictor, which is freely available, was developed using 8,000 samples from 82 Illumina DNA methylation array datasets, encompassing 51 healthy tissues and cell types. I found that DNA methylation age has the following properties: first, it is close to zero for embryonic and induced pluripotent stem cells; second, it correlates with cell passage number; third, it gives rise to a highly heritable measure of age acceleration; and, fourth, it is applicable to chimpanzee tissues. Analysis of 6,000 cancer samples from 32 datasets showed that all of the considered 20 cancer types exhibit significant age acceleration, with an average of 36 years. Low age-acceleration of cancer tissue is associated with a high number of somatic mutations and TP53 mutations, while mutations in steroid receptors greatly accelerate DNA methylation age in breast cancer. Finally, I characterize the 353 CpG sites that together form an aging clock in terms of chromatin states and tissue variance. Conclusions I propose that DNA methylation age measures the cumulative effect of an epigenetic maintenance system. This novel epigenetic clock can be used to address a host of questions in developmental biology, cancer and aging research.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Alzheimers Dis Rep
                Journal ID (iso-abbrev): J Alzheimers Dis Rep
                Journal ID (publisher-id): ADR
                Title: Journal of Alzheimer's Disease Reports
                Publisher: IOS Press (Nieuwe Hemweg 6B, 1013 BG Amsterdam, The Netherlands )
                ISSN (Electronic): 2542-4823
                Publication date (Electronic, preprint): 15 May 2023
                Publication date (Electronic, pub): 31 May 2023
                Publication date (Electronic, collection): 2023
                Volume: 7
                Issue: 1
                Pages: 475-503
                Affiliations
                [a ] Centre for Precision Health, Edith Cowan University , Joondalup, Western Australia, Australia
                [b ]Collaborative Genomics and Translation Group, Edith Cowan University , Joondalup, Western Australia, Australia
                [c ] School of Medical and Health Sciences, Edith Cowan University , Joondalup, Western Australia, Australia
                [d ] Curtin Medical School, Curtin University , Bentley, Western Australia, Australia
                [e ]CSIRO Health and Biosecurity, Australian e-Health Research Centre , Floreat, Western Australia
                Author notes
                [* ]Correspondence to: Prof. Simon M. Laws, Centre for Precision Health, Edith Cowan University, 270 Joondalup Drive, Joondalup, 6027, Western Australia, Australia. Tel.: +61 8 6304 5128; Fax: +61 8 6304 2493; E-mail: s.laws@ 123456ecu.edu.au .
                Article
                Publisher ID: ADR220109
                DOI: 10.3233/ADR-220109
                PMC ID: 10259073
                PubMed ID: 37313495
                SO-VID: b9c4a500-ce7d-4eb3-a322-84c16dd4345b
                Copyright © © 2023 – The authors. Published by IOS Press
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial (CC BY-NC 4.0) License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 20 December 2022
                Date accepted : 23 April 2023
                Categories
                Subject: Review

                Keywords: aging,alzheimer’s disease,dementia,dna methylation,epigenetics
                Data availability:
                Keywords: aging, alzheimer’s disease, dementia, dna methylation, epigenetics

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