Epigenetic Clock: DNA Methylation in Aging

Jiang, Shuang; Guo, Yuchen

doi:10.1155/2020/1047896

Cited by 37 publications

(30 citation statements)

References 105 publications

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“…Most of these epigenetic alterations contribute to cognitive decline during aging (reviewed by Harman and Martin, 2020 ). DNA methylation is a process, by which methyl groups are added to cytosine residues, primarily in the regions rich in cytosine-guanine dinucleotides, CpG, which are grouped in so called CpG islands (reviewed in Jiang and Guo, 2020 ). In neuronal cells, CpG methylation plays a critical role in neural plasticity (Martinowich et al, 2003 ; Miller et al, 2010 ).…”

Section: Selected Aspects Of Cellular Senescence and Their Role In Brmentioning

confidence: 99%

Cellular Senescence in Brain Aging

Sikora

Bielak-Żmijewska

Dudkowska

et al. 2021

Front. Aging Neurosci.

140

115

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Aging of the brain can manifest itself as a memory and cognitive decline, which has been shown to frequently coincide with changes in the structural plasticity of dendritic spines. Decreased number and maturity of spines in aged animals and humans, together with changes in synaptic transmission, may reflect aberrant neuronal plasticity directly associated with impaired brain functions. In extreme, a neurodegenerative disease, which completely devastates the basic functions of the brain, may develop. While cellular senescence in peripheral tissues has recently been linked to aging and a number of aging-related disorders, its involvement in brain aging is just beginning to be explored. However, accumulated evidence suggests that cell senescence may play a role in the aging of the brain, as it has been documented in other organs. Senescent cells stop dividing and shift their activity to strengthen the secretory function, which leads to the acquisition of the so called senescence-associated secretory phenotype (SASP). Senescent cells have also other characteristics, such as altered morphology and proteostasis, decreased propensity to undergo apoptosis, autophagy impairment, accumulation of lipid droplets, increased activity of senescence-associated-β-galactosidase (SA-β-gal), and epigenetic alterations, including DNA methylation, chromatin remodeling, and histone post-translational modifications that, in consequence, result in altered gene expression. Proliferation-competent glial cells can undergo senescence both in vitro and in vivo, and they likely participate in neuroinflammation, which is characteristic for the aging brain. However, apart from proliferation-competent glial cells, the brain consists of post-mitotic neurons. Interestingly, it has emerged recently, that non-proliferating neuronal cells present in the brain or cultivated in vitro can also have some hallmarks, including SASP, typical for senescent cells that ceased to divide. It has been documented that so called senolytics, which by definition, eliminate senescent cells, can improve cognitive ability in mice models. In this review, we ask questions about the role of senescent brain cells in brain plasticity and cognitive functions impairments and how senolytics can improve them. We will discuss whether neuronal plasticity, defined as morphological and functional changes at the level of neurons and dendritic spines, can be the hallmark of neuronal senescence susceptible to the effects of senolytics.

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Section: Selected Aspects Of Cellular Senescence and Their Role In Brmentioning

confidence: 99%

Cellular Senescence in Brain Aging

Sikora

Bielak-Żmijewska

Dudkowska

et al. 2021

Front. Aging Neurosci.

140

115

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“…However, to date there is no clear agreement on whether the epigenome has a central role in ageing (is it the cause or the consequence? ), and neither is a consensus on what the epigenetic clocks might mean, which are the role that methylation marks do play on ageing and health or even the involvement of them in the rejuvenation process (Gladyshev, 2020;Niehrs & Calkhoven, 2020;Bertucci & Parrott, 2020;Zhang & Gladyshev, 2020;Jiang & Guo, 2020;Field et al, 2018;Horvath & Raj, 2018).…”

Section: A Coherent Information-based Conception Of Both Phenomena: Lmentioning

confidence: 99%

The Principle of Continuous Biological Information Flow as the Fundamental Foundation for the Biological Sciences. Implications for Ageing Research

Marsellach¹

2020

Preprint

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The current state of biological knowledge contains an unresolved paradox: life as a continuity in the face of the phenomena of ageing. In this manuscript I propose a theoretical framework that offers a solution for this apparent contradiction. The framework proposed is based on a rethinking of what ageing is at a molecular level, as well as on a rethinking of the mechanisms in charge of the flow of information from one generation to the following ones. I propose an information-based conception of ageing instead of the widely accepted damage-based conception of ageing and propose a full recovery of the chromosome theory of inheritance to describe the intergenerational flow of information. Altogether the proposed framework allows a precise and unique definition of what life is: a continuous flow of biological information. The proposed framework also implies that ageing is merely a consequence of the way in which epigenetically-coded phenotypic characteristics are passed from one generation to the next ones.

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“…EPIGENETIC REGULATION OF FERROPTOSIS VIA DNA METHYLATION DNA methylation level is the most promising indicator to estimate biological aging. DNA methylation level increases with aging at specific loci, however, genome undergoes hypomethylation globally [72]. As discussed above that BRD4 regulate ferroptosis, however, its expression is epigenetically regulated via DNA methylation.…”

Section: Epigenetic Regulation Of Ferroptosis Via Histone Modificationmentioning

confidence: 95%

Implication of ferroptosis in aging

et al. 2021

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Life is indeed continuously going through the irreversible and inevitable process of aging. The rate of aging process depends on various factors and varies individually. These factors include various environmental stimuli including exposure to toxic chemicals, psychological stress whereas suffering with various illnesses specially the chronic diseases serve as endogenous triggers. The basic underlying mechanism for all kinds of stresses is now known to be manifested as production of excessive ROS, exhaustion of ROS neutralizing antioxidant enzymes and proteins leading to imbalance in oxidation and antioxidant processes with subsequent oxidative stress induced inflammation affecting the cells, tissues, organs and the whole body. All these factors lead to conventional cell death either through necrosis, apoptosis, or autophagy. Currently, a newly identified mechanism of iron dependent regulated cell death called ferroptosis, is of special interest for its implication in pathogenesis of various diseases such as cardiovascular disease, neurological disorders, cancers, and various other age-related disorders (ARD). In ferroptosis, the cell death occur neither by conventional apoptosis, necrosis nor by autophagy, rather dysregulated iron in the cell mediates excessive lipid peroxidation of accumulated lethal lipids. It is not surprising to assume its role in aging as previous research have identified some solid cues on the subject. In this review, we will highlight the factual evidences to support the possible role and implication of ferroptosis in aging in order to declare the need to identify and explore the interventions to prevent excessive ferroptosis leading to accelerated aging and associated liabilities of aging.

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Epigenetic Clock: DNA Methylation in Aging

Cited by 37 publications

References 105 publications

Cellular Senescence in Brain Aging

Cellular Senescence in Brain Aging

The Principle of Continuous Biological Information Flow as the Fundamental Foundation for the Biological Sciences. Implications for Ageing Research

Implication of ferroptosis in aging

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