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Simultaneous profiling of 3D genome structure and DNA methylation in single human cells.在单个人类细胞中同时分析 3D 基因组结构和 DNA 甲基化。
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Improved precision of epigenetic clock estimates across tissues and its implication for biological ageing.改善跨组织的表观遗传时钟估计的精度及其对生物衰老的影响。
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Dynamic Enhancer DNA Methylation as Basis for Transcriptional and Cellular Heterogeneity of ESCs.动态增强子DNA甲基化作为胚胎干细胞转录和细胞异质性的基础
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Neuroepigenetic signatures of age and sex in the living human brain.人类活体大脑中年龄和性别的神经表观遗传学特征。
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Age Mosaicism across Multiple Scales in Adult Tissues.成年组织中多尺度的年龄镶嵌现象。
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当功能追随形式:衰老神经元的核区室结构和表观遗传景观。

When function follows form: Nuclear compartment structure and the epigenetic landscape of the aging neuron.

机构信息

Department of Cellular and Molecular Medicine, University of California San Diego, La Jolla, CA, USA.

Nuclear Architecture in Neural Plasticity and Aging, German Center for Neurodegenerative Diseases (DZNE), Dresden, Germany.

出版信息

Exp Gerontol. 2020 May;133:110876. doi: 10.1016/j.exger.2020.110876. Epub 2020 Feb 14.

DOI:10.1016/j.exger.2020.110876
PMID:32068088
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7086016/
Abstract

The human brain is affected by cellular aging. Neurons are primarily generated during embryogenesis and early life with a limited capacity for renewal and replacement, making them some of the oldest cells in the human body. Our present understanding of neurodegenerative diseases points towards advanced neuronal age as a prerequisite for the development of these disorders. While significant progress has been made in understanding the relationship between aging and neurological disease, it will be essential to delve further into the molecular mechanisms of neuronal aging in order to develop therapeutic interventions targeting age-related brain dysfunction. In this mini review, we highlight recent findings on the relationship between the aging of nuclear structures and changes in the epigenetic landscape during neuronal aging and disease.

摘要

人类大脑受到细胞衰老的影响。神经元主要在胚胎发生和生命早期生成,其更新和替换能力有限,因此成为人体中最古老的细胞之一。我们目前对神经退行性疾病的理解表明,神经元的高龄是这些疾病发展的前提。虽然我们在理解衰老与神经疾病之间的关系方面已经取得了重大进展,但深入研究神经元衰老的分子机制对于开发针对与年龄相关的大脑功能障碍的治疗干预措施至关重要。在这篇简短的综述中,我们强调了最近在核结构衰老与神经元衰老和疾病期间表观遗传景观变化之间关系的发现。