The broken Alzheimer's disease genome.

IF 11.1 Q1 CELL BIOLOGY
Cell genomics Pub Date : 2024-05-08 Epub Date: 2024-05-01 DOI:10.1016/j.xgen.2024.100555
Cláudio Gouveia Roque, Hemali Phatnani, Ulrich Hengst
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引用次数: 0

Abstract

The complex pathobiology of late-onset Alzheimer's disease (AD) poses significant challenges to therapeutic and preventative interventions. Despite these difficulties, genomics and related disciplines are allowing fundamental mechanistic insights to emerge with clarity, particularly with the introduction of high-resolution sequencing technologies. After all, the disrupted processes at the interface between DNA and gene expression, which we call the broken AD genome, offer detailed quantitative evidence unrestrained by preconceived notions about the disease. In addition to highlighting biological pathways beyond the classical pathology hallmarks, these advances have revitalized drug discovery efforts and are driving improvements in clinical tools. We review genetic, epigenomic, and gene expression findings related to AD pathogenesis and explore how their integration enables a better understanding of the multicellular imbalances contributing to this heterogeneous condition. The frontiers opening on the back of these research milestones promise a future of AD care that is both more personalized and predictive.

破碎的阿尔茨海默病基因组
晚发性阿尔茨海默病(AD)的病理生物学非常复杂,给治疗和预防干预带来了巨大挑战。尽管存在这些困难,但基因组学和相关学科,尤其是高分辨率测序技术的引入,使基本的机理认识得以清晰呈现。毕竟,DNA 与基因表达界面的中断过程(我们称之为 "破碎的 AD 基因组")提供了详细的定量证据,不受对该疾病先入为主的观念的限制。除了强调经典病理学特征之外的生物学途径之外,这些进展还为药物发现工作注入了新的活力,并推动了临床工具的改进。我们回顾了与多发性硬化症发病机制相关的遗传学、表观基因组学和基因表达研究成果,并探讨了如何通过整合这些研究成果更好地理解导致这种异质性疾病的多细胞失衡。这些具有里程碑意义的研究成果所开辟的前沿领域有望为未来的注意力缺失症治疗提供更加个性化和更具预测性的服务。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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CiteScore
7.10
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0.00%
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