综述解读

组蛋白修饰站在 AD 的衰老、神经炎症与代谢交汇处

来源:Aging Cell · PMID 42934178 · DOI 10.1111/acel.70785** · 来源:IMA 知识库《文献层·文献监控卡片》2026-10-29 期 · 摘要级(file_id dGBunAeRiRlm,下载实测 692,872 B) · 摘要级,未获取付费墙全文

数据日期 2026-10-29 · 生成时间 2026-10-29 06:03

证据级别:摘要级。本条依据 PubMed 结构化摘要与元数据撰写,付费墙全文未获取、未逐节核验,本站未做任何数值推算补全。

研究问题

Aging, neuroinflammation and metabolic dysfunction are tightly intertwined in Alzheimer's disease (AD), but how transient pathological signals become persistent cellular states remains poorly understood.

方法

Histone post-translational modifications (PTMs) provide a dynamic interface between extracellular stimuli, cellular metabolism and chromatin state.

核心结论

This Review examines how canonical histone modifications and emerging metabolite-derived acylations regulate inflammatory and stress-responsive programmes across microglia, astrocytes and neurons during aging and AD.;We discuss how amyloid-β, tau pathology, metabolic dysfunction and innate immune signaling converge on histone-modifying machinery, and how reciprocal interactions between metabolism and chromatin may stabilize disease-associated cell states.;Particular attention is given to cellular senescence and neuroimmune memory, while emphasizing the context dependence of individual histone marks across cell types, genomic regions and disease stages.;We further evaluate evidence for causality using three criteria: perturbation, persistence and reversibility. ‖ 结论:This framework distinguishes chromatin states that accompany ongoing pathology from those capable of sustaining pathological cell states beyond their initiating signals.

局限

未能获取全文,具体设计细节、失访与统计学处理无法核验。

对本项目的价值

★★★☆☆ 脑老化是最大未满足需求,也是终点最难量化的领域;biomarker 与认知读数选择最敏感。

原文题录

  • 英文标题:Histone Modifications at the Intersection of Aging, Neuroinflammation and Metabolism in Alzheimer's Disease.
  • 期刊与标识:Aging Cell · PMID 42934178 · DOI 10.1111/acel.70785**

C 级证据分级:C 级(预印本 / 观点评论,非原始研究)

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