数据日期 2026-10-29 · 生成时间 2026-10-29 06:03
研究问题
This review focuses on the mechanisms underlying brain aging and SASP activation, as well as the signaling pathways involved in inflammaging and its links to immunosenescence, BBB damage, and neurodegeneration, which together facilitate the development and progression of neurodegenerative diseases and pathological aging.
方法
（全文无独立方法节，正文亦未给出可抽取的实验动作句）
核心结论
In addition, NF-κB regulates proinflammatory molecules, including CCAAT-binding protein β (C/EBPβ), bromodomain-containing protein 4 (BRD4), lysine methyltransferase MLL1, and euchromatic histone lysine methyltransferase 2 (EHMT2) [18,43].；Transcription Factors NF-κB, TGF-β and HMGB1 NF-κB-mediated signaling pathways are the primary regulators of innate immunity and induce SASP and inflammation during cellular senescence [95,96].；Similarly, transforming growth factor-β (TGF-β) activated kinase 1 (TAK1) and its two regulatory subunits, TAB1 and TAB2, which are part of different PRR pathways, converge on NF-κB activation: TAK1 activates IKK, which phosphorylates IκBα and thereby promotes NF-κB activation [100,101,102]. ‖ 结论：Therefore, approaches to preventing these conditions may focus on maintaining the BBB through therapeutic strategies that either open it to deliver drugs to the CNS or reinforce it to slow the progression of neurodegenerative diseases.
局限
全文未设独立 limitations 节；结构上为综述/二次研究，因果推断强度受限。
对本项目的价值
★★★☆☆ 细胞衰老清除/重编程是项目干预管线的核心支柱之一。命中核心 细胞衰老；设计 单细胞。
全文来源
PMC JATS 全文（正文 80,381 字符，已过标题/DOI 逐字归属校验）
原文题录
- 英文标题：Brain Aging and Cellular Senescence Trigger Neuroimmunological Dysregulation and Neurodegeneration.
- 期刊与标识：Brain Sci · PMID 42939272 · DOI 10.3390/brainsci16101019**
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