时间标签：数据日期 2026-11-05 · 生成时间 2026-11-05 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/11/02 – 2026/11/06 ｜ 情报发生日期 2026-11-05
研究问题
The therapeutic goal should therefore be restoration of homeostatic immune–endothelial communication rather than indiscriminate suppression of inflammation.6Discussion and future perspectivesThe major unresolved question is whether immune activation or vascular dysfunction initiates the age-associated cycle.；Single-cell and spatial approaches should therefore move beyond the question of whether ‘microglia’ or ‘endothelial cells’ are activated and instead identify which cellular states interact, where, and at what stage.；It is a dynamic interface capable of determining whether an aging neurovascular system remains compensated or progresses toward persistent inflammation, vascular failure, and neurodegeneration.
方法
These observations suggest that neuroinflammation and vascular dysfunction are not merely parallel consequences of aging.；We therefore focus on how aging primes both sides of this interface, how bidirectional signaling destabilizes neurovascular homeostasis, and how this state may progress from physiological aging toward neurodegenerative disease.；We therefore focus on how aging primes both sides of this interface, how bidirectional signaling destabilizes neurovascular homeostasis, and how this state may progress from physiological aging toward neurodegenerative disease (Figure 1).Figure 1Overview of immune-endothelial crosstalk in the aging neurovascular unit.
核心结论
Increasing evidence indicates that age-related cognitive decline cannot be explained solely by neuronal pathology.；Human dynamic contrast-enhanced magnetic resonance imaging has demonstrated age-associated increases in BBB permeability in the hippocampus, particularly in the CA1 and dentate gyrus, with greater disruption in individuals with mild cognitive impairment (10).；These observations suggest that neuroinflammation and vascular dysfunction are not merely parallel consequences of aging.
局限
This finding should not, however, be interpreted as evidence that NLRP3 universally initiates BBB aging; the experimental context involved peripheral inflammation rather than uncomplicated physiological aging.Microglia themselves can also exert temporally opposing vascular effects.；However, compared with AD and VCID, the temporal and causal contribution of aging-specific immune–endothelial signaling to PD remains less well established.Regional and cellular heterogeneity further complicates these comparisons.；However, CNS delivery remains a substantial obstacle, motivating continued development of barrier-targeted delivery technologies (95).Clinical translation remains much less mature.
对本项目的价值
中高价值：属「衰老细胞清除 / SASP 轴」方向；细胞衰老 / senolytics / SASP栏目可用作本项目文献库与综述素材。 ｜ 价值分 3.1/5（★★★☆☆）
全文来源
PubMed PMC JATS（正文 26,569 字符，题名指纹 0.9，已过 PubMed PMCID 官方关联 + 题名指纹 + 正文长度归属校验）
原文题录
- 中文题名：衰老中神经炎症与血管功能障碍交汇处的免疫-内皮串扰
- 英文标题：Immune-endothelial crosstalk at the nexus of neuroinflammation and vascular dysfunction in aging.
- 期刊与标识：Frontiers in immunology · PMID 42974162 · DOI 10.3389/fimmu.2026.1972284 · PMC PMC13725442