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Peer-reviewedCC BY 4.0Frontiers in Immunology

Neurovascular-immune-clearance remodeling in brain aging

  • Yuxin Liu1,2
  • Ronghao Yang1,2
  • Haocai Chang1,2
  1. 1MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, College of Biophotonics, School of Optoelectronic Science and Engineering, South China Normal University
  2. 2Guangdong Provincial Key Laboratory of Laser Life Science, College of Biophotonics, School of Optoelectronic Science and Engineering, South China Normal University
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Abstract

Brain aging involves concurrent changes in cerebral vessels, immune regulation, and waste clearance, yet these processes are often studied separately. This fragmented approach limits understanding of how dysfunction in one system influences the others and contributes to age-related neurological disorders. This review summarizes current evidence on the neurovascular-immune-clearance axis, focusing on neurovascular unit deterioration, impaired glymphatic and meningeal lymphatic transport, neuroimmune remodeling, and the cell-specific mechanisms that connect these processes. We further compare their shared and disease-dependent roles in Alzheimer’s disease, vascular cognitive impairment, and late-life depression. Available imaging, fluid, proteomic, and epigenetic biomarkers are evaluated for their ability to measure different components of this axis, and emerging interventions are organized according to their predominant effects on vascular support, clearance function, immune signaling, and cellular senescence. Current evidence indicates that brain aging is characterized by interacting and partially compensable functional bottlenecks rather than a single linear pathological pathway. Integrating these mechanisms provides a framework for interpreting heterogeneous aging phenotypes, selecting complementary biomarkers, and developing mechanism-guided interventions. Future progress will depend on longitudinal human validation and direct demonstration that target engagement produces durable neurological benefit.

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Cite

BibTeXRIS
BibTeX
@article{liu2026neurovascularimmuneclearance,
  title = {{Neurovascular-immune-clearance remodeling in brain aging}},
  author = {Yuxin Liu and Ronghao Yang and Haocai Chang},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = oct,
  doi = {10.3389/fimmu.2026.1950144},
  url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1950144/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Neurovascular-immune-clearance remodeling in brain aging
AU  - Yuxin Liu
AU  - Ronghao Yang
AU  - Haocai Chang
PY  - 2026
DA  - 2026/10/29
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.1950144
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1950144/full
AB  - Brain aging involves concurrent changes in cerebral vessels, immune regulation, and waste clearance, yet these processes are often studied separately. This fragmented approach limits understanding of how dysfunction in one system influences the others and contributes to age-related neurological disorders. This review summarizes current evidence on the neurovascular-immune-clearance axis, focusing on neurovascular unit deterioration, impaired glymphatic and meningeal lymphatic transport, neuroimmune remodeling, and the cell-specific mechanisms that connect these processes. We further compare their shared and disease-dependent roles in Alzheimer’s disease, vascular cognitive impairment, and late-life depression. Available imaging, fluid, proteomic, and epigenetic biomarkers are evaluated for their ability to measure different components of this axis, and emerging interventions are organized according to their predominant effects on vascular support, clearance function, immune signaling, and cellular senescence. Current evidence indicates that brain aging is characterized by interacting and partially compensable functional bottlenecks rather than a single linear pathological pathway. Integrating these mechanisms provides a framework for interpreting heterogeneous aging phenotypes, selecting complementary biomarkers, and developing mechanism-guided interventions. Future progress will depend on longitudinal human validation and direct demonstration that target engagement produces durable neurological benefit.
SN  - 1664-3224
ER  -