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<p>Alzheimer’s disease (AD) progression is tightly linked to neuroinflammation driven by central-peripheral immune imbalance, with microglial/astrocytic activation, blood-brain barrier disruption, and cytokine dysregulation forming a vicious cycle. Exosomes, as nanoscale extracellular vesicles, emerge as potent modulators by crossing the blood-brain barrier and delivering functional cargos (miR-146a, miR-124, TREM2, IL-10) to target immune and neuronal cells. They induce M2 microglial polarization, inhibit A1 astrocyte transformation, and balance Treg/Th17 subsets, while suppressing NF-κB and NLRP3 inflammasome pathways to reduce pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) and elevate anti-inflammatory IL-10. Additionally, exosomes enhance Aβ/tau clearance via promoting phagocytosis and autophagy, and repair the blood-brain barrier to mitigate peripheral immune infiltration. Derived from MSCs, immune cells, or traditional Chinese medicines, exosomes exhibit low immunogenicity and high biocompatibility, with preclinical and pilot clinical data confirming 30%–50% improvement in cognitive scores and 40%–60% reductions in cerebrospinal fluid IL-1β, TNF-α, and IL-6 levels in AD models and patients. These findings highlight exosomes as a multitargeted strategy to ameliorate neuroinflammation and halt AD neurodegeneration.</p>

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Exosomes in Alzheimer’s disease: neuroinflammation mitigation via immune modulation and inflammatory pathway targeting

  • 期刊论文

  • 发表日期：

    2026年4月16日

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  • Hongtao Jia,
  • Yonghai Meng,
  • Nan Zhao,
  • Yan Liu

摘要

Alzheimer’s disease (AD) progression is tightly linked to neuroinflammation driven by central-peripheral immune imbalance, with microglial/astrocytic activation, blood-brain barrier disruption, and cytokine dysregulation forming a vicious cycle. Exosomes, as nanoscale extracellular vesicles, emerge as potent modulators by crossing the blood-brain barrier and delivering functional cargos (miR-146a, miR-124, TREM2, IL-10) to target immune and neuronal cells. They induce M2 microglial polarization, inhibit A1 astrocyte transformation, and balance Treg/Th17 subsets, while suppressing NF-κB and NLRP3 inflammasome pathways to reduce pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) and elevate anti-inflammatory IL-10. Additionally, exosomes enhance Aβ/tau clearance via promoting phagocytosis and autophagy, and repair the blood-brain barrier to mitigate peripheral immune infiltration. Derived from MSCs, immune cells, or traditional Chinese medicines, exosomes exhibit low immunogenicity and high biocompatibility, with preclinical and pilot clinical data confirming 30%–50% improvement in cognitive scores and 40%–60% reductions in cerebrospinal fluid IL-1β, TNF-α, and IL-6 levels in AD models and patients. These findings highlight exosomes as a multitargeted strategy to ameliorate neuroinflammation and halt AD neurodegeneration.