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<p>Asthma is increasingly recognized as a systemic inflammatory syndrome that extends beyond the respiratory tract, with emerging evidence highlighting its relevance to neuroinflammation. The lung–brain axis—via interconnected inflammatory, vascular, metabolic, neural, and microbial pathways—provides a framework for understanding how chronic pulmonary disease may sustain or exacerbate neuroinflammatory processes. Mechanistically, asthma promotes blood–brain barrier disruption, systemic inflammation that seeds central neuroinflammation, oxidative stress, mitochondrial dysfunction, gut–lung–brain microbial crosstalk, and sleep fragmentation, all of which are biologically plausible drivers of sustained neuroinflammatory states and consequent neurodegenerative vulnerability. Epidemiological studies link asthma to increased risks of all-cause dementia and Alzheimer’s disease, though cohort findings vary. Neuroimaging and biomarker evidence further support neuroinflammatory involvement, revealing altered hippocampal metabolism, white matter abnormalities, elevated plasma glial fibrillary acidic protein and neurofilament light chains, and cerebrospinal fluid markers of synaptic injury in severe or poorly controlled asthma—each reflecting neuroinflammatory or neurodegenerative sequelae. Links with Parkinson’s disease and other neurodegenerative disorders remain more preliminary. Notably, asthma severity, phenotype, exacerbation frequency, and corticosteroid burden modulate neurological risk, suggesting that optimal disease control—potentially enhanced by biologic therapies—may confer neuroprotective benefits by dampening neuroinflammation. In conclusion, asthma should not be viewed solely as an airway disorder but as a potentially modifiable contributor to long-term brain vulnerability via neuroinflammatory pathways within the lung–brain axis. Future longitudinal studies integrating detailed phenotyping, biomarkers, and neuroimaging are needed to establish causality and guide anti-neuroinflammatory therapeutic strategies.</p>

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Unknotting the nexus of asthma and neuroinflammation: from brain network alterations to therapeutic implications

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月15日

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  • Wenjie Hu,
  • Yanan Zou,
  • Junbo Yin,
  • Lei Liu,
  • Yujie Ding,
  • Xingzhe Gao,
  • Yan Li,
  • Xiangyi Kong

摘要

Asthma is increasingly recognized as a systemic inflammatory syndrome that extends beyond the respiratory tract, with emerging evidence highlighting its relevance to neuroinflammation. The lung–brain axis—via interconnected inflammatory, vascular, metabolic, neural, and microbial pathways—provides a framework for understanding how chronic pulmonary disease may sustain or exacerbate neuroinflammatory processes. Mechanistically, asthma promotes blood–brain barrier disruption, systemic inflammation that seeds central neuroinflammation, oxidative stress, mitochondrial dysfunction, gut–lung–brain microbial crosstalk, and sleep fragmentation, all of which are biologically plausible drivers of sustained neuroinflammatory states and consequent neurodegenerative vulnerability. Epidemiological studies link asthma to increased risks of all-cause dementia and Alzheimer’s disease, though cohort findings vary. Neuroimaging and biomarker evidence further support neuroinflammatory involvement, revealing altered hippocampal metabolism, white matter abnormalities, elevated plasma glial fibrillary acidic protein and neurofilament light chains, and cerebrospinal fluid markers of synaptic injury in severe or poorly controlled asthma—each reflecting neuroinflammatory or neurodegenerative sequelae. Links with Parkinson’s disease and other neurodegenerative disorders remain more preliminary. Notably, asthma severity, phenotype, exacerbation frequency, and corticosteroid burden modulate neurological risk, suggesting that optimal disease control—potentially enhanced by biologic therapies—may confer neuroprotective benefits by dampening neuroinflammation. In conclusion, asthma should not be viewed solely as an airway disorder but as a potentially modifiable contributor to long-term brain vulnerability via neuroinflammatory pathways within the lung–brain axis. Future longitudinal studies integrating detailed phenotyping, biomarkers, and neuroimaging are needed to establish causality and guide anti-neuroinflammatory therapeutic strategies.