<p>Cognitive impairment is a prevalent extrapulmonary manifestation of COPD. However, existing reviews have not yet systematically linked COPD-related dysregulation of brain functional networks with clinical indicators. This review bridges this gap by elucidating the pathway from pulmonary pathology to cognitive deficits via central network dysfunction, synthesizing evidence across four dimensions: clinical manifestations; physiological and pathological mechanisms; fMRI-based brain network disorders; and promising treatments. Chronic hypoxia-induced neuroinflammation, oxidative stress, and systemic inflammation propagated via the lung-brain axis were the main pathogenesis of COPD-CI. Cognitive deficits in COPD patients primarily manifest as executive function and visuospatial impairment, with some reality distinctive neural network features showing aberrant functional connectivity between the default mode network and visual network. Long-term oxygen therapy, anti-inflammatory regimens, and cognitive rehabilitation demonstrate benefits in improving cognition. Large sample, cross-sectional study is needed in the future studies, and multimodal neuroimaging should be used to delineate spatiotemporal network dynamics in COPD-CI.</p>

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Aberrant brain functional network in COPD patients with cognitive impairment: clinical manifestations, mechanisms and therapeutic strategies

  • Jia-kai He,
  • Xin-yu Han,
  • Yun-sheng Tan,
  • Zi-ang Yao,
  • Yuan-li Dong,
  • Cui-ling Feng

摘要

Cognitive impairment is a prevalent extrapulmonary manifestation of COPD. However, existing reviews have not yet systematically linked COPD-related dysregulation of brain functional networks with clinical indicators. This review bridges this gap by elucidating the pathway from pulmonary pathology to cognitive deficits via central network dysfunction, synthesizing evidence across four dimensions: clinical manifestations; physiological and pathological mechanisms; fMRI-based brain network disorders; and promising treatments. Chronic hypoxia-induced neuroinflammation, oxidative stress, and systemic inflammation propagated via the lung-brain axis were the main pathogenesis of COPD-CI. Cognitive deficits in COPD patients primarily manifest as executive function and visuospatial impairment, with some reality distinctive neural network features showing aberrant functional connectivity between the default mode network and visual network. Long-term oxygen therapy, anti-inflammatory regimens, and cognitive rehabilitation demonstrate benefits in improving cognition. Large sample, cross-sectional study is needed in the future studies, and multimodal neuroimaging should be used to delineate spatiotemporal network dynamics in COPD-CI.