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<p>Perioperative neurocognitive disorders (PND), including postoperative delirium, delayed neurocognitive recovery, and postoperative cognitive dysfunction, are common complications in older surgical patients and are associated with impaired recovery, reduced quality of life, and increased postoperative morbidity. Current management remains largely supportive and preventive, and effective targeted therapies are still lacking. Electroacupuncture (EA), as a minimally invasive neuromodulatory intervention, has attracted increasing attention because of its potential multi-target regulatory effects. This review summarizes current mechanistic and clinical evidence regarding EA for PND. Preclinical studies suggest that EA may modulate several interacting pathological processes, including neuroinflammation, oxidative stress, autophagy dysfunction, ferroptosis, mitochondrial injury, microbiota-gut-brain axis dysregulation, and hippocampal synaptic plasticity. Recent PND/POCD animal studies further support EA-related regulation of NLRP3 inflammasome activation, cGAS–STING signaling, SIRT1/NRF2/GPX4-mediated ferroptosis, AMPK/SIRT1/FOXO1/PINK1/Parkin-related autophagy pathways, and MAPK-related synaptic plasticity. Clinical studies and meta-analyses suggest that EA and related acupoint-based electrical stimulation techniques may reduce early postoperative cognitive decline and improve short-term cognitive outcomes in older surgical patients. However, the overall evidence remains limited by heterogeneous stimulation protocols, variable acupoint prescriptions, incomplete blinding, short follow-up, and reliance on cognitive screening scales. Several proposed mechanisms are still partly inferred from non-PND models. Future studies should use standardized EA protocols, clinically relevant PND models, dynamic mechanistic assessments, and adequately powered sham-controlled trials to clarify the therapeutic role of EA in PND.</p>

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Advances in electroacupuncture for perioperative neurocognitive disorders: mechanisms and clinical evidence

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月8日

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  • Shirong Wei,
  • Sitong Zhou,
  • Junwen Tu,
  • Tong Zhi,
  • Yungong Wang,
  • Qihong Shen,
  • Chaobo Ni,
  • Ming Yao,
  • Huadong Ni

摘要

Perioperative neurocognitive disorders (PND), including postoperative delirium, delayed neurocognitive recovery, and postoperative cognitive dysfunction, are common complications in older surgical patients and are associated with impaired recovery, reduced quality of life, and increased postoperative morbidity. Current management remains largely supportive and preventive, and effective targeted therapies are still lacking. Electroacupuncture (EA), as a minimally invasive neuromodulatory intervention, has attracted increasing attention because of its potential multi-target regulatory effects. This review summarizes current mechanistic and clinical evidence regarding EA for PND. Preclinical studies suggest that EA may modulate several interacting pathological processes, including neuroinflammation, oxidative stress, autophagy dysfunction, ferroptosis, mitochondrial injury, microbiota-gut-brain axis dysregulation, and hippocampal synaptic plasticity. Recent PND/POCD animal studies further support EA-related regulation of NLRP3 inflammasome activation, cGAS–STING signaling, SIRT1/NRF2/GPX4-mediated ferroptosis, AMPK/SIRT1/FOXO1/PINK1/Parkin-related autophagy pathways, and MAPK-related synaptic plasticity. Clinical studies and meta-analyses suggest that EA and related acupoint-based electrical stimulation techniques may reduce early postoperative cognitive decline and improve short-term cognitive outcomes in older surgical patients. However, the overall evidence remains limited by heterogeneous stimulation protocols, variable acupoint prescriptions, incomplete blinding, short follow-up, and reliance on cognitive screening scales. Several proposed mechanisms are still partly inferred from non-PND models. Future studies should use standardized EA protocols, clinically relevant PND models, dynamic mechanistic assessments, and adequately powered sham-controlled trials to clarify the therapeutic role of EA in PND.