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<p>Relevant studies on acupuncture-moxibustion intervening Alzheimer disease (AD) were collected, sorted out, and summarized, and acupuncture-moxibustion plays its role in treating AD via the following aspects: inhibiting abnormal activation of microglia and astrocytes; correcting imbalanced polarization of microglia; upregulating the expression of triggering receptor expressed on myeloid cells 2 (TREM2) and component 1q (C1q); downregulating nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3); regulating the release of proinflammatory/anti-inflammatory factors; reducing the release of cyclooxygenase-2 (COX-2) and transforming growth factor-β1 (TGF-β1); suppressing the abnormal activation of Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3), nuclear factor-κB (NF-κB), high mobility group box 1 (HMGB1)/receptor for advanced glycation end products (RAGE), and p38 mitogen-activated protein kinase (p38 MAPK) pathways; and upregulating molecule levels of the interleukin (IL)-33/growth stimulating gene 2 protein (ST2) pathway.</p>

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Research progress on neuroinflammatory mechanisms of acupuncture-moxibustion intervening Alzheimer disease

  • 期刊论文

  • 发表日期：

    2026年4月24日

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  • Li Li,
  • Xingke Yan,
  • Cui Ma,
  • Yuting Wei,
  • Tingting Dou,
  • Wenting Xie

摘要

Relevant studies on acupuncture-moxibustion intervening Alzheimer disease (AD) were collected, sorted out, and summarized, and acupuncture-moxibustion plays its role in treating AD via the following aspects: inhibiting abnormal activation of microglia and astrocytes; correcting imbalanced polarization of microglia; upregulating the expression of triggering receptor expressed on myeloid cells 2 (TREM2) and component 1q (C1q); downregulating nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3); regulating the release of proinflammatory/anti-inflammatory factors; reducing the release of cyclooxygenase-2 (COX-2) and transforming growth factor-β1 (TGF-β1); suppressing the abnormal activation of Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3), nuclear factor-κB (NF-κB), high mobility group box 1 (HMGB1)/receptor for advanced glycation end products (RAGE), and p38 mitogen-activated protein kinase (p38 MAPK) pathways; and upregulating molecule levels of the interleukin (IL)-33/growth stimulating gene 2 protein (ST2) pathway.