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<p>Neuroinflammation, driven by dysregulated microglial polarization, is a hallmark of Alzheimer’s disease (AD). Recently, the triggering receptor expressed on myeloid cells 2 (TREM2), a key regulator of microglial function, has emerged as a promising therapeutic target for AD. This study aimed to investigate the therapeutic potential and mechanism of action of the natural compound β-asarone in AD models. Our results demonstrate that β-asarone significantly improved cognitive function, reduced hippocampal neuronal damage, and decreased both Aβ deposition and Tau hyperphosphorylation in 3×Tg-AD mice. Mechanistically, β-asarone upregulated TREM2 expression, activated the PI3K/AKT pathway, and inhibited GSK3β activity, thereby promoting the polarization of microglia from the pro-inflammatory M1 phenotype toward the anti-inflammatory M2 phenotype and alleviating neuroinflammation. This study is the first to elucidate that β-asarone ameliorates AD pathology by modulating microglial polarization via the TREM2/PI3K/AKT/GSK3β signaling axis, providing experimental evidence supporting its potential as an immunomodulatory therapeutic agent for AD.</p> Graphical Abstract <p></p>

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β-Asarone Mediates the Alleviation of Neuroinflammation in Alzheimer’s Disease Via Modulation of the TREM2/PI3K/AKT Signaling Pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月24日

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  • Na Yang,
  • Jiajun Jiang,
  • Jianhong Shi,
  • Xuan Liu,
  • Chenshi Yu,
  • Shunyuan Guo,
  • Chengliang Zhang,
  • Feng Gao,
  • Zijian Yang,
  • Huina Feng,
  • Qiuyan Weng,
  • Tao Qiu,
  • Changyu Li,
  • Liting Ji

摘要

Neuroinflammation, driven by dysregulated microglial polarization, is a hallmark of Alzheimer’s disease (AD). Recently, the triggering receptor expressed on myeloid cells 2 (TREM2), a key regulator of microglial function, has emerged as a promising therapeutic target for AD. This study aimed to investigate the therapeutic potential and mechanism of action of the natural compound β-asarone in AD models. Our results demonstrate that β-asarone significantly improved cognitive function, reduced hippocampal neuronal damage, and decreased both Aβ deposition and Tau hyperphosphorylation in 3×Tg-AD mice. Mechanistically, β-asarone upregulated TREM2 expression, activated the PI3K/AKT pathway, and inhibited GSK3β activity, thereby promoting the polarization of microglia from the pro-inflammatory M1 phenotype toward the anti-inflammatory M2 phenotype and alleviating neuroinflammation. This study is the first to elucidate that β-asarone ameliorates AD pathology by modulating microglial polarization via the TREM2/PI3K/AKT/GSK3β signaling axis, providing experimental evidence supporting its potential as an immunomodulatory therapeutic agent for AD.

Graphical Abstract