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<p>Neuroinflammation is increasingly recognized as a key feature in the development of Alzheimer’s disease (AD), with tumor necrosis factor-alpha (TNF-α) playing a crucial role in initiating inflammatory responses. Continuous activation of TNF-α leads to synaptic dysfunction, neuronal loss, and worsening of amyloid and tau pathology. Specifically, the upregulation of the pro-inflammatory cytokine TNF-α in the brain activates its receptors (TNFR1 &amp; TNFR2). Targeting TNF-α through selective inhibition presents a promising therapeutic strategy for regulating neuroinflammatory responses without compromising systemic immunity. This review discusses current insights into TNF-α signaling in AD progression and examines the effectiveness of selective TNF-α inhibitors in preclinical and clinical studies. We also highlighted specific TNF-α inhibitors, including small molecules and gene therapy approaches, for chronic inflammatory conditions and discussed the limitations and future directions of the current review. Targeted TNF-α inhibition could serve as a novel, disease-modifying treatment for AD, especially when combined with multi-targeted approaches addressing amyloid burden, tau pathology, oxidative stress, and neuroinflammation.</p>

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Selective Inhibition of Tumor Necrosis Factor for Attenuating Alzheimer’s Disease: Strategies Targeting Neuroinflammation

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月14日

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  • Janakiraman Pillai Udaiyappan,
  • Rengasamy Balakrishnan,
  • Manivasagam Muthukumaran Tamilarasan,
  • Balamuralikrishnan Balasubramanian,
  • Kasim Sakran Abass

摘要

Neuroinflammation is increasingly recognized as a key feature in the development of Alzheimer’s disease (AD), with tumor necrosis factor-alpha (TNF-α) playing a crucial role in initiating inflammatory responses. Continuous activation of TNF-α leads to synaptic dysfunction, neuronal loss, and worsening of amyloid and tau pathology. Specifically, the upregulation of the pro-inflammatory cytokine TNF-α in the brain activates its receptors (TNFR1 & TNFR2). Targeting TNF-α through selective inhibition presents a promising therapeutic strategy for regulating neuroinflammatory responses without compromising systemic immunity. This review discusses current insights into TNF-α signaling in AD progression and examines the effectiveness of selective TNF-α inhibitors in preclinical and clinical studies. We also highlighted specific TNF-α inhibitors, including small molecules and gene therapy approaches, for chronic inflammatory conditions and discussed the limitations and future directions of the current review. Targeted TNF-α inhibition could serve as a novel, disease-modifying treatment for AD, especially when combined with multi-targeted approaches addressing amyloid burden, tau pathology, oxidative stress, and neuroinflammation.