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<p>Ageing has been recognized as the leading risk factor for Alzheimer’s disease (AD), with an intricate interplay of oxidative stress, neuroinflammation, and cellular senescence implicated in its pathogenesis. Mitochondrial dysfunction has been linked to redox imbalance and excessive production of reactive oxygen species (ROS), which disrupt homeostasis and damage both mitochondrial and nuclear DNA, thereby promoting amyloid-β accumulation and cognitive decline. Chronic activation of inflammasome signaling in microglia and astrocytes, characterized by the upregulation of NLRP3 and NF-κB, has been linked to the establishment of a neuroinflammatory environment, leading to synaptic loss and exacerbating tau pathology. Additionally, the accumulation of senescent glial and neuronal cells has been shown to drive the senescence-associated secretory phenotype (SASP), further amplifying inflammation and oxidative damage. Promising therapeutic interventions, including mitochondria-targeted antioxidants and senolytics, have been evaluated; however, translational challenges persist, such as the heterogeneity of biomarker measures and the insufficient delivery of antioxidants. A proposed roadmap emphasizes the importance of monitoring oxidative and inflammatory biomarkers, implementing combinatorial therapies, and personalizing interventions to enhance resilience in the ageing brain and delay the onset of AD.</p>

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Interplay of oxidative stress and neuroinflammation in alzheimer’s: insights into age-driven pathogenesis

  • 期刊论文

  • 发表日期：

    2026年3月10日

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  • Sayed Mohammad Firdous,
  • Shibam Chakrabortty,
  • Vaishali R. Undale,
  • Shouvik Mallik,
  • Mostafa Gouda

摘要

Ageing has been recognized as the leading risk factor for Alzheimer’s disease (AD), with an intricate interplay of oxidative stress, neuroinflammation, and cellular senescence implicated in its pathogenesis. Mitochondrial dysfunction has been linked to redox imbalance and excessive production of reactive oxygen species (ROS), which disrupt homeostasis and damage both mitochondrial and nuclear DNA, thereby promoting amyloid-β accumulation and cognitive decline. Chronic activation of inflammasome signaling in microglia and astrocytes, characterized by the upregulation of NLRP3 and NF-κB, has been linked to the establishment of a neuroinflammatory environment, leading to synaptic loss and exacerbating tau pathology. Additionally, the accumulation of senescent glial and neuronal cells has been shown to drive the senescence-associated secretory phenotype (SASP), further amplifying inflammation and oxidative damage. Promising therapeutic interventions, including mitochondria-targeted antioxidants and senolytics, have been evaluated; however, translational challenges persist, such as the heterogeneity of biomarker measures and the insufficient delivery of antioxidants. A proposed roadmap emphasizes the importance of monitoring oxidative and inflammatory biomarkers, implementing combinatorial therapies, and personalizing interventions to enhance resilience in the ageing brain and delay the onset of AD.