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<p>Neuroinflammation and tau aggregation are hallmarks of tauopathies. Microglial NLRP3 inflammasome activation, initiated by tau, is a key mediator in these diseases, resulting in the release of pro-inflammatory IL-1β and neuronal damage. However, microglia can also present with other disease-associated states such as cellular senescence, which can be driven by tau. Senescent microglia are characterized by a sustained cytokine release, exacerbating disease progression.</p>

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Wie Tau die Reaktionen von Mikroglia in Tauopathien beeinflusst

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月4日

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  • Jana Caroline Hollenbeck,
  • Christina Ising

摘要

Neuroinflammation and tau aggregation are hallmarks of tauopathies. Microglial NLRP3 inflammasome activation, initiated by tau, is a key mediator in these diseases, resulting in the release of pro-inflammatory IL-1β and neuronal damage. However, microglia can also present with other disease-associated states such as cellular senescence, which can be driven by tau. Senescent microglia are characterized by a sustained cytokine release, exacerbating disease progression.