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Inflammasomes in Alzheimer's Progression: Nrf2 as a Preventive Target

Rubén López-Hernández1, María Magdalena de la Torre-Álamo2, Belén García-Bueno2

  • 1Molecular Inflammation Group, Pathophysiology of the Inflammation and Oxidative Stress Lab, Biomedical Research Institute of Murcia (IMIB), University Clinical Hospital Virgen de la Arrixaca, 30120 Murcia, Spain.

Antioxidants (Basel, Switzerland)
|February 26, 2025
PubMed

Insights

Alzheimer's disease involves inflammasomes like NLRP3, activated by amyloid plaques and Tau tangles. Targeting NLRP3 and promoting Nrf2 offers a strategy to reduce neuroinflammation and combat Alzheimer's pathology.

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Alzheimer's disease (AD) is characterized by amyloid plaques (Aβ1-42) and Tau tangles, leading to neuronal loss.
  • Neuroinflammation, driven by microglial activation and inflammatory mediators, significantly contributes to AD progression.
  • Inflammasomes, especially NLRP3, are increasingly recognized for their role in AD pathogenesis, promoting cytokine release and pyroptosis.

Purpose of the Study:

  • To review current understanding of inflammasome involvement in Alzheimer's disease.
  • To explore therapeutic strategies targeting neuroinflammation in AD.
  • To highlight the potential of Nrf2 as a therapeutic target for AD.

Main Methods:

  • Literature review of studies on Alzheimer's disease, neuroinflammation, inflammasomes (NLRP3, ASC), and Nrf2.
  • Analysis of mechanisms linking Aβ1-42 and Tau pathology to inflammasome activation.
  • Examination of autophagic clearance defects in relation to inflammasome accumulation.

Main Results:

  • Aβ1-42 and hyperphosphorylated Tau activate NLRP3 inflammasomes, exacerbating neuroinflammation.
  • ASC speck formation accelerates Aβ aggregation and sustains inflammation.
  • Defective autophagic clearance of inflammasomes contributes to chronic inflammation in AD.

Conclusions:

  • Inhibiting NLRP3 inflammasome activation and promoting ASC speck degradation are potential therapeutic avenues for AD.
  • The transcription factor Nrf2 shows promise for AD treatment due to its anti-inflammatory and antioxidant properties.
  • Targeting inflammasome-driven neuroinflammation via Nrf2 modulation could offer a novel therapeutic strategy for Alzheimer's disease.
Keywords:
ASCAlzheimer’sAβ proteinsNrf2inflammasome NLRP3inflammation

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