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Alzheimer's disease involves brain inflammation. Activated microglia release ASC specks, promoting amyloid-beta aggregation and pathology spread, which can be inhibited.

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Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Alzheimer's disease (AD) is characterized by amyloid beta and tau pathology.
  • Emerging evidence highlights innate immune pathway activation as a critical factor in AD progression.

Purpose of the Study:

  • To investigate the role of microglia-mediated immune responses in Alzheimer's disease pathogenesis.
  • To explore the mechanism of ASC speck-induced pathology seeding and potential inhibition strategies.

Main Methods:

  • Utilized in vivo two-photon imaging and in vitro live imaging.
  • Performed biochemical analysis of protein-protein interactions.

Main Results:

  • Microglia activation by aggregated proteins or nucleic acids leads to inflammatory mediator release.
  • Sustained NLRP3 inflammasome activation causes pyroptosis and ASC speck release.
  • ASC specks enhance beta-amyloid aggregation, contributing to pathology spread.

Conclusions:

  • The described mechanism explains pathology propagation within and between brain regions.
  • Evidence for in vivo and in vitro ASC speck-induced seeding will be presented.
  • Inhibitory effects of biologicals and pharmacological agents will be demonstrated.