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Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • Alzheimer's disease (AD) involves amyloid-beta (Aβ) plaques and tau pathology.
  • TREM2 gene variants are associated with AD risk, affecting microglial responses.
  • The role of TREM2 in microglial function regarding tau pathology is not fully understood.

Purpose of the Study:

  • To investigate the role of TREM2 and microglial function in the seeding and spreading of tau pathology in Alzheimer's disease models.
  • To determine if microglial depletion and repopulation affect Aβ-driven tau propagation.

Main Methods:

  • Utilized TREM2 knockout (TREM2KO) mouse models and microglial ablation/repopulation strategies.
  • Assessed tau seeding and spreading in the presence and absence of microglia and TREM2.
  • Analyzed disease-associated microglia (DAM) gene expression.

Main Results:

  • Both TREM2 deficiency and microglial ablation significantly enhanced tau seeding and spreading around Aβ plaques.
  • Microglial repopulation around plaques did not restore protective functions; instead, it showed reduced DAM gene expression and increased tau pathology.
  • TREM2-dependent activation of the DAM phenotype is critical for mitigating Aβ-induced tau propagation.

Conclusions:

  • TREM2-dependent microglial activation, specifically the DAM phenotype, is essential for delaying the pathological spread of tau aggregates in Alzheimer's disease.
  • Loss of TREM2 function or microglial dysfunction exacerbates tau seeding and spreading, highlighting the protective role of activated microglia.