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Basic Science and Pathogenesis.

Evan J Messenger1, Sydney Baar1, Logan M Bedford1

  • 1Indiana University School of Medicine, Indianapolis, IN, USA.

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Summary
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Phospholipase C gamma 2 (PLCG2) is crucial for Alzheimer's disease (AD) innate immunity and TREM2 signaling. Its deficiency impacts microglial response and amyloid pathology, revealing distinct pathways from TREM2 deficiency.

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Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • Genes linked to Alzheimer's disease (AD) risk are often expressed in microglia and influence innate immunity.
  • Phospholipase C gamma 2 (PLCG2) is a key mediator of microglial transmembrane signaling, downstream of receptors like TREM2.
  • Genetic variants in PLCG2 have been shown to modify AD risk.

Purpose of the Study:

  • To investigate the mechanisms by which PLCG2 influences AD pathology and microglial function.
  • To understand the interplay between PLCG2 and TREM2 signaling in the context of AD.

Main Methods:

  • Utilized the 5xFAD murine model of AD to study the effects of PLCG2 ablation on amyloid pathology and microglial response.
  • Examined the functional and transcriptomic consequences of TREM2 deficiency to dissect PLCG2's role in TREM2 signaling.
  • Performed transcriptomic analysis (RNA-Seq) and immunohistochemistry on knockout mouse models.

Main Results:

  • PLCG2 deficiency reduced TREM2 expression, while TREM2 deficiency did not affect PLCG2, suggesting PLCG2's role in TREM2 induction.
  • Both PLCG2 and TREM2 knockout in 5xFAD mice increased LAMP1 area per plaque, indicating heightened plaque neurotoxicity.
  • Transcriptomic analysis revealed overlapping immune response pathways but distinct transcriptional profiles between PLCG2 and TREM2 knockouts, particularly in cell migration and adhesion.

Conclusions:

  • PLCG2 plays a significant role in the innate immune response to amyloid pathology and TREM2 signaling in AD.
  • The study identifies key pathways influenced by PLCG2 that are critical for microglial function in AD pathogenesis.