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Basic Science and Pathogenesis.

Pablo Zaragoza-Ballester1,2,3, Briggitte Nuscher4,5, Daniel Alcolea6,7

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APOEε4 carriage lowers TREM2 response in early dementia with Lewy bodies (DLB), but higher TREM2 levels in prodromal DLB correlate with slower cognitive decline, indicating a protective role for microglial activation.

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Area of Science:

  • Neuroscience
  • Genetics
  • Immunology

Background:

  • APOEε4 is a known risk factor for Alzheimer's Disease (AD) and dementia with Lewy bodies (DLB).
  • TREM2-mediated microglial activation is implicated in AD pathogenesis and may interact with APOE.
  • DLB often presents with AD copathology, necessitating investigation into these interactions within DLB.

Purpose of the Study:

  • To investigate the interplay between TREM2 response, APOEε4 carriage, and AD copathology in DLB.
  • To determine how these factors influence the progression of DLB.
  • To examine the role of microglial activation in early-stage DLB.

Main Methods:

  • Measured cerebrospinal fluid (CSF) cleaved soluble TREM2 (cTREM2) in 76 DLB patients (prodromal DLB and DLB-dementia).
  • Assessed APOEε4 carriage and core AD biomarkers (Aβ42, t-tau, p-tau181).
  • Utilized [18F]Florbetapir-PET imaging in a subset of patients and conducted clinical follow-up.

Main Results:

  • APOEε4 carriers showed significantly lower cTREM2 levels in prodromal DLB compared to non-carriers.
  • Lower cTREM2 levels in prodromal DLB were independently associated with APOEε4 carriage.
  • Elevated cTREM2 levels in prodromal DLB correlated with higher AD biomarkers and slower cognitive decline, while this association was absent in DLB-dementia.

Conclusions:

  • APOEε4 carriage attenuates TREM2-dependent microglial response in prodromal DLB.
  • Higher cTREM2 levels in early DLB suggest a protective role for microglial activation.
  • These findings highlight an early modulation of TREM2 response by APOEε4 impacting DLB progression.