Association between soluble TREM2, APOE genotype, Alzheimer's copathology and disease evolution in dementia with Lewy bodies

APOEε4 carriage attenuates the TREM2-dependent microglial response in prodromal DLB, as reflected by lower CSF cTREM2 levels. Elevated cTREM2 levels in the prodromal phase are associated with slower cognitive decline, suggesting a protective role of microglial activation during early disease stages. These findings suggest an early modulation of TREM2-driven microglial response by APOEε4 which influences DLB progression.

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Publication Details

Journal
Alzheimer s & Dementia
Published
2025-12-01
DOI
https://doi.org/10.1002/alz70855_102529
Primary Topic
Neuroinflammation and Neurodegeneration Mechanisms
Type
article
Field-Weighted Citation Impact
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article

Association between soluble TREM2, APOE genotype, Alzheimer's copathology and disease evolution in dementia with Lewy bodies

Estrella Morenas‐Rodríguez, Adolfo Gómez‐Grande, Alexandre Bejanin, Juan M. Fortea et al.
Alzheimer s & Dementia
Neuroinflammation and Neurodegeneration Mechanisms
article

Association between soluble TREM2, APOE genotype, Alzheimer's copathology and disease evolution in dementia with Lewy bodies

Estrella Morenas‐Rodríguez, Adolfo Gómez‐Grande, Alexandre Bejanin, Juan M. Fortea, Christian Haass, Daniel Alcolea, Alberto Lleó, Isabel Sala, Valle Camacho, Lídia Vaqué‐Alcázar, Elena Vera, Álex Fernández‐León, Íñigo Rodríguez‐Baz, Pablo Zaragoza‐Ballester, Briggitte Nuscher
article en

Abstract

APOEε4 carriage attenuates the TREM2-dependent microglial response in prodromal DLB, as reflected by lower CSF cTREM2 levels. Elevated cTREM2 levels in the prodromal phase are associated with slower cognitive decline, suggesting a protective role of microglial activation during early disease stages. These findings suggest an early modulation of TREM2-driven microglial response by APOEε4 which influences DLB progression.

Alzheimer s & DementiaVol. 21(S1)
Universidad Complutense de Madrid (ES), Universitat Autònoma de Barcelona (ES), Instituto de Salud Carlos III (ES), German Center for Neurodegenerative Diseases (DE), Hospital de Sant Pau (ES), Research Institute Hospital 12 de Octubre (ES), Biomedical Research Networking Center on Neurodegenerative Diseases (ES), Hospital Universitario 12 De Octubre (ES), Munich Cluster for Systems Neurology (DE), Fundació Catalana per a la Recerca i la Innovació (ES), Ludwig-Maximilians-Universität München (DE)
Openalex Percentile: Top 39%
Neuroinflammation and Neurodegeneration Mechanisms
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