TREM2 function impedes tau seeding in neuritic plaques

Variants in the triggering receptor expressed on myeloid cells 2 (TREM2) have been associated with increased risk for sporadic, late-onset Alzheimer’s disease (AD). Here we show that germline knockout of Trem2 or the TREM2(R47H) variant reduce microgliosis around amyloid-β (Aβ) plaques and facilitat...

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Detalles Bibliográficos
Autores principales: Leyns, Cheryl E.G., Gratuze, Maud, Narasimhan, Sneha, Jain, Nimansha, Koscal, Lauren J., Jiang, Hong, Manis, Melissa, Colonna, Marco, Lee, Virginia M.Y., Ulrich, Jason D., Holtzman, David M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2019
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6660358/
https://www.ncbi.nlm.nih.gov/pubmed/31235932
http://dx.doi.org/10.1038/s41593-019-0433-0
Descripción
Sumario:Variants in the triggering receptor expressed on myeloid cells 2 (TREM2) have been associated with increased risk for sporadic, late-onset Alzheimer’s disease (AD). Here we show that germline knockout of Trem2 or the TREM2(R47H) variant reduce microgliosis around amyloid-β (Aβ) plaques and facilitate the seeding and spreading of neuritic plaque (NP) tau aggregates. These findings demonstrate a key role for TREM2 and microglia in limiting development of peri-plaque tau pathologies.

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