%0 Journal Article
%A Kedia, Shreeya
%A Ji, Hao
%A Feng, Ruoqing
%A Androvic, Peter
%A Spieth, Lena
%A Liu, Lu
%A Franz, Jonas
%A Zdiarstek, Hanna
%A Anderson, Katrin Perez
%A Kaboglu, Cem Busra
%A Liu, Qian
%A Mattugini, Nicola
%A Cherif, Fatma
%A Prtvar, Danilo
%A Cantuti-Castelvetri, Ludovico
%A Liesz, Arthur
%A Schifferer, Martina
%A Stadelmann, Christine
%A Tahirovic, Sabina
%A Gokce, Ozgun
%A Simons, Mikael
%T T cell-mediated microglial activation triggers myelin pathology in a mouse model of amyloidosis.
%J Nature neuroscience
%V 27
%N 8
%@ 1097-6256
%C New York, NY
%I Nature America
%M DZNE-2024-01002
%P 1468 - 1474
%D 2024
%X Age-related myelin damage induces inflammatory responses, yet its involvement in Alzheimer's disease remains uncertain, despite age being a major risk factor. Using a mouse model of Alzheimer's disease, we found that amyloidosis itself triggers age-related oligodendrocyte and myelin damage. Mechanistically, CD8+ T cells promote the progressive accumulation of abnormally interferon-activated microglia that display myelin-damaging activity. Thus, our data suggest that immune responses against myelinating oligodendrocytes may contribute to neurodegenerative diseases with amyloidosis.
%K Animals
%K Microglia: pathology
%K Microglia: metabolism
%K Microglia: immunology
%K Myelin Sheath: pathology
%K Myelin Sheath: metabolism
%K Mice
%K Disease Models, Animal
%K Amyloidosis: pathology
%K Alzheimer Disease: pathology
%K Alzheimer Disease: metabolism
%K Alzheimer Disease: immunology
%K CD8-Positive T-Lymphocytes: immunology
%K Mice, Transgenic
%K Oligodendroglia: pathology
%K Oligodendroglia: metabolism
%K Mice, Inbred C57BL
%F PUB:(DE-HGF)16
%9 Journal Article
%2 pmc:PMC11303250
%$ pmid:38937583
%R 10.1038/s41593-024-01682-8
%U https://pub.dzne.de/record/271134