TY  - JOUR
AU  - Kedia, Shreeya
AU  - Ji, Hao
AU  - Feng, Ruoqing
AU  - Androvic, Peter
AU  - Spieth, Lena
AU  - Liu, Lu
AU  - Franz, Jonas
AU  - Zdiarstek, Hanna
AU  - Anderson, Katrin Perez
AU  - Kaboglu, Cem Busra
AU  - Liu, Qian
AU  - Mattugini, Nicola
AU  - Cherif, Fatma
AU  - Prtvar, Danilo
AU  - Cantuti-Castelvetri, Ludovico
AU  - Liesz, Arthur
AU  - Schifferer, Martina
AU  - Stadelmann, Christine
AU  - Tahirovic, Sabina
AU  - Gokce, Ozgun
AU  - Simons, Mikael
TI  - T cell-mediated microglial activation triggers myelin pathology in a mouse model of amyloidosis.
JO  - Nature neuroscience
VL  - 27
IS  - 8
SN  - 1097-6256
CY  - New York, NY
PB  - Nature America
M1  - DZNE-2024-01002
SP  - 1468 - 1474
PY  - 2024
AB  - 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.
KW  - Animals
KW  - Microglia: pathology
KW  - Microglia: metabolism
KW  - Microglia: immunology
KW  - Myelin Sheath: pathology
KW  - Myelin Sheath: metabolism
KW  - Mice
KW  - Disease Models, Animal
KW  - Amyloidosis: pathology
KW  - Alzheimer Disease: pathology
KW  - Alzheimer Disease: metabolism
KW  - Alzheimer Disease: immunology
KW  - CD8-Positive T-Lymphocytes: immunology
KW  - Mice, Transgenic
KW  - Oligodendroglia: pathology
KW  - Oligodendroglia: metabolism
KW  - Mice, Inbred C57BL
LB  - PUB:(DE-HGF)16
C2  - pmc:PMC11303250
C6  - pmid:38937583
DO  - DOI:10.1038/s41593-024-01682-8
UR  - https://pub.dzne.de/record/271134
ER  -