ORCID: https://orcid.org/0000-0002-6233-0705; Franz, Jonas
ORCID: https://orcid.org/0000-0001-7523-6622; Zdiarstek, Hanna
ORCID: https://orcid.org/0009-0009-1341-3107; Anderson, Katrin Perez; Kaboglu, Cem
ORCID: https://orcid.org/0000-0002-7887-1602; Liu, Qian; Mattugini, Nicola; Cherif, Fatma; Prtvar, Danilo
ORCID: https://orcid.org/0009-0004-8251-1441; Cantuti-Castelvetri, Ludovico
ORCID: https://orcid.org/0000-0002-0642-1610; Liesz, Arthur
ORCID: https://orcid.org/0000-0002-9069-2594; Schifferer, Martina
ORCID: https://orcid.org/0000-0002-0500-8218; Stadelmann, Christine
ORCID: https://orcid.org/0000-0003-1766-5458; Tahirovic, Sabina
ORCID: https://orcid.org/0000-0003-4403-9559; Gokce, Ozgun
ORCID: https://orcid.org/0000-0001-6319-404X und Simons, Mikael
ORCID: https://orcid.org/0000-0001-5329-192X
(2024):
T cell-mediated microglial activation triggers myelin pathology in a mouse model of amyloidosis.
In: Nature Neuroscience, Bd. 27, Nr. 8: S. 1468-1474
[PDF, 21MB]

Abstract
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.
Dokumententyp: | Zeitschriftenartikel |
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Fakultät: | Medizin > Adolf-Butenandt-Institut
Medizin > Munich Cluster for Systems Neurology (SyNergy) Medizin > Institut für Schlaganfall- und Demenzforschung (ISD) |
Themengebiete: | 600 Technik, Medizin, angewandte Wissenschaften > 610 Medizin und Gesundheit |
URN: | urn:nbn:de:bvb:19-epub-122905-5 |
ISSN: | 1097-6256 |
Sprache: | Englisch |
Dokumenten ID: | 122905 |
Datum der Veröffentlichung auf Open Access LMU: | 06. Dez. 2024 07:09 |
Letzte Änderungen: | 06. Dez. 2024 07:09 |
DFG: | Gefördert durch die Deutsche Forschungsgemeinschaft (DFG) - 390857198 |