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Amyloid-beta impairs TOM1-mediated IL-1R1 signaling.

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dc.contributor.authorMartini, Alessandra Cadete
dc.contributor.authorGomez-Arboledas, Angela
dc.contributor.authorForner, Stefania
dc.contributor.authorRodriguez-Ortiz, Carlos J
dc.contributor.authorMcQuade, Amanda
dc.contributor.authorDanhash, Emma
dc.contributor.authorPhan, Jimmy
dc.contributor.authorJavonillo, Dominic
dc.contributor.authorHa, Jordan-Vu
dc.contributor.authorTram, Melanie
dc.contributor.authorTrujillo-Estrada, Laura
dc.contributor.authorda Cunha, Celia
dc.contributor.authorAger, Rahasson R
dc.contributor.authorDavila, Jose C
dc.contributor.authorKitazawa, Masashi
dc.contributor.authorBlurton-Jones, Mathew
dc.contributor.authorGutierrez, Antonia
dc.contributor.authorBaglietto-Vargas, David
dc.contributor.authorMedeiros, Rodrigo
dc.contributor.authorLaFerla, Frank M
dc.date.accessioned2024-02-10T20:02:13Z
dc.date.available2024-02-10T20:02:13Z
dc.date.issued2019-09-30
dc.descriptionCorrection for Cadete Martini et al., Amyloid-beta impairs TOM1-mediated IL-1R1 signaling. Proc Natl Acad Sci USA. 2019 Nov 19;116(47):23860. doi: 10.1073/pnas.1918411116. PMID: 31740603
dc.description.abstractDefects in interleukin-1β (IL-1β)-mediated cellular responses contribute to Alzheimer's disease (AD). To decipher the mechanism associated with its pathogenesis, we investigated the molecular events associated with the termination of IL-1β inflammatory responses by focusing on the role played by the target of Myb1 (TOM1), a negative regulator of the interleukin-1β receptor-1 (IL-1R1). We first show that TOM1 steady-state levels are reduced in human AD hippocampi and in the brain of an AD mouse model versus respective controls. Experimentally reducing TOM1 affected microglia activity, substantially increased amyloid-beta levels, and impaired cognition, whereas enhancing its levels was therapeutic. These data show that reparation of the TOM1-signaling pathway represents a therapeutic target for brain inflammatory disorders such as AD. A better understanding of the age-related changes in the immune system will allow us to craft therapies to limit detrimental aspects of inflammation, with the broader purpose of sharply reducing the number of people afflicted by AD.
dc.format.number42es_ES
dc.format.page21198-21206es_ES
dc.format.volume116es_ES
dc.identifier.doi10.1073/pnas.1914088116
dc.identifier.e-issn1091-6490es_ES
dc.identifier.journalProceedings of the National Academy of Sciences of the United States of Americaes_ES
dc.identifier.otherhttp://hdl.handle.net/10668/14569
dc.identifier.pubmedID31570577es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/17915
dc.language.isoeng
dc.rights.accessRightsopen accesses_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subject3xTg-AD
dc.subjectAlzheimer’s disease
dc.subjectIL-1R1
dc.subjectTOM1
dc.subjectTarget of Myb1
dc.titleAmyloid-beta impairs TOM1-mediated IL-1R1 signaling.
dc.typeresearch article
dc.type.hasVersionVoR
dspace.entity.typePublication
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