Cited time in webofscience Cited time in scopus

Full metadata record

DC Field Value Language
dc.contributor.author Nam, Hyeri -
dc.contributor.author Lee, Younghwan -
dc.contributor.author Kim, Boil -
dc.contributor.author Lee, Ji-Won -
dc.contributor.author Hwang, Seohyeon -
dc.contributor.author An, Hyun-Kyu -
dc.contributor.author Chung, Kyung Min -
dc.contributor.author Park, Youngjin -
dc.contributor.author Hong, Jihyun -
dc.contributor.author Kim, Kyungjin -
dc.contributor.author Kim, Eun-Kyoung -
dc.contributor.author Choe, Han Kyoung -
dc.contributor.author Yu, Seong-Woon -
dc.date.accessioned 2022-10-26T08:00:07Z -
dc.date.available 2022-10-26T08:00:07Z -
dc.date.created 2022-06-16 -
dc.date.issued 2022-04 -
dc.identifier.issn 2041-1723 -
dc.identifier.uri http://hdl.handle.net/20.500.11750/16935 -
dc.description.abstract Hyperimmunity is associated with Alzheimer disease. Here the authors show that the Presenilin 2 N141I mutation causes overproduction of clock-controlled cytokines and memory deficits through suppression of REV-ERB alpha gene by hypermethylation. Hyperimmunity drives the development of Alzheimer disease (AD). The immune system is under the circadian control, and circadian abnormalities aggravate AD progress. Here, we investigate how an AD-linked mutation deregulates expression of circadian genes and induces cognitive decline using the knock-in (KI) mice heterozygous for presenilin 2 N141I mutation. This mutation causes selective overproduction of clock gene-controlled cytokines through the DNA hypermethylation-mediated repression of REV-ERB alpha in innate immune cells. The KI/+ mice are vulnerable to otherwise innocuous, mild immune challenges. The antipsychotic chlorpromazine restores the REV-ERB alpha level by normalizing DNA methylation through the inhibition of PI3K/AKT1 pathway, and prevents the overexcitation of innate immune cells and cognitive decline in KI/+ mice. These results highlight a pathogenic link between this AD mutation and immune cell overactivation through the epigenetic suppression of REV-ERB alpha. -
dc.language English -
dc.publisher Nature Publishing Group -
dc.title Presenilin 2 N141I mutation induces hyperactive immune response through the epigenetic repression of REV-ERB alpha -
dc.type Article -
dc.identifier.doi 10.1038/s41467-022-29653-2 -
dc.identifier.wosid 000783759500004 -
dc.identifier.scopusid 2-s2.0-85128276917 -
dc.identifier.bibliographicCitation Nature Communications, v.13, no.1 -
dc.description.isOpenAccess TRUE -
dc.subject.keywordPlus GLYCOGEN-SYNTHASE KINASE-3 -
dc.subject.keywordPlus ALZHEIMERS-DISEASE -
dc.subject.keywordPlus INFLAMMATORY RESPONSES -
dc.subject.keywordPlus AMYLOID HYPOTHESIS -
dc.subject.keywordPlus DNA METHYLATION -
dc.subject.keywordPlus HOST RESPONSE -
dc.subject.keywordPlus CLOCK -
dc.subject.keywordPlus CHLORPROMAZINE -
dc.subject.keywordPlus DYNAMICS -
dc.subject.keywordPlus SLEEP -
dc.citation.number 1 -
dc.citation.title Nature Communications -
dc.citation.volume 13 -
dc.description.journalRegisteredClass scie -
dc.description.journalRegisteredClass scopus -
dc.relation.journalResearchArea Science & Technology - Other Topics -
dc.relation.journalWebOfScienceCategory Multidisciplinary Sciences -
dc.type.docType Article -

qrcode

  • twitter
  • facebook
  • mendeley

Items in Repository are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE