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dc.contributor.authorHughes, Craig
dc.contributor.authorChoi, Minee L.
dc.contributor.authorYi, Jee-Hyun
dc.contributor.authorKim, Seung-Chan
dc.contributor.authorDrews, Anna
dc.contributor.authorGeorge-Hyslop, Peter St.
dc.contributor.authorBryant, Clare
dc.contributor.authorGandhi, Sonia
dc.contributor.authorCho, Kwangwook
dc.contributor.authorKlenerman, David
dc.date.accessioned2021-02-17T16:39:07Z
dc.date.available2021-02-17T16:39:07Z
dc.date.issued2020-02-18
dc.date.submitted2019-06-12
dc.identifier.others42003-020-0792-9
dc.identifier.other792
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/317794
dc.descriptionFunder: Alzheimer's Research UK (ARUK); doi: https://doi.org/10.13039/501100002283
dc.description.abstractAbstract: The molecular events causing memory loss and neuronal cell death in Alzheimer’s disease (AD) over time are still unknown. Here we found that picomolar concentrations of soluble oligomers of synthetic beta amyloid (Aβ42) aggregates incubated with BV2 cells or rat astrocytes caused a sensitised response of Toll-like receptor 4 (TLR4) with time, leading to increased production of TNF-α. Aβ aggregates caused long term potentiation (LTP) deficit in hippocampal slices and predominantly neuronal cell death in co-cultures of astrocytes and neurons, which was blocked by TLR4 antagonists. Soluble Aβ aggregates cause LTP deficit and neuronal death via an autocrine/paracrine mechanism due to TLR4 signalling. These findings suggest that the TLR4-mediated inflammatory response may be a key pathophysiological process in AD.
dc.languageen
dc.publisherNature Publishing Group UK
dc.rightsAttribution 4.0 International (CC BY 4.0)en
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/en
dc.subjectArticle
dc.subject/631/250/371
dc.subject/692/617/375/365/1283
dc.subject/13/21
dc.subject/96/63
dc.subject/9
dc.subjectarticle
dc.titleBeta amyloid aggregates induce sensitised TLR4 signalling causing long-term potentiation deficit and rat neuronal cell death
dc.typeArticle
dc.date.updated2021-02-17T16:39:06Z
prism.issueIdentifier1
prism.publicationNameCommunications Biology
prism.volume3
dc.identifier.doi10.17863/CAM.64909
dcterms.dateAccepted2020-01-24
rioxxterms.versionofrecord10.1038/s42003-020-0792-9
rioxxterms.versionVoR
rioxxterms.licenseref.urihttp://creativecommons.org/licenses/by/4.0/
dc.contributor.orcidGeorge-Hyslop, Peter St. [0000-0003-0796-7209]
dc.contributor.orcidBryant, Clare [0000-0002-2924-0038]
dc.identifier.eissn2399-3642


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Attribution 4.0 International (CC BY 4.0)
Except where otherwise noted, this item's licence is described as Attribution 4.0 International (CC BY 4.0)