Show simple item record

dc.contributor.authorMak, Elijahen
dc.contributor.authorPadilla, Concepcionen
dc.contributor.authorAnnus, Tiinaen
dc.contributor.authorWilson, Liam Ren
dc.contributor.authorHong, Youngen
dc.contributor.authorFryer, Timothyen
dc.contributor.authorColes, Jonathanen
dc.contributor.authorAigbirhio, Franklinen
dc.contributor.authorMenon, Daviden
dc.contributor.authorNestor, Peter Jen
dc.contributor.authorZaman, Shahiden
dc.contributor.authorHolland, Anthonyen
dc.date.accessioned2019-03-08T00:30:37Z
dc.date.available2019-03-08T00:30:37Z
dc.date.issued2019-08en
dc.identifier.issn0197-4580
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/290323
dc.description.abstractABSTRACT OBJECTIVE: Older adults with Down Syndrome (DS) often have Alzheimer’s disease (AD) neuropathologies. While PET imaging studies of amyloid deposition (Aβ) have been associated with worse clinical prognosis and cognitive impairment, their relationships with cortical thickness remain unclear in people with DS. METHODS: In a sample of 44 DS adults who underwent cognitive assessments, [11C]-PiB PET and T1-MPRAGE, we used mixed effect models to evaluate the spatial relationships between Aβ binding with patterns of cortical thickness. Partial Spearman correlations were used to delineate the topography of local Aβ-associated cortical thinning. RESULTS: [11C]-PiB BPND was negatively associated with decreased cortical thickness. Locally, regional [11C]-PiB retention was negatively correlated with cortical thickness in widespread cortices, predominantly in temporo-parietal regions. CONCLUSION: Contrary to the prevailing evidence in established AD, we propose that our findings implicate Aβ in spatial patterns of atrophy that recapitulated the “cortical signature” of neurodegeneration in AD, conferring support to recent recommendations for earlier disease- interventions.
dc.description.sponsorshipAlzheimer's Research UK Health Foundation CLARE
dc.format.mediumPrint-Electronicen
dc.languageengen
dc.publisherElsevier BV
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectCerebral Cortexen
dc.subjectHumansen
dc.subjectDown Syndromeen
dc.subjectAtrophyen
dc.subjectPositron-Emission Tomographyen
dc.subjectDiffusion Magnetic Resonance Imagingen
dc.subjectAdulten
dc.subjectAgeden
dc.subjectMiddle Ageden
dc.subjectFemaleen
dc.subjectMaleen
dc.subjectAmyloid beta-Peptidesen
dc.subjectAmyloidogenic Proteinsen
dc.titleDelineating the topography of amyloid-associated cortical atrophy in Down syndrome.en
dc.typeArticle
prism.endingPage202
prism.publicationDate2019en
prism.publicationNameNeurobiology of agingen
prism.startingPage196
prism.volume80en
dc.identifier.doi10.17863/CAM.37553
dcterms.dateAccepted2019-02-25en
rioxxterms.versionofrecord10.1016/j.neurobiolaging.2019.02.018en
rioxxterms.versionAM
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2019-08en
dc.contributor.orcidMak, Elijah [0000-0002-6437-8024]
dc.contributor.orcidColes, Jonathan [0000-0003-4013-679X]
dc.contributor.orcidAigbirhio, Franklin [0000-0001-9453-5257]
dc.contributor.orcidMenon, David [0000-0002-3228-9692]
dc.contributor.orcidZaman, Shahid [0000-0003-1639-6014]
dc.contributor.orcidHolland, Anthony [0000-0003-4107-130X]
dc.identifier.eissn1558-1497
rioxxterms.typeJournal Article/Reviewen
pubs.funder-project-idMRC (G1002252)
pubs.funder-project-idMRC (G0900903)
cam.orpheus.successThu Jan 30 10:49:17 GMT 2020 - Embargo updated*
rioxxterms.freetoread.startdate2020-08-31


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record

Attribution-NonCommercial-NoDerivatives 4.0 International
Except where otherwise noted, this item's licence is described as Attribution-NonCommercial-NoDerivatives 4.0 International