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dc.contributor.authorPadilla, Concepcion
dc.contributor.authorMontal, Victor
dc.contributor.authorWalpert, Madeleine J
dc.contributor.authorHong, Young
dc.contributor.authorFryer, Timothy
dc.contributor.authorColes, Jonathan
dc.contributor.authorAigbirhio, Franklin I
dc.contributor.authorHartley, Sigan L
dc.contributor.authorCohen, Ann D
dc.contributor.authorTudorascu, Dana L
dc.contributor.authorChristian, Bradley T
dc.contributor.authorHanden, Benjamin L
dc.contributor.authorKlunk, William E
dc.contributor.authorHolland, Anthony
dc.contributor.authorZaman, Shahid
dc.date.accessioned2022-01-28T00:30:37Z
dc.date.available2022-01-28T00:30:37Z
dc.date.issued2022
dc.identifier.issn2352-8729
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/332969
dc.description.abstractIntroduction: The Down syndrome population has a high prevalence for dementia, often showing their first clinical symptoms in their 40s. Methods: In a longitudinal cohort, we investigate whether amyloid deposition at time point 1 (TP1) could predict cortical thickness change at time point 2 (TP2). The association between tau burden and cortical thickness was also examined at time point 3 (TP3). Results: Between TP1 and TP2 there was pronounced cortical thinning in temporo-parietal cortices and cortical thickening in the frontal cortex. Baseline amyloid burden was strongly associated to cortical thinning progression, especially in the temporo-parietal regions. At TP3, tau deposition negatively correlated with cortical atrophy in regions where tau usually accumulates at later Braak stages. Discussion: A higher amount of amyloid accumulation triggers a cascade of changes of disease-causing processes that eventually lead to dementia. As expected, we found that regions where tau usually accumulates were those also displaying high levels of cortical atrophy.
dc.description.sponsorshipThis research was generously supported by different grants from the Medical Research Council (grant ID number: 98480), the Alzheimer’s Research UK (grant ID number: ARUK-PG2015-23), and the National Institute of Health of the USA (grant ID number: U01AG051406-01 Neurodegeneration in Aging Down Syndrome, NiAD). Additional support came from the NIHR Cambridge Biomedical Research Centre, the NIHR Collaborations in Leadership for Applied Health Research and Care (CLAHRC) for the East of England, the NIHR Cambridge Dementia Biomedical Research Unit, the Down Syndrome Association, and the Health Foundation.
dc.publisherWiley Open Access
dc.rightsAll Rights Reserved
dc.rights.urihttp://www.rioxx.net/licenses/all-rights-reserved
dc.titleCortical atrophy and amyloid and tau deposition in Down syndrome: A longitudinal study.
dc.typeArticle
dc.publisher.departmentDepartment of Medicine
dc.date.updated2022-01-26T16:25:09Z
prism.publicationNameAlzheimers Dement (Amst)
dc.identifier.doi10.17863/CAM.80393
dcterms.dateAccepted2022-01-10
rioxxterms.versionofrecord10.1002/dad2.12288
rioxxterms.versionAM
dc.contributor.orcidPadilla, Concepcion [0000-0003-4102-6787]
dc.contributor.orcidColes, Jonathan [0000-0003-4013-679X]
dc.contributor.orcidHolland, Anthony [0000-0003-4107-130X]
dc.contributor.orcidZaman, Shahid [0000-0003-1639-6014]
dc.identifier.eissn2352-8729
rioxxterms.typeJournal Article/Review
cam.orpheus.successTue Apr 12 08:22:32 BST 2022 - Embargo updated
cam.orpheus.counter4
cam.depositDate2022-01-26
pubs.licence-identifierapollo-deposit-licence-2-1
pubs.licence-display-nameApollo Repository Deposit Licence Agreement
rioxxterms.freetoread.startdate2022-12-31


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