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dc.contributor.authorMak, Elijah
dc.contributor.authorDonaghy, Paul C
dc.contributor.authorMcKiernan, Elizabeth
dc.contributor.authorFirbank, Michael J
dc.contributor.authorLloyd, Jim
dc.contributor.authorPetrides, George S
dc.contributor.authorThomas, Alan J
dc.contributor.authorO'Brien, John
dc.date.accessioned2018-12-01T00:30:57Z
dc.date.available2018-12-01T00:30:57Z
dc.date.issued2019-01
dc.identifier.issn0197-4580
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/286205
dc.description.abstractAlthough dementia with Lewy bodies (DLB) is a synucleinopathy, it is frequently accompanied by beta amyloid (Aβ) accumulation. Elucidating the relationships of Aβ with gray matter atrophy in DLB may yield insights regarding the contributions of comorbid Alzheimer's disease to its disease progression. Twenty healthy controls and 25 DLB subjects underwent clinical assessment, [18F]-Florbetapir, and 3T magnetic resonance imaging. FreeSurfer was used to estimate cortical thickness and subcortical volumes, and PetSurfer was used to quantify [18F]-Florbetapir standardized uptake value ratio. Principal component analysis was used to identify the dominant Aβ component for correlations with regional cortical thickness, hippocampal subfields, and subcortical structures. Relative to healthy controls, the DLB group demonstrated increased Aβ in widespread regions encompassing the frontal and temporoparietal cortices, whereas cortical thinning was restricted to the temporal lobe. Among DLB subjects, the Aβ component was significantly associated with more severe hippocampal and subiculum atrophy. These findings may reflect an early process of superimposed AD-like atrophy in DLB, thereby conferring support for the therapeutic potential of anti-Aβ interventions in people with DLB.
dc.description.sponsorshipNIHR Newcastle Biomedical Research Centre; Eli Lilly and Company
dc.format.mediumPrint-Electronic
dc.languageeng
dc.publisherElsevier BV
dc.subjectHippocampus
dc.subjectHumans
dc.subjectLewy Body Disease
dc.subjectAlzheimer Disease
dc.subjectAtrophy
dc.subjectDisease Progression
dc.subjectPositron-Emission Tomography
dc.subjectMagnetic Resonance Imaging
dc.subjectAged
dc.subjectAged, 80 and over
dc.subjectMiddle Aged
dc.subjectFemale
dc.subjectMale
dc.subjectAmyloid beta-Peptides
dc.titleBeta amyloid deposition maps onto hippocampal and subiculum atrophy in dementia with Lewy bodies.
dc.typeArticle
prism.endingPage81
prism.publicationDate2019
prism.publicationNameNeurobiol Aging
prism.startingPage74
prism.volume73
dc.identifier.doi10.17863/CAM.33517
dcterms.dateAccepted2018-09-06
rioxxterms.versionofrecord10.1016/j.neurobiolaging.2018.09.004
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2019-01
dc.contributor.orcidMak, Elijah [0000-0002-6437-8024]
dc.contributor.orcidO'Brien, John [0000-0002-0837-5080]
dc.identifier.eissn1558-1497
rioxxterms.typeJournal Article/Review
rioxxterms.freetoread.startdate2019-09-12


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