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dc.contributor.authorSheikh-Bahaei, Nasim
dc.contributor.authorManavaki, Roido
dc.contributor.authorSajjadi, S Ahmad
dc.contributor.authorPriest, Andrew N
dc.contributor.authorO'Brien, John T
dc.contributor.authorGillard, Jonathan H
dc.date.accessioned2019-04-11T23:30:16Z
dc.date.available2019-04-11T23:30:16Z
dc.date.issued2019
dc.identifier.issn1387-2877
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/291527
dc.description.abstractBACKGROUND: Despite the well-documented relationship between lobar cerebral microbleeds (lCMB) and Alzheimer's disease (AD), there is limited knowledge about the role of lCMB in AD pathology. OBJECTIVE: To understand the nature of this relationship, we investigated the association between lCMB, amyloid load, perfusion, and metabolism. METHODS: Participants with AD, mild cognitive impairment (MCI), and healthy controls were recruited and scanned with 11C-Pittsburg-Compound B (PiB), Fluorodeoxyglucose (FDG) PET, and susceptibility-weighted MRI. Early PiB-PET frames were used to estimate perfusion. The association between lCMB and PET uptake in each anatomical lobe was measured using multiple regression models. RESULTS: The presence of lCMB predicted increased total (p < 0.001) and regional (p = 0.0002) PiB uptake, as well as decreased cerebral perfusion (p = 0.03). Cases with lCMB had hypometabolism in their temporal lobe (p = 0.04). CONCLUSION: There are significant relationships between lCMBs and various markers of AD pathology. lCMB has a spatial association with Aβ load and a complex effect on perfusion and metabolism.
dc.format.mediumPrint
dc.languageeng
dc.publisherIOS Press
dc.rightsAll rights reserved
dc.subjectBrain
dc.subjectHumans
dc.subjectCerebral Hemorrhage
dc.subjectAlzheimer Disease
dc.subjectFluorodeoxyglucose F18
dc.subjectPositron-Emission Tomography
dc.subjectMagnetic Resonance Imaging
dc.subjectAged
dc.subjectAged, 80 and over
dc.subjectFemale
dc.subjectMale
dc.subjectAmyloid beta-Peptides
dc.subjectCognitive Dysfunction
dc.titleCorrelation of Lobar Cerebral Microbleeds with Amyloid, Perfusion, and Metabolism in Alzheimer's Disease.
dc.typeArticle
prism.endingPage1497
prism.issueIdentifier4
prism.publicationDate2019
prism.publicationNameJ Alzheimers Dis
prism.startingPage1489
prism.volume68
dc.identifier.doi10.17863/CAM.38687
dcterms.dateAccepted2019-02-06
rioxxterms.versionofrecord10.3233/JAD-180443
rioxxterms.versionAM
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2019-01
dc.contributor.orcidSheikh-Bahaei, Nasim [0000-0001-7029-7215]
dc.contributor.orcidManavaki, Roido [0000-0002-4384-6626]
dc.contributor.orcidO'Brien, John [0000-0002-0837-5080]
dc.identifier.eissn1875-8908
rioxxterms.typeJournal Article/Review
pubs.funder-project-idCambridge University Hospitals NHS Foundation Trust (CUH) (unknown)
rioxxterms.freetoread.startdate2020-03-18


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