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dc.contributor.authorMak, Elijahen
dc.contributor.authorGabel, Silvyen
dc.contributor.authorMirette, Habiben
dc.contributor.authorSu, Lien
dc.contributor.authorWilliams, Guyen
dc.contributor.authorWaldman, Adamen
dc.contributor.authorWells, Katieen
dc.contributor.authorRitchie, Karenen
dc.contributor.authorRitchie, Craigen
dc.contributor.authorO'Brien, Johnen
dc.date.accessioned2017-01-09T14:49:21Z
dc.date.available2017-01-09T14:49:21Z
dc.date.issued2017-05en
dc.identifier.issn1568-1637
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/261784
dc.description.abstractThe last decade has witnessed a proliferation of neuroimaging studies characterising brain changes associated with Alzheimer's disease (AD), where both widespread atrophy and 'signature' brain regions have been implicated. In parallel, a prolonged latency period has been established in AD, with abnormal cerebral changes beginning many years before symptom onset. This raises the possibility of early therapeutic intervention, even before symptoms, when treatments could have the greatest effect on disease-course modification. Two important prerequisites of this endeavour are (1) accurate characterisation or risk stratification and (2) monitoring of progression using neuroimaging outcomes as a surrogate biomarker in those without symptoms but who will develop AD, here referred to as preclinical AD. Structural neuroimaging modalities have been used to identify brain changes related to risk factors for AD, such as familial genetic mutations, risk genes (for example apolipoprotein epsilon-4 allele), and/or family history. In this review, we summarise structural imaging findings in preclinical AD. Overall, the literature suggests early vulnerability in characteristic regions, such as the medial temporal lobe structures and the precuneus, as well as white matter tracts in the fornix, cingulum and corpus callosum. We conclude that while structural markers are promising, more research and validation studies are needed before future secondary prevention trials can adopt structural imaging biomarkers as either stratification or surrogate biomarkers.
dc.description.sponsorshipThis study was supported by the National Institute for Health Research (NIHR, RG64473), Cambridge Biomedical Research Centre and Biomedical Research Unit in Dementia, and the Alzheimer's Society. Elijah Mak was in the receipt of the Gates Cambridge studentship.
dc.format.mediumPrint-Electronicen
dc.languageengen
dc.language.isoenen
dc.publisherElsevier
dc.subjectHumansen
dc.subjectDementiaen
dc.subjectAlzheimer Diseaseen
dc.subjectAtrophyen
dc.subjectDisease Progressionen
dc.subjectAsymptomatic Diseasesen
dc.subjectNeuroimagingen
dc.subjectConnectomeen
dc.subjectGray Matteren
dc.subjectBiomarkersen
dc.titleStructural neuroimaging in preclinical dementia: From microstructural deficits and grey matter atrophy to macroscale connectomic changes.en
dc.typeArticle
prism.endingPage264
prism.publicationDate2017en
prism.publicationNameAgeing research reviewsen
prism.startingPage250
prism.volume35en
dc.identifier.doi10.17863/CAM.6998
dcterms.dateAccepted2016-10-19en
rioxxterms.versionofrecord10.1016/j.arr.2016.10.001en
rioxxterms.versionAMen
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2017-05en
dc.contributor.orcidMak, Elijah [0000-0002-6437-8024]
dc.contributor.orcidWilliams, Guy [0000-0001-5223-6654]
dc.contributor.orcidO'Brien, John [0000-0002-0837-5080]
dc.identifier.eissn1872-9649
rioxxterms.typeJournal Article/Reviewen
pubs.funder-project-idCambridge University Hospitals NHS Foundation Trust (CUH) (unknown)
pubs.funder-project-idCambridge University Hospitals NHS Foundation Trust (CUH) (unknown)
rioxxterms.freetoread.startdate2017-10-21


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