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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorBUSATTO FILHO, Geraldo
dc.contributor.authorDURAN, Fabio Luiz de Souza
dc.contributor.authorSQUARZONI, Paula
dc.contributor.authorCOUTINHO, Artur Martins Novaes
dc.contributor.authorROSA, Pedro Gomes Penteado
dc.contributor.authorTORRALBO, Leticia
dc.contributor.authorPACHI, Clarice Gameiro da Fonseca
dc.contributor.authorCOSTA, Naomi Antunes da
dc.contributor.authorPORTO, Fabio Henrique de Gobbi
dc.contributor.authorCARVALHO, Cleudiana Lima
dc.contributor.authorBRUCKI, Sonia Maria Dozzi
dc.contributor.authorNITRINI, Ricardo
dc.contributor.authorFORLENZA, Orestes Vicente
dc.contributor.authorLEITE, Claudia da Costa
dc.contributor.authorBUCHPIGUEL, Carlos Alberto
dc.contributor.authorFARIA, Daniele de Paula
dc.date.accessioned2021-02-18T13:41:31Z-
dc.date.available2021-02-18T13:41:31Z-
dc.date.issued2021
dc.identifier.citationJOURNAL OF NEUROSCIENCE RESEARCH, v.99, n.2, p.481-501, 2021
dc.identifier.issn0360-4012
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/39340-
dc.description.abstractChanges in hippocampal subfield volumes (HSV) along the Alzheimer's disease (AD) continuum have been scarcely investigated to date in elderly subjects classified based on the presence of beta-amyloid aggregation and signs of neurodegeneration. We classified patients (either sex) with mild dementia compatible with AD (n = 35) or amnestic mild cognitive impairment (n = 39), and cognitively unimpaired subjects (either sex;n = 26) using [C-11]PIB-PET to assess beta-amyloid aggregation (A+) and [F-18]FDG-PET to account for neurodegeneration ((N)+). Magnetic resonance imaging-based automated methods were used for HSV and white matter hyperintensity (WMH) measurements. Significant HSV reductions were found in A+(N)+ subjects in the presubiculum/subiculum complex and molecular layer, related to worse memory performance. In both the A+(N)+ and A+(N)- categories, subicular volumes were inversely correlated with the degree of A beta deposition. The A-(N)+ subgroup showed reduced HSV relative to the A-(N)- subgroup also in the subiculum/presubiculum. Combining all (N)- subjects, HSV were lower in subjects presenting significant cognitive decline irrespective of A+/A- classification (controlling for WMH load); these between-group differences were detected again in the presubiculum, but also involved the CA4 and granular layer. These findings demonstrate that differential HSV reductions are detectable both in (N)+ and (N)- categories along the AD continuum, and are directly related to the severity of cognitive deficits. HSV reductions are larger both in A+(N)+ and A+(N)- subjects in direct proportion to the degree of A beta deposition. The meaningful HSV reductions detected in the A-(N)+ subgroup highlights the strength of biomarker-based classifications outside of the classical AD continuum.eng
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao PauloFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [2012/50239-6, 2018/15167-1]
dc.language.isoeng
dc.publisherWILEYeng
dc.relation.ispartofJournal of Neuroscience Research
dc.rightsrestrictedAccesseng
dc.subjectAlzheimer's diseaseeng
dc.subjectcognitive impairmenteng
dc.subjecthippocampus subfieldseng
dc.subjectMRIeng
dc.subjectNIA-AA research frameworkeng
dc.subjectPET imagingeng
dc.subject.othermild cognitive impairmenteng
dc.subject.otherwhite-matter hyperintensitieseng
dc.subject.othercerebral glucose-metabolismeng
dc.subject.otherassociation workgroupseng
dc.subject.otherdiagnostic guidelineseng
dc.subject.othercerebrospinal-fluideng
dc.subject.othernational instituteeng
dc.subject.othervessel diseaseeng
dc.subject.othercsf biomarkerseng
dc.subject.othertau pathologyeng
dc.titleHippocampal subregional volume changes in elders classified using positron emission tomography-based Alzheimer's biomarkers of beta-amyloid deposition and neurodegenerationeng
dc.typearticleeng
dc.rights.holderCopyright WILEYeng
dc.identifier.doi10.1002/jnr.24739
dc.identifier.pmid33073383
dc.subject.wosNeuroscienceseng
dc.type.categoryoriginal articleeng
dc.type.versionpublishedVersioneng
hcfmusp.description.beginpage481
hcfmusp.description.endpage501
hcfmusp.description.issue2
hcfmusp.description.volume99
hcfmusp.origemWOS
hcfmusp.origem.idWOS:000579608200001
hcfmusp.origem.id2-s2.0-85092621195
hcfmusp.publisher.cityHOBOKENeng
hcfmusp.publisher.countryUSAeng
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dc.description.indexMEDLINEeng
dc.identifier.eissn1097-4547
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