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Prediction of Alzheimer's disease pathophysiology based on cortical thickness patterns

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dc.contributor.authorHwang, Jihye-
dc.contributor.authorKim, Chan Mi-
dc.contributor.authorJeon, Seun-
dc.contributor.authorLee, Jong Min-
dc.contributor.authorHong, Yun Jeong-
dc.contributor.authorRoh, Jee Hoon-
dc.contributor.authorLee, Jae-Hong-
dc.contributor.authorKoh, Jae-Young-
dc.contributor.authorNa, Duk L.-
dc.date.accessioned2022-07-15T19:45:50Z-
dc.date.available2022-07-15T19:45:50Z-
dc.date.issued2015-12-
dc.identifier.issn2352-8729-
dc.identifier.issn2352-8729-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/155658-
dc.description.abstractIntroduction: Recent studies have shown that pathologically defined subtypes of Alzheimer's disease (AD) represent distinctive atrophy patterns and clinical characteristics. We investigated whether a cortical thickness-based clustering method can reflect such findings. Methods: A total of 77 AD subjects from the Alzheimer's Disease Neuroimaging Initiative 2 data set who underwent 3-T magnetic resonance imaging, [18F]-fluorodeoxyglucose-positron emission tomography (PET), [18F]-Florbetapir PET, and cerebrospinal fluid (CSF) tests were enrolled. After clustering based on cortical thickness, diverse imaging and biofluid biomarkers were compared between these groups. Results: Three cortical thinning patterns were noted: medial temporal (MT; 19.5%), diffuse (55.8%), and parietal dominant (P; 24.7%) atrophy subtypes. The P subtype was the youngest and represented more glucose hypometabolism in the parietal and occipital cortices and marked amyloid-beta accumulation in most brain regions. The MT subtype revealed more glucose hypometabolism in the left hippocampus and bilateral frontal cortices and less performance in memory tests. CSF test results did not differ between the groups. Discussion: Cortical thickness patterns can reflect pathophysiological and clinical changes in AD.-
dc.format.extent10-
dc.language영어-
dc.language.isoENG-
dc.publisherElsevier BV-
dc.titlePrediction of Alzheimer's disease pathophysiology based on cortical thickness patterns-
dc.typeArticle-
dc.publisher.location네델란드-
dc.identifier.doi10.1016/j.dadm.2015.11.008-
dc.identifier.scopusid2-s2.0-84962798256-
dc.identifier.bibliographicCitationAlzheimer's and Dementia: Diagnosis, Assessment and Disease Monitoring, v.2, no.1, pp 58 - 67-
dc.citation.titleAlzheimer's and Dementia: Diagnosis, Assessment and Disease Monitoring-
dc.citation.volume2-
dc.citation.number1-
dc.citation.startPage58-
dc.citation.endPage67-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscopus-
dc.subject.keywordPlusamyloid beta protein-
dc.subject.keywordPlusadult-
dc.subject.keywordPlusaged-
dc.subject.keywordPlusAlzheimer disease-
dc.subject.keywordPlusArticle-
dc.subject.keywordPlusbrain atrophy-
dc.subject.keywordPlusbrain region-
dc.subject.keywordPluscerebrospinal fluid analysis-
dc.subject.keywordPluscontrolled study-
dc.subject.keywordPluscortical thickness (brain)-
dc.subject.keywordPlusdisease marker-
dc.subject.keywordPlusfemale-
dc.subject.keywordPlusfrontal cortex-
dc.subject.keywordPlusglucose metabolism-
dc.subject.keywordPlushippocampus-
dc.subject.keywordPlushuman-
dc.subject.keywordPlusleft hemisphere-
dc.subject.keywordPlusmajor clinical study-
dc.subject.keywordPlusmale-
dc.subject.keywordPlusmedial temporal lobe-
dc.subject.keywordPlusmemory test-
dc.subject.keywordPlusneuroimaging-
dc.subject.keywordPlusnuclear magnetic resonance imaging-
dc.subject.keywordPlusoccipital cortex-
dc.subject.keywordPlusparietal cortex-
dc.subject.keywordPluspathophysiology-
dc.subject.keywordPluspositron emission tomography-
dc.subject.keywordPlusprediction-
dc.subject.keywordAuthorAlzheimer's disease-
dc.subject.keywordAuthorAlzheimer's Disease Neuroimaging Initiative-
dc.subject.keywordAuthorCortical thickness-
dc.subject.keywordAuthorMagnetic resonance imaging-
dc.subject.keywordAuthorPositron emission tomography-
dc.identifier.urlhttps://alz-journals.onlinelibrary.wiley.com/doi/10.1016/j.dadm.2015.11.008-
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