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Prediction of Alzheimer's disease pathophysiology based on cortical thickness patternsopen access

Authors
Hwang, JihyeKim, Chan MiJeon, SeunLee, Jong MinHong, Yun JeongRoh, Jee HoonLee, Jae-HongKoh, Jae-YoungNa, Duk L.
Issue Date
Dec-2015
Publisher
Elsevier Inc.
Keywords
Alzheimer' s disease; Alzheimer' s Disease Neuroimaging Initiative; Cortical thickness; Magnetic resonance imaging; Positron emission tomography
Citation
Alzheimer's and Dementia: Diagnosis, Assessment and Disease Monitoring, v.2, no.1, pp.58 - 67
Indexed
SCOPUS
Journal Title
Alzheimer's and Dementia: Diagnosis, Assessment and Disease Monitoring
Volume
2
Number
1
Start Page
58
End Page
67
URI
https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/155658
DOI
10.1016/j.dadm.2015.11.008
ISSN
2352-8729
Abstract
Introduction: 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.
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