TY - JOUR
T1 - Association of Subcortical Structural Shapes With Tau, Amyloid, and Cortical Atrophy in Early-Onset and Late-Onset Alzheimer’s Disease
AU - Lee, Eun Chong
AU - Kang, Jae Myeong
AU - Seo, Seongho
AU - Seo, Ha Eun
AU - Lee, Sang Yoon
AU - Park, Kee Hyung
AU - Na, Duk L.
AU - Noh, Young
AU - Seong, Joon Kyung
N1 - Funding Information:
Funding. This study was supported by a grant from the Korea Healthcare Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (Grant No: HI14C1135), a grant from the Brain Research Program of the National Research Foundation (NRF) funded by the Korean Government (MSIT) (No. 2018M3C7A1056889); by Institute of Information & communications Technology Planning & Evaluation (IITP) grant funded by the Korean Government (MSIT) [No. 2019-0-00079, Department of Artificial Intelligence (Korea University)]; and by Brain Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science and ICT (No. 2020M3C7A101835721).
Funding Information:
This study was supported by a grant from the Korea Healthcare Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (Grant No: HI14C1135), a grant from the Brain Research Program of the National Research Foundation (NRF) funded by the Korean Government (MSIT) (No. 2018M3C7A1056889); by Institute of Information & communications Technology Planning & Evaluation (IITP) grant funded by the Korean Government (MSIT) [No. 2019-0-00079,
Publisher Copyright:
© Copyright © 2020 Lee, Kang, Seo, Seo, Lee, Park, Na, Noh and Seong.
PY - 2020/10/26
Y1 - 2020/10/26
N2 - The objectives of this study were to compare the topographical subcortical shape and to investigate the effects of tau or amyloid burden on atrophic patterns in early onset Alzheimer’s disease (EOAD) and late-onset Alzheimer’s disease (LOAD). One hundred and sixty-one participants (53 EOAD, 44 LOAD, 33 young controls, and 31 older controls) underwent [18F]THK5351 positron emission tomography (PET), [18F]flutemetamol (FLUTE) PET, and 3T MRI scans. We used surface-based analysis to evaluate subcortical structural shape, permutation-based statistics for group comparisons, and Spearman’s correlations to determine associations with THK, FLUTE, cortical thickness, and neuropsychological test results. When compared to their age-matched controls, EOAD patients exhibited shape reduction in the bilateral amygdala, hippocampus, caudate, and putamen, while in LOAD patients, the bilateral amygdala and hippocampus showed decreased shapes. In EOAD, widespread subcortical shrinkage, with less association of the hippocampus, correlated with THK retention and cortical thinning, while in LOAD patients, subcortical structures were limited which had significant correlation with THK or mean cortical thickness. Subcortical structural shape showed less correlation with FLUTE global retention in both EOAD and LOAD. Multiple cognitive domains, except memory function, correlated with the bilateral amygdala, caudate, and putamen in EOAD patients, while more restricted regions in the subcortical structures were correlated with neuropsychological test results in LOAD patients. Subcortical structures were associated with AD hallmarks in EOAD. However, the correlation was limited in LOAD. Moreover, relationship between subcortical structural atrophy and cognitive decline were quite different between EOAD and LOAD. These findings suggest that the effects of Alzheimer’s pathologies on subcortical structural changes in EOAD and LOAD and they may have different courses of pathomechanism.
AB - The objectives of this study were to compare the topographical subcortical shape and to investigate the effects of tau or amyloid burden on atrophic patterns in early onset Alzheimer’s disease (EOAD) and late-onset Alzheimer’s disease (LOAD). One hundred and sixty-one participants (53 EOAD, 44 LOAD, 33 young controls, and 31 older controls) underwent [18F]THK5351 positron emission tomography (PET), [18F]flutemetamol (FLUTE) PET, and 3T MRI scans. We used surface-based analysis to evaluate subcortical structural shape, permutation-based statistics for group comparisons, and Spearman’s correlations to determine associations with THK, FLUTE, cortical thickness, and neuropsychological test results. When compared to their age-matched controls, EOAD patients exhibited shape reduction in the bilateral amygdala, hippocampus, caudate, and putamen, while in LOAD patients, the bilateral amygdala and hippocampus showed decreased shapes. In EOAD, widespread subcortical shrinkage, with less association of the hippocampus, correlated with THK retention and cortical thinning, while in LOAD patients, subcortical structures were limited which had significant correlation with THK or mean cortical thickness. Subcortical structural shape showed less correlation with FLUTE global retention in both EOAD and LOAD. Multiple cognitive domains, except memory function, correlated with the bilateral amygdala, caudate, and putamen in EOAD patients, while more restricted regions in the subcortical structures were correlated with neuropsychological test results in LOAD patients. Subcortical structures were associated with AD hallmarks in EOAD. However, the correlation was limited in LOAD. Moreover, relationship between subcortical structural atrophy and cognitive decline were quite different between EOAD and LOAD. These findings suggest that the effects of Alzheimer’s pathologies on subcortical structural changes in EOAD and LOAD and they may have different courses of pathomechanism.
KW - Alzheimer’s disease
KW - amyloid
KW - cortical thickness
KW - magnetic resonance imaging
KW - positron emission tomography
KW - subcortical shape analysis
KW - tau
UR - http://www.scopus.com/inward/record.url?scp=85095726743&partnerID=8YFLogxK
U2 - 10.3389/fnagi.2020.563559
DO - 10.3389/fnagi.2020.563559
M3 - Article
AN - SCOPUS:85095726743
VL - 12
JO - Frontiers in Aging Neuroscience
JF - Frontiers in Aging Neuroscience
SN - 1663-4365
M1 - 563559
ER -