Involvement of the Precuneus/Posterior Cingulate Cortex Is Significant for the Development of Alzheimer's Disease: A PET (THK5351, PiB) and Resting fMRI Study
: Imaging studies in Alzheimer's disease (AD) have yet to answer the underlying questions concerning the relationship among tau retention, neuroinflammation, network disruption and cognitive decline. We compared the spatial retention patterns of F-THK5351 and resting state network (RSN) disrupt...
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| Published in | Frontiers in aging neuroscience Vol. 10; p. 304 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Switzerland
Frontiers Research Foundation
05.10.2018
Frontiers Media S.A |
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| Online Access | Get full text |
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| Abstract | : Imaging studies in Alzheimer's disease (AD) have yet to answer the underlying questions concerning the relationship among tau retention, neuroinflammation, network disruption and cognitive decline. We compared the spatial retention patterns of
F-THK5351 and resting state network (RSN) disruption in patients with early AD and healthy controls.
: We enrolled 23
C-Pittsburgh compound B (PiB)-positive patients with early AD and 24
C-PiB-negative participants as healthy controls. All participants underwent resting state functional MRI and
F-THK5351 PET scans. We used scaled subprofile modeling/principal component analysis (SSM/PCA) to reduce the complexity of multivariate data and to identify patterns that exhibited the largest statistical effects (variances) in THK5351 concentration in AD and healthy controls.
: SSM/PCA identified a significant spatial THK5351 pattern composed by mainly three clusters including precuneus/posterior cingulate cortex (PCC), right and left dorsolateral prefrontal cortex (DLPFC) which accounted for 23.6% of the total subject voxel variance of the data and had 82.6% sensitivity and 79.1% specificity in discriminating AD from healthy controls. There was a significant relationship between the intensity of the
F-THK5351 covariation pattern and cognitive scores in AD. The spatial patterns of
F-THK5351 uptake showed significant similarity with intrinsic functional connectivity, especially in the PCC network. Seed-based connectivity analysis from the PCC showed significant decrease in connectivity over widespread brain regions in AD patients. An evaluation of an autopsied AD patient with Braak V showed that
F-THK5351 retention corresponded to tau deposition, monoamine oxidase-B (MAO-B) and astrogliosis in the precuneus/PCC.
: We identified an AD-specific spatial pattern of
F-THK5351 retention in the precuneus/PCC, an important connectivity hub region in the brain. Disruption of the functional connections of this important network hub may play an important role in developing dementia in AD. |
|---|---|
| AbstractList | Background
: Imaging studies in Alzheimer’s disease (AD) have yet to answer the underlying questions concerning the relationship among tau retention, neuroinflammation, network disruption and cognitive decline. We compared the spatial retention patterns of
18
F-THK5351 and resting state network (RSN) disruption in patients with early AD and healthy controls.
Methods
: We enrolled 23
11
C-Pittsburgh compound B (PiB)-positive patients with early AD and 24
11
C-PiB-negative participants as healthy controls. All participants underwent resting state functional MRI and
18
F-THK5351 PET scans. We used scaled subprofile modeling/principal component analysis (SSM/PCA) to reduce the complexity of multivariate data and to identify patterns that exhibited the largest statistical effects (variances) in THK5351 concentration in AD and healthy controls.
Findings
: SSM/PCA identified a significant spatial THK5351 pattern composed by mainly three clusters including precuneus/posterior cingulate cortex (PCC), right and left dorsolateral prefrontal cortex (DLPFC) which accounted for 23.6% of the total subject voxel variance of the data and had 82.6% sensitivity and 79.1% specificity in discriminating AD from healthy controls. There was a significant relationship between the intensity of the
18
F-THK5351 covariation pattern and cognitive scores in AD. The spatial patterns of
18
F-THK5351 uptake showed significant similarity with intrinsic functional connectivity, especially in the PCC network. Seed-based connectivity analysis from the PCC showed significant decrease in connectivity over widespread brain regions in AD patients. An evaluation of an autopsied AD patient with Braak V showed that
18
F-THK5351 retention corresponded to tau deposition, monoamine oxidase-B (MAO-B) and astrogliosis in the precuneus/PCC.
Interpretation
: We identified an AD-specific spatial pattern of
18
F-THK5351 retention in the precuneus/PCC, an important connectivity hub region in the brain. Disruption of the functional connections of this important network hub may play an important role in developing dementia in AD. Background: Imaging studies in Alzheimer’s disease (AD) have yet to answer the underlying questions concerning the relationship among tau retention, neuroinflammation, network disruption and cognitive decline. We compared the spatial retention patterns of 18F-THK5351 and resting state network (RSN) disruption in patients with early AD and healthy controls.Methods: We enrolled 23 11C-Pittsburgh compound B (PiB)-positive patients with early AD and 24 11C-PiB-negative participants as healthy controls. All participants underwent resting state functional MRI and 18F-THK5351 PET scans. We used scaled subprofile modeling/principal component analysis (SSM/PCA) to reduce the complexity of multivariate data and to identify patterns that exhibited the largest statistical effects (variances) in THK5351 concentration in AD and healthy controls.Findings: SSM/PCA identified a significant spatial THK5351 pattern composed by mainly three clusters including precuneus/posterior cingulate cortex (PCC), right and left dorsolateral prefrontal cortex (DLPFC) which accounted for 23.6% of the total subject voxel variance of the data and had 82.6% sensitivity and 79.1% specificity in discriminating AD from healthy controls. There was a significant relationship between the intensity of the 18F-THK5351 covariation pattern and cognitive scores in AD. The spatial patterns of 18F-THK5351 uptake showed significant similarity with intrinsic functional connectivity, especially in the PCC network. Seed-based connectivity analysis from the PCC showed significant decrease in connectivity over widespread brain regions in AD patients. An evaluation of an autopsied AD patient with Braak V showed that 18F-THK5351 retention corresponded to tau deposition, monoamine oxidase-B (MAO-B) and astrogliosis in the precuneus/PCC.Interpretation: We identified an AD-specific spatial pattern of 18F-THK5351 retention in the precuneus/PCC, an important connectivity hub region in the brain. Disruption of the functional connections of this important network hub may play an important role in developing dementia in AD. : Imaging studies in Alzheimer's disease (AD) have yet to answer the underlying questions concerning the relationship among tau retention, neuroinflammation, network disruption and cognitive decline. We compared the spatial retention patterns of F-THK5351 and resting state network (RSN) disruption in patients with early AD and healthy controls. : We enrolled 23 C-Pittsburgh compound B (PiB)-positive patients with early AD and 24 C-PiB-negative participants as healthy controls. All participants underwent resting state functional MRI and F-THK5351 PET scans. We used scaled subprofile modeling/principal component analysis (SSM/PCA) to reduce the complexity of multivariate data and to identify patterns that exhibited the largest statistical effects (variances) in THK5351 concentration in AD and healthy controls. : SSM/PCA identified a significant spatial THK5351 pattern composed by mainly three clusters including precuneus/posterior cingulate cortex (PCC), right and left dorsolateral prefrontal cortex (DLPFC) which accounted for 23.6% of the total subject voxel variance of the data and had 82.6% sensitivity and 79.1% specificity in discriminating AD from healthy controls. There was a significant relationship between the intensity of the F-THK5351 covariation pattern and cognitive scores in AD. The spatial patterns of F-THK5351 uptake showed significant similarity with intrinsic functional connectivity, especially in the PCC network. Seed-based connectivity analysis from the PCC showed significant decrease in connectivity over widespread brain regions in AD patients. An evaluation of an autopsied AD patient with Braak V showed that F-THK5351 retention corresponded to tau deposition, monoamine oxidase-B (MAO-B) and astrogliosis in the precuneus/PCC. : We identified an AD-specific spatial pattern of F-THK5351 retention in the precuneus/PCC, an important connectivity hub region in the brain. Disruption of the functional connections of this important network hub may play an important role in developing dementia in AD. Abstract Background: Imaging studies in Alzheimer’s disease have yet to answer the underlying questions concerning the relationship among tau retention, neuroinflammation, network disruption, and cognitive decline. We compared the spatial retention patterns of 18F-THK5351 and resting state network disruption in patients with early Alzheimer’s disease and healthy controls. Methods: We enrolled 23 11C-Pittsburgh compound B (PiB)-positive patients with early Alzheimer’s disease and 24 11C-PiB-negative participants as healthy controls. All participants underwent resting state functional MRI and 18F-THK5351 PET scans. We used scaled subprofile modeling/principal component analysis (SSM/PCA) to reduce the complexity of multivariate data and to identify patterns that exhibited the largest statistical effects (variances) in THK5351 concentration in Alzheimer’s disease and healthy controls. Findings: SSM/PCA identified a significant spatial THK5351 pattern composed by mainly three clusters including precuneus/posterior cingulate cortex, right and left dorsolateral prefrontal cortex which accounted for 23.6% of the total subject voxel variance of the data and had 82.6% sensitivity and 79.1% specificity in discriminating Alzheimer’s disease from healthy controls. There was a significant relationship between the intensity of the 18F-THK5351 covariation pattern and cognitive scores in Alzheimer’s disease. The spatial patterns of 18F-THK5351 uptake showed significant similarity with intrinsic functional connectivity, especially in the precuneus/posterior cingulate cortex network. Seed-based connectivity analysis from the precuneus/posterior cingulate cortex showed significant decrease in connectivity over widespread brain regions in Alzheimer’s disease patients. An evaluation of an autopsied Alzheimer’s disease patient with Braak V showed that 18F-THK5351 retention corresponded to tau deposition, monoamine oxidase-B and astrogliosis in the precuneus/posterior cingulate cortex. Interpretation: We identified an Alzheimer’s disease-specific spatial pattern of 18F-THK5351 retention in the precuneus/posterior cingulate cortex, an important connectivity hub region in the brain. Disruption of the functional connections of this important network hub may play an important role in developing dementia in Alzheimer’s disease. |
| Author | Ohdake, Reiko Kato, Katsuhiko Riku, Yuichi Harada, Ryuichi Okamura, Nobuyuki Katsuno, Masahisa Masuda, Michihito Ogura, Aya Watanabe, Hirohisa Bagarinao, Epifanio Ishigaki, Shinsuke Imai, Kazunori Yamaguchi, Hiroshi Miyao, Shinichi Yanai, Kazuhiko Hara, Kazuhiro Naganawa, Shinji Kawabata, Kazuya Sobue, Gen Yoshida, Mari Yokoi, Takamasa |
| AuthorAffiliation | 6 Department of Pharmacology, Tohoku University School of Medicine , Sendai , Japan 8 Department of Neuropathology, Institute for Medical Science of Aging, Aichi Medical University , Nagakute , Japan 2 Brain and Mind Research Center, Nagoya University , Nagoya , Japan 4 Department of Radiological and Medical Laboratory Sciences, Nagoya University Graduate School of Medicine , Nagoya , Japan 1 Department of Neurology, Nagoya University Graduate School of Medicine , Nagoya , Japan 3 Department of Neurology, Meitetsu Hospital , Nagoya , Japan 7 Division of Pharmacology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University , Sendai , Japan 5 Department of Radiology, Nagoya University Graduate School of Medicine , Nagoya , Japan |
| AuthorAffiliation_xml | – name: 2 Brain and Mind Research Center, Nagoya University , Nagoya , Japan – name: 7 Division of Pharmacology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University , Sendai , Japan – name: 1 Department of Neurology, Nagoya University Graduate School of Medicine , Nagoya , Japan – name: 3 Department of Neurology, Meitetsu Hospital , Nagoya , Japan – name: 5 Department of Radiology, Nagoya University Graduate School of Medicine , Nagoya , Japan – name: 8 Department of Neuropathology, Institute for Medical Science of Aging, Aichi Medical University , Nagakute , Japan – name: 6 Department of Pharmacology, Tohoku University School of Medicine , Sendai , Japan – name: 4 Department of Radiological and Medical Laboratory Sciences, Nagoya University Graduate School of Medicine , Nagoya , Japan |
| Author_xml | – sequence: 1 givenname: Takamasa surname: Yokoi fullname: Yokoi, Takamasa organization: Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan – sequence: 2 givenname: Hirohisa surname: Watanabe fullname: Watanabe, Hirohisa organization: Brain and Mind Research Center, Nagoya University, Nagoya, Japan – sequence: 3 givenname: Hiroshi surname: Yamaguchi fullname: Yamaguchi, Hiroshi organization: Brain and Mind Research Center, Nagoya University, Nagoya, Japan – sequence: 4 givenname: Epifanio surname: Bagarinao fullname: Bagarinao, Epifanio organization: Brain and Mind Research Center, Nagoya University, Nagoya, Japan – sequence: 5 givenname: Michihito surname: Masuda fullname: Masuda, Michihito organization: Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan – sequence: 6 givenname: Kazunori surname: Imai fullname: Imai, Kazunori organization: Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan – sequence: 7 givenname: Aya surname: Ogura fullname: Ogura, Aya organization: Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan – sequence: 8 givenname: Reiko surname: Ohdake fullname: Ohdake, Reiko organization: Brain and Mind Research Center, Nagoya University, Nagoya, Japan – sequence: 9 givenname: Kazuya surname: Kawabata fullname: Kawabata, Kazuya organization: Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan – sequence: 10 givenname: Kazuhiro surname: Hara fullname: Hara, Kazuhiro organization: Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan – sequence: 11 givenname: Yuichi surname: Riku fullname: Riku, Yuichi organization: Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan – sequence: 12 givenname: Shinsuke surname: Ishigaki fullname: Ishigaki, Shinsuke organization: Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan – sequence: 13 givenname: Masahisa surname: Katsuno fullname: Katsuno, Masahisa organization: Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan – sequence: 14 givenname: Shinichi surname: Miyao fullname: Miyao, Shinichi organization: Department of Neurology, Meitetsu Hospital, Nagoya, Japan – sequence: 15 givenname: Katsuhiko surname: Kato fullname: Kato, Katsuhiko organization: Department of Radiological and Medical Laboratory Sciences, Nagoya University Graduate School of Medicine, Nagoya, Japan – sequence: 16 givenname: Shinji surname: Naganawa fullname: Naganawa, Shinji organization: Department of Radiology, Nagoya University Graduate School of Medicine, Nagoya, Japan – sequence: 17 givenname: Ryuichi surname: Harada fullname: Harada, Ryuichi organization: Department of Pharmacology, Tohoku University School of Medicine, Sendai, Japan – sequence: 18 givenname: Nobuyuki surname: Okamura fullname: Okamura, Nobuyuki organization: Division of Pharmacology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Japan – sequence: 19 givenname: Kazuhiko surname: Yanai fullname: Yanai, Kazuhiko organization: Department of Pharmacology, Tohoku University School of Medicine, Sendai, Japan – sequence: 20 givenname: Mari surname: Yoshida fullname: Yoshida, Mari organization: Department of Neuropathology, Institute for Medical Science of Aging, Aichi Medical University, Nagakute, Japan – sequence: 21 givenname: Gen surname: Sobue fullname: Sobue, Gen organization: Brain and Mind Research Center, Nagoya University, Nagoya, Japan |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30344488$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | 2018. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. Copyright © 2018 Yokoi, Watanabe, Yamaguchi, Bagarinao, Masuda, Imai, Ogura, Ohdake, Kawabata, Hara, Riku, Ishigaki, Katsuno, Miyao, Kato, Naganawa, Harada, Okamura, Yanai, Yoshida and Sobue. 2018 Yokoi, Watanabe, Yamaguchi, Bagarinao, Masuda, Imai, Ogura, Ohdake, Kawabata, Hara, Riku, Ishigaki, Katsuno, Miyao, Kato, Naganawa, Harada, Okamura, Yanai, Yoshida and Sobue |
| Copyright_xml | – notice: 2018. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: Copyright © 2018 Yokoi, Watanabe, Yamaguchi, Bagarinao, Masuda, Imai, Ogura, Ohdake, Kawabata, Hara, Riku, Ishigaki, Katsuno, Miyao, Kato, Naganawa, Harada, Okamura, Yanai, Yoshida and Sobue. 2018 Yokoi, Watanabe, Yamaguchi, Bagarinao, Masuda, Imai, Ogura, Ohdake, Kawabata, Hara, Riku, Ishigaki, Katsuno, Miyao, Kato, Naganawa, Harada, Okamura, Yanai, Yoshida and Sobue |
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| Keywords | MRI positron emission tomography (PET) 18F-THK5351 11C-PiB MAO-B resting state network astrocyte |
| Language | English |
| License | This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
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| Snippet | : Imaging studies in Alzheimer's disease (AD) have yet to answer the underlying questions concerning the relationship among tau retention, neuroinflammation,... Abstract Background: Imaging studies in Alzheimer’s disease have yet to answer the underlying questions concerning the relationship among tau retention,... Background : Imaging studies in Alzheimer’s disease (AD) have yet to answer the underlying questions concerning the relationship among tau retention,... Background: Imaging studies in Alzheimer’s disease (AD) have yet to answer the underlying questions concerning the relationship among tau retention,... |
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| SubjectTerms | 11C-PiB 18F-THK5351 Aging Amine oxidase (flavin-containing) Brain mapping Brain research Cognition & reasoning Cognitive ability Cortex (cingulate) Cortex (parietal) Dementia Dementia disorders Functional magnetic resonance imaging Gliosis Hospitals Inflammation MAO-B Medicine Memory MRI Neural networks Neurodegeneration Neuroimaging Neurology Neuroscience Pathology Positron emission tomography positron emission tomography (PET) Prefrontal cortex Principal components analysis resting state network Retention Tau protein University graduates |
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| Title | Involvement of the Precuneus/Posterior Cingulate Cortex Is Significant for the Development of Alzheimer's Disease: A PET (THK5351, PiB) and Resting fMRI Study |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/30344488 https://www.proquest.com/docview/2300632785/abstract/ https://search.proquest.com/docview/2125309778 https://pubmed.ncbi.nlm.nih.gov/PMC6182068 https://doaj.org/article/18bbf7f4c87f4874afbcd69527b13a5e |
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