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In vivo retention of (18)F-AV-1451 in corticobasal syndrome

OBJECTIVE: To study the usefulness of (18)F-AV-1451 PET in patients with corticobasal syndrome (CBS). METHODS: We recruited 8 patients with CBS, 17 controls, 31 patients with Alzheimer disease (AD), and 11 patients with progressive supranuclear palsy (PSP) from the Swedish BioFINDER study. All patie...

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Autores principales: Smith, Ruben, Schöll, Michael, Widner, Håkan, van Westen, Danielle, Svenningsson, Per, Hägerström, Douglas, Ohlsson, Tomas, Jögi, Jonas, Nilsson, Christer, Hansson, Oskar
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Lippincott Williams & Wilkins 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5580862/
https://www.ncbi.nlm.nih.gov/pubmed/28754841
http://dx.doi.org/10.1212/WNL.0000000000004264
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author Smith, Ruben
Schöll, Michael
Widner, Håkan
van Westen, Danielle
Svenningsson, Per
Hägerström, Douglas
Ohlsson, Tomas
Jögi, Jonas
Nilsson, Christer
Hansson, Oskar
author_facet Smith, Ruben
Schöll, Michael
Widner, Håkan
van Westen, Danielle
Svenningsson, Per
Hägerström, Douglas
Ohlsson, Tomas
Jögi, Jonas
Nilsson, Christer
Hansson, Oskar
author_sort Smith, Ruben
collection PubMed
description OBJECTIVE: To study the usefulness of (18)F-AV-1451 PET in patients with corticobasal syndrome (CBS). METHODS: We recruited 8 patients with CBS, 17 controls, 31 patients with Alzheimer disease (AD), and 11 patients with progressive supranuclear palsy (PSP) from the Swedish BioFINDER study. All patients underwent clinical assessment, (18)F-AV-1451 PET, MRI, and quantification of β-amyloid pathology. A subset of participants also underwent (18)F-FDG-PET. RESULTS: In the 8 patients with CBS, 6 had imaging findings compatible with the corticobasal degeneration pathology and 2 with typical AD pathology. In the 6 patients with CBS without typical AD pathology, there were substantial retentions of (18)F-AV-1451 in the motor cortex, corticospinal tract, and basal ganglia contralateral to the most affected body side. These patients could be clearly distinguished from patients with AD dementia or PSP using (18)F-AV-1451. However, cortical atrophy was more widespread than the cortical retention of (18)F-AV1451 in these CBS cases, and cortical AV-1451 uptake did not correlate with cortical thickness or glucose hypometabolism. These results are in sharp contrast to AD dementia, where (18)F-AV-1451 retention was more widespread than cortical atrophy, and correlated well with cortical thickness and hypometabolism. CONCLUSIONS: Patients with CBS without typical AD pathology exhibited AV-1451 retention in the motor cortex, corticospinal tract, and basal ganglia contralateral to the affected body side, clearly different from controls and patients with AD dementia or PSP. However, cortical atrophy measured with MRI and decreased (18)F-fluorodeoxyglucose uptake were more widespread than (18)F-AV-1451 uptake and probably represent earlier, yet less specific, markers of CBS. CLASSIFICATION OF EVIDENCE: This study provides Class III evidence that (18)F-AV-1451 PET distinguishes between CBS and AD or PSP.
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spelling pubmed-55808622017-09-08 In vivo retention of (18)F-AV-1451 in corticobasal syndrome Smith, Ruben Schöll, Michael Widner, Håkan van Westen, Danielle Svenningsson, Per Hägerström, Douglas Ohlsson, Tomas Jögi, Jonas Nilsson, Christer Hansson, Oskar Neurology Article OBJECTIVE: To study the usefulness of (18)F-AV-1451 PET in patients with corticobasal syndrome (CBS). METHODS: We recruited 8 patients with CBS, 17 controls, 31 patients with Alzheimer disease (AD), and 11 patients with progressive supranuclear palsy (PSP) from the Swedish BioFINDER study. All patients underwent clinical assessment, (18)F-AV-1451 PET, MRI, and quantification of β-amyloid pathology. A subset of participants also underwent (18)F-FDG-PET. RESULTS: In the 8 patients with CBS, 6 had imaging findings compatible with the corticobasal degeneration pathology and 2 with typical AD pathology. In the 6 patients with CBS without typical AD pathology, there were substantial retentions of (18)F-AV-1451 in the motor cortex, corticospinal tract, and basal ganglia contralateral to the most affected body side. These patients could be clearly distinguished from patients with AD dementia or PSP using (18)F-AV-1451. However, cortical atrophy was more widespread than the cortical retention of (18)F-AV1451 in these CBS cases, and cortical AV-1451 uptake did not correlate with cortical thickness or glucose hypometabolism. These results are in sharp contrast to AD dementia, where (18)F-AV-1451 retention was more widespread than cortical atrophy, and correlated well with cortical thickness and hypometabolism. CONCLUSIONS: Patients with CBS without typical AD pathology exhibited AV-1451 retention in the motor cortex, corticospinal tract, and basal ganglia contralateral to the affected body side, clearly different from controls and patients with AD dementia or PSP. However, cortical atrophy measured with MRI and decreased (18)F-fluorodeoxyglucose uptake were more widespread than (18)F-AV-1451 uptake and probably represent earlier, yet less specific, markers of CBS. CLASSIFICATION OF EVIDENCE: This study provides Class III evidence that (18)F-AV-1451 PET distinguishes between CBS and AD or PSP. Lippincott Williams & Wilkins 2017-08-22 /pmc/articles/PMC5580862/ /pubmed/28754841 http://dx.doi.org/10.1212/WNL.0000000000004264 Text en Copyright © 2017 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License 4.0 (CC BY) (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Article
Smith, Ruben
Schöll, Michael
Widner, Håkan
van Westen, Danielle
Svenningsson, Per
Hägerström, Douglas
Ohlsson, Tomas
Jögi, Jonas
Nilsson, Christer
Hansson, Oskar
In vivo retention of (18)F-AV-1451 in corticobasal syndrome
title In vivo retention of (18)F-AV-1451 in corticobasal syndrome
title_full In vivo retention of (18)F-AV-1451 in corticobasal syndrome
title_fullStr In vivo retention of (18)F-AV-1451 in corticobasal syndrome
title_full_unstemmed In vivo retention of (18)F-AV-1451 in corticobasal syndrome
title_short In vivo retention of (18)F-AV-1451 in corticobasal syndrome
title_sort in vivo retention of (18)f-av-1451 in corticobasal syndrome
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5580862/
https://www.ncbi.nlm.nih.gov/pubmed/28754841
http://dx.doi.org/10.1212/WNL.0000000000004264
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