Cortical [18 F]PI-2620 Binding Differentiates Corticobasal Syndrome Subtypes
© 2021 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society..
BACKGROUND: Corticobasal syndrome is associated with cerebral protein aggregates composed of 4-repeat (~50% of cases) or mixed 3-repeat/4-repeat tau isoforms (~25% of cases) or nontauopathies (~25% of cases).
OBJECTIVES: The aim of this single-center study was to investigate the diagnostic value of the tau PET-ligand [18 F]PI-2620 in patients with corticobasal syndrome.
METHODS: Forty-five patients (71.5 ± 7.6 years) with corticobasal syndrome and 14 age-matched healthy controls underwent [18 F]PI-2620-PET. Beta-amyloid status was determined by cerebral β-amyloid PET and/or CSF analysis. Subcortical and cortical [18 F]PI-2620 binding was quantitatively and visually compared between β-amyloid-positive and -negative patients and controls. Regional [18 F]PI-2620 binding was correlated with clinical and demographic data.
RESULTS: Twenty-four percent (11 of 45) were β-amyloid-positive. Significantly elevated [18 F]PI-2620 distribution volume ratios were observed in both β-amyloid-positive and β-amyloid-negative patients versus controls in the dorsolateral prefrontal cortex and basal ganglia. Cortical [18 F]PI-2620 PET positivity was distinctly higher in β-amyloid-positive compared with β-amyloid-negative patients with pronounced involvement of the dorsolateral prefrontal cortex. Semiquantitative analysis of [18 F]PI-2620 PET revealed a sensitivity of 91% for β-amyloid-positive and of 65% for β-amyloid-negative cases, which is in excellent agreement with prior clinicopathological data. Regardless of β-amyloid status, hemispheric lateralization of [18 F]PI-2620 signal reflected contralateral predominance of clinical disease severity.
CONCLUSIONS: Our data indicate a value of [18 F]PI-2620 for evaluating corticobasal syndrome, providing quantitatively and regionally distinct signals in β-amyloid-positive as well as β-amyloid-negative corticobasal syndrome. In corticobasal syndrome, [18 F]PI-2620 may potentially serve for a differential diagnosis and for monitoring disease progression. © 2021 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2021 |
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Erschienen: |
2021 |
Enthalten in: |
Zur Gesamtaufnahme - volume:36 |
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Enthalten in: |
Movement disorders : official journal of the Movement Disorder Society - 36(2021), 9 vom: 02. Sept., Seite 2104-2115 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Palleis, Carla [VerfasserIn] |
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Links: |
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Themen: |
Alzheimer's disease |
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Anmerkungen: |
Date Completed 13.10.2021 Date Revised 13.10.2021 published: Print-Electronic Citation Status MEDLINE |
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doi: |
10.1002/mds.28624 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM325040443 |
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100 | 1 | |a Palleis, Carla |e verfasserin |4 aut | |
245 | 1 | 0 | |a Cortical [18 F]PI-2620 Binding Differentiates Corticobasal Syndrome Subtypes |
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500 | |a Date Revised 13.10.2021 | ||
500 | |a published: Print-Electronic | ||
500 | |a Citation Status MEDLINE | ||
520 | |a © 2021 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society. | ||
520 | |a BACKGROUND: Corticobasal syndrome is associated with cerebral protein aggregates composed of 4-repeat (~50% of cases) or mixed 3-repeat/4-repeat tau isoforms (~25% of cases) or nontauopathies (~25% of cases) | ||
520 | |a OBJECTIVES: The aim of this single-center study was to investigate the diagnostic value of the tau PET-ligand [18 F]PI-2620 in patients with corticobasal syndrome | ||
520 | |a METHODS: Forty-five patients (71.5 ± 7.6 years) with corticobasal syndrome and 14 age-matched healthy controls underwent [18 F]PI-2620-PET. Beta-amyloid status was determined by cerebral β-amyloid PET and/or CSF analysis. Subcortical and cortical [18 F]PI-2620 binding was quantitatively and visually compared between β-amyloid-positive and -negative patients and controls. Regional [18 F]PI-2620 binding was correlated with clinical and demographic data | ||
520 | |a RESULTS: Twenty-four percent (11 of 45) were β-amyloid-positive. Significantly elevated [18 F]PI-2620 distribution volume ratios were observed in both β-amyloid-positive and β-amyloid-negative patients versus controls in the dorsolateral prefrontal cortex and basal ganglia. Cortical [18 F]PI-2620 PET positivity was distinctly higher in β-amyloid-positive compared with β-amyloid-negative patients with pronounced involvement of the dorsolateral prefrontal cortex. Semiquantitative analysis of [18 F]PI-2620 PET revealed a sensitivity of 91% for β-amyloid-positive and of 65% for β-amyloid-negative cases, which is in excellent agreement with prior clinicopathological data. Regardless of β-amyloid status, hemispheric lateralization of [18 F]PI-2620 signal reflected contralateral predominance of clinical disease severity | ||
520 | |a CONCLUSIONS: Our data indicate a value of [18 F]PI-2620 for evaluating corticobasal syndrome, providing quantitatively and regionally distinct signals in β-amyloid-positive as well as β-amyloid-negative corticobasal syndrome. In corticobasal syndrome, [18 F]PI-2620 may potentially serve for a differential diagnosis and for monitoring disease progression. © 2021 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a Research Support, Non-U.S. Gov't | |
650 | 4 | |a Alzheimer's disease | |
650 | 4 | |a PET | |
650 | 4 | |a corticobasal syndrome | |
650 | 4 | |a four-repeat tauopathies | |
650 | 4 | |a tau | |
650 | 7 | |a Amyloid beta-Peptides |2 NLM | |
700 | 1 | |a Brendel, Matthias |e verfasserin |4 aut | |
700 | 1 | |a Finze, Anika |e verfasserin |4 aut | |
700 | 1 | |a Weidinger, Endy |e verfasserin |4 aut | |
700 | 1 | |a Bötzel, Kai |e verfasserin |4 aut | |
700 | 1 | |a Danek, Adrian |e verfasserin |4 aut | |
700 | 1 | |a Beyer, Leonie |e verfasserin |4 aut | |
700 | 1 | |a Nitschmann, Alexander |e verfasserin |4 aut | |
700 | 1 | |a Kern, Maike |e verfasserin |4 aut | |
700 | 1 | |a Biechele, Gloria |e verfasserin |4 aut | |
700 | 1 | |a Rauchmann, Boris-Stephan |e verfasserin |4 aut | |
700 | 1 | |a Häckert, Jan |e verfasserin |4 aut | |
700 | 1 | |a Höllerhage, Matthias |e verfasserin |4 aut | |
700 | 1 | |a Stephens, Andrew W |e verfasserin |4 aut | |
700 | 1 | |a Drzezga, Alexander |e verfasserin |4 aut | |
700 | 1 | |a van Eimeren, Thilo |e verfasserin |4 aut | |
700 | 1 | |a Villemagne, Victor L |e verfasserin |4 aut | |
700 | 1 | |a Schildan, Andreas |e verfasserin |4 aut | |
700 | 1 | |a Barthel, Henryk |e verfasserin |4 aut | |
700 | 1 | |a Patt, Marianne |e verfasserin |4 aut | |
700 | 1 | |a Sabri, Osama |e verfasserin |4 aut | |
700 | 0 | |a German Imaging Initiative for Tauopathies (GII4T) |e verfasserin |4 aut | |
700 | 1 | |a Bartenstein, Peter |e verfasserin |4 aut | |
700 | 1 | |a Perneczky, Robert |e verfasserin |4 aut | |
700 | 1 | |a Haass, Christian |e verfasserin |4 aut | |
700 | 1 | |a Levin, Johannes |e verfasserin |4 aut | |
700 | 1 | |a Höglinger, Günter U |e verfasserin |4 aut | |
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