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| Hauptseite > Publikationsdatenbank > Cortical [18F]PI‐2620 Binding Differentiates Corticobasal Syndrome Subtypes > print |
| Hauptseite > Publikationsdatenbank > Cortical [18F]PI‐2620 Binding Differentiates Corticobasal Syndrome Subtypes > print |
| 001 | 904371 | ||
| 005 | 20230123101900.0 | ||
| 024 | 7 | _ | |a 10.1002/mds.28624 |2 doi |
| 024 | 7 | _ | |a 0885-3185 |2 ISSN |
| 024 | 7 | _ | |a 1531-8257 |2 ISSN |
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| 037 | _ | _ | |a FZJ-2021-05941 |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Palleis, Carla |0 P:(DE-HGF)0 |b 0 |
| 245 | _ | _ | |a Cortical [18F]PI‐2620 Binding Differentiates Corticobasal Syndrome Subtypes |
| 260 | _ | _ | |a New York, NY |c 2021 |b Wiley |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1667372222_15986 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
| 336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 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).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.Keywords: Alzheimer's disease; PET; corticobasal syndrome; four-repeat tauopathies; tau. |
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| 700 | 1 | _ | |a Brendel, Matthias |0 P:(DE-HGF)0 |b 1 |
| 700 | 1 | _ | |a Finze, Anika |0 P:(DE-HGF)0 |b 2 |
| 700 | 1 | _ | |a Weidinger, Endy |0 P:(DE-HGF)0 |b 3 |
| 700 | 1 | _ | |a Bötzel, Kai |0 P:(DE-HGF)0 |b 4 |
| 700 | 1 | _ | |a Danek, Adrian |0 P:(DE-HGF)0 |b 5 |
| 700 | 1 | _ | |a Beyer, Leonie |0 P:(DE-HGF)0 |b 6 |
| 700 | 1 | _ | |a Nitschmann, Alexander |0 P:(DE-HGF)0 |b 7 |
| 700 | 1 | _ | |a Kern, Maike |0 P:(DE-HGF)0 |b 8 |
| 700 | 1 | _ | |a Biechele, Gloria |0 P:(DE-HGF)0 |b 9 |
| 700 | 1 | _ | |a Rauchmann, Boris-Stephan |0 P:(DE-HGF)0 |b 10 |
| 700 | 1 | _ | |a Häckert, Jan |0 P:(DE-HGF)0 |b 11 |
| 700 | 1 | _ | |a Höllerhage, Matthias |0 P:(DE-HGF)0 |b 12 |
| 700 | 1 | _ | |a Stephens, Andrew W. |0 P:(DE-HGF)0 |b 13 |
| 700 | 1 | _ | |a Drzezga, Alexander |0 P:(DE-Juel1)177611 |b 14 |
| 700 | 1 | _ | |a Eimeren, Thilo |0 P:(DE-HGF)0 |b 15 |
| 700 | 1 | _ | |a Villemagne, Victor L. |0 P:(DE-HGF)0 |b 16 |
| 700 | 1 | _ | |a Schildan, Andreas |0 P:(DE-HGF)0 |b 17 |
| 700 | 1 | _ | |a Barthel, Henryk |0 P:(DE-HGF)0 |b 18 |
| 700 | 1 | _ | |a Patt, Marianne |0 P:(DE-HGF)0 |b 19 |
| 700 | 1 | _ | |a Sabri, Osama |0 P:(DE-HGF)0 |b 20 |
| 700 | 1 | _ | |a Bartenstein, Peter |0 P:(DE-HGF)0 |b 21 |
| 700 | 1 | _ | |a Perneczky, Robert |0 P:(DE-HGF)0 |b 22 |
| 700 | 1 | _ | |a Haass, Christian |0 P:(DE-HGF)0 |b 23 |
| 700 | 1 | _ | |a Levin, Johannes |0 P:(DE-HGF)0 |b 24 |e Corresponding author |
| 700 | 1 | _ | |a Höglinger, Günter U. |0 P:(DE-HGF)0 |b 25 |e Corresponding author |
| 773 | _ | _ | |a 10.1002/mds.28624 |g Vol. 36, no. 9, p. 2104 - 2115 |0 PERI:(DE-600)2041249-6 |n 9 |p 2104 - 2115 |t Movement disorders |v 36 |y 2021 |x 0885-3185 |
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