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| 001 | 155385 | ||
| 005 | 20240611120547.0 | ||
| 024 | 7 | _ | |a 10.1002/mds.28624 |2 doi |
| 024 | 7 | _ | |a pmid:33951244 |2 pmid |
| 024 | 7 | _ | |a 0885-3185 |2 ISSN |
| 024 | 7 | _ | |a 1531-8257 |2 ISSN |
| 024 | 7 | _ | |a altmetric:105350439 |2 altmetric |
| 037 | _ | _ | |a DZNE-2021-00625 |
| 041 | _ | _ | |a English |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Palleis, Carla |0 P:(DE-2719)9000852 |b 0 |e First author |
| 245 | _ | _ | |a Cortical [18 F]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 1718025011_5320 |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 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).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.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.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.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. |
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| 588 | _ | _ | |a Dataset connected to DataCite |
| 650 | _ | 7 | |a Alzheimer's disease |2 Other |
| 650 | _ | 7 | |a PET |2 Other |
| 650 | _ | 7 | |a corticobasal syndrome |2 Other |
| 650 | _ | 7 | |a four-repeat tauopathies |2 Other |
| 650 | _ | 7 | |a tau |2 Other |
| 650 | _ | 2 | |a Alzheimer Disease: diagnostic imaging |2 MeSH |
| 650 | _ | 2 | |a Amyloid beta-Peptides |2 MeSH |
| 650 | _ | 2 | |a Diagnosis, Differential |2 MeSH |
| 650 | _ | 2 | |a Humans |2 MeSH |
| 650 | _ | 2 | |a Positron-Emission Tomography |2 MeSH |
| 650 | _ | 2 | |a Syndrome |2 MeSH |
| 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-2719)9000882 |b 3 |
| 700 | 1 | _ | |a Bötzel, Kai |b 4 |
| 700 | 1 | _ | |a Danek, Adrian |0 P:(DE-2719)2810712 |b 5 |u dzne |
| 700 | 1 | _ | |a Beyer, Leonie |b 6 |
| 700 | 1 | _ | |a Nitschmann, Alexander |b 7 |
| 700 | 1 | _ | |a Kern, Maike |b 8 |
| 700 | 1 | _ | |a Biechele, Gloria |b 9 |
| 700 | 1 | _ | |a Rauchmann, Boris Stephan |0 P:(DE-2719)9001808 |b 10 |u dzne |
| 700 | 1 | _ | |a Häckert, Jan |b 11 |
| 700 | 1 | _ | |a Höllerhage, Matthias |0 P:(DE-2719)2813308 |b 12 |
| 700 | 1 | _ | |a Stephens, Andrew W |b 13 |
| 700 | 1 | _ | |a Drzezga, Alexander |0 P:(DE-2719)2811239 |b 14 |
| 700 | 1 | _ | |a Eimeren, Thilo |0 P:(DE-2719)2812285 |b 15 |
| 700 | 1 | _ | |a Villemagne, Victor L |b 16 |
| 700 | 1 | _ | |a Schildan, Andreas |b 17 |
| 700 | 1 | _ | |a Barthel, Henryk |b 18 |
| 700 | 1 | _ | |a Patt, Marianne |b 19 |
| 700 | 1 | _ | |a Sabri, Osama |0 P:(DE-2719)2814810 |b 20 |
| 700 | 1 | _ | |a Tauopathies, German Imaging Initiative for |0 P:(DE-HGF)0 |b 21 |e Collaboration Author |
| 700 | 1 | _ | |a Bartenstein, Peter |b 22 |
| 700 | 1 | _ | |a Perneczky, Robert |0 P:(DE-2719)2812234 |b 23 |
| 700 | 1 | _ | |a Haass, Christian |0 P:(DE-2719)2202037 |b 24 |
| 700 | 1 | _ | |a Levin, Johannes |0 P:(DE-2719)2811659 |b 25 |
| 700 | 1 | _ | |a Höglinger, Günter |0 P:(DE-2719)2811373 |b 26 |e Last author |
| 773 | _ | _ | |a 10.1002/mds.28624 |g p. mds.28624 |0 PERI:(DE-600)2041249-6 |n 9 |p 2104 - 2115 |t Movement disorders |v 36 |y 2021 |x 1531-8257 |
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