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Cortical [18F]PI-2620 Binding Differentiates Corticobasal Syndrome Subtypes

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 [18F]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 [18F]PI-2620-PET. Beta-amyloid status was determined by cerebral β-amyloid PET and/or CSF analysis. Subcortical and cortical [18F]PI-2620 binding was quantitatively and visually compared between β-amyloid-positive and -negative patients and controls. Regional [18F]PI-2620 binding was correlated with clinical and demographic data.
Results

Twenty-four percent (11 of 45) were β-amyloid-positive. Significantly elevated [18F]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 [18F]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 [18F]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 [18F]PI-2620 signal reflected contralateral predominance of clinical disease severity.
Conclusions

Our data indicate a value of [18F]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, [18F]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

Identiferoai:union.ndltd.org:DRESDEN/oai:qucosa:de:qucosa:85768
Date05 June 2023
CreatorsPalleis, Carla, Brendel, Matthias, Finze, Anika, Weidinger, Endy, Bötzel, Kai, Danek, Adrian, Beyer, Leonie, Nitschmann, Alexander, Kern, Maike, Biechele, Gloria, Rauchmann, Boris-Stephan, Häckert, Jan, Höllerhage, Matthias, Stephens, Andrew W., Drzezga, Alexander, van Eimeren, Thilo, Villemagne, Victor L., Schildan, Andreas, Barthel, Henryk, Patt, Marianne, Sabri, Osama, for Tauopathies (GII4T), German Imaging Initiative, Bartenstein, Peter, Perneczky, Robert, Haass, Christian, Levin, Johannes, Höglinger, Günter U.
PublisherWiley-Blackwell
Source SetsHochschulschriftenserver (HSSS) der SLUB Dresden
LanguageEnglish
Detected LanguageEnglish
Typeinfo:eu-repo/semantics/publishedVersion, doc-type:article, info:eu-repo/semantics/article, doc-type:Text
Rightsinfo:eu-repo/semantics/openAccess
Relation0885-3185

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