Carla Palleis1,2, Matthias Brendel3,4, Johannes Levin1,2,4, Günter U Höglinger2,4,5, Anika Finze3, Endy Weidinger1,2, Kai Bötzel1, Adrian Danek1, Leonie Beyer3, Alexander Nitschmann3, Maike Kern3, Gloria Biechele3, Boris-Stephan Rauchmann6,7, Jan Häckert7, Matthias Höllerhage5, Andrew W Stephens8, Alexander Drzezga9,10,11, Thilo van Eimeren9,10,12, Victor L Villemagne13, Andreas Schildan14, Henryk Barthel14, Marianne Patt14, Osama Sabri14, Peter Bartenstein3,4, Robert Perneczky2,4,7,15, Christian Haass2,4,16. 1. Department of Neurology, Ludwig-Maximilians-University, Munich, Germany. 2. German Center for Neurodegenerative Diseases (DZNE), Munich, Germany. 3. Department of Nuclear Medicine, Ludwig-Maximilians-University, Munich, Germany. 4. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. 5. Department of Neurology, Hannover Medical School, Hannover, Germany. 6. Department of Radiology, Ludwig-Maximilians-University, Munich, Germany. 7. Department of Psychiatry and Psychotherapy, Ludwig-Maximilians-University, Munich, Germany. 8. Life Molecular Imaging GmbH, Berlin, Germany. 9. Department of Nuclear Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany. 10. German Center for Neurodegenerative Diseases (DZNE), Bonn-Cologne, Germany. 11. Institute of Neuroscience and Medicine (INM-2), Molecular Organization of the Brain, Forschungszentrum Jülich, Julich, Germany. 12. Department of Neurology, University Hospital Cologne, Cologne, Germany. 13. Department of Psychiatry, The University of Pittsburgh, Pittsburgh, Pennsylvania, USA. 14. Department of Nuclear Medicine, University of Leipzig, Leipzig, Germany. 15. Ageing Epidemiology (AGE) Research Unit, School of Public Health, Imperial College, London, United Kingdom. 16. Chair of Metabolic Biochemistry, Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-University, Munich, Germany.
Abstract
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.
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.
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