Palleis, Carla and Sauerbeck, Julia and Beyer, Leonie and Harris, Stefanie and Schmitt, Julia and Morenas-Rodriguez, Estrella and Finze, Anika and Nitschmann, Alexander and Ruch-Rubinstein, Francois and Eckenweber, Florian and Biechele, Gloria and Blume, Tanja and Shi, Yuan and Weidinger, Endy and Prix, Catharina and Boetzel, Kai and Danek, Adrian and Rauchmann, Boris-Stephan and Stoecklein, Sophia and Lindner, Simon and Unterrainer, Marcus and Albert, Nathalie L. and Wetzel, Christian and Rupprecht, Rainer and Rominger, Axel and Bartenstein, Peter and Herms, Jochen and Perneczky, Robert and Haass, Christian and Levin, Johannes and Hoeglinger, Guenter U. and Brendel, Matthias (2021) In Vivo Assessment of Neuroinflammation in 4-Repeat Tauopathies. MOVEMENT DISORDERS, 36 (4). pp. 883-894. ISSN 0885-3185, 1531-8257
Full text not available from this repository. (Request a copy)Abstract
Background Neuroinflammation has received growing interest as a therapeutic target in neurodegenerative disorders, including 4-repeat tauopathies. Objectives The aim of this cross-sectional study was to investigate 18 kDa translocator protein positron emission tomography (PET) as a biomarker for microglial activation in the 4-repeat tauopathies corticobasal degeneration and progressive supranuclear palsy. Methods Specific binding of the 18 kDa translocator protein tracer F-18-GE-180 was determined by serial PET during pharmacological depletion of microglia in a 4-repeat tau mouse model. The 18 kDa translocator protein PET was performed in 30 patients with corticobasal syndrome (68 +/- 9 years, 16 women) and 14 patients with progressive supranuclear palsy (69 +/- 9 years, 8 women), and 13 control subjects (70 +/- 7 years, 7 women). Group comparisons and associations with parameters of disease progression were assessed by region-based and voxel-wise analyses. Results Tracer binding was significantly reduced after pharmacological depletion of microglia in 4-repeat tau mice. Elevated 18 kDa translocator protein labeling was observed in the subcortical brain areas of patients with corticobasal syndrome and progressive supranuclear palsy when compared with controls and was most pronounced in the globus pallidus internus, whereas only patients with corticobasal syndrome showed additionally elevated tracer binding in motor and supplemental motor areas. The 18 kDa translocator protein labeling was not correlated with parameters of disease progression in corticobasal syndrome and progressive supranuclear palsy but allowed sensitive detection in patients with 4-repeat tauopathies by a multiregion classifier. Conclusions Our data indicate that F-18-GE-180 PET detects microglial activation in the brain of patients with 4-repeat tauopathy, fitting to predilection sites of the phenotype. The 18 kDa translocator protein PET has a potential for monitoring neuroinflammation in 4-repeat tauopathies. (c) 2020 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | PROGRESSIVE SUPRANUCLEAR PALSY; GLUCOSE-METABOLISM; WILD-TYPE; DISEASE; BRAIN; ACTIVATION; MICROGLIA; TRACER; DEGENERATION; DIAGNOSIS; corticobasal syndrome; four‐ repeat tauopathies; progressive supranuclear palsy; sTREM2; translocator protein |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Psychiatrie und Psychotherapie |
| Depositing User: | Petra Gürster |
| Date Deposited: | 21 Apr 2021 09:06 |
| Last Modified: | 21 Apr 2021 09:06 |
| URI: | https://pred.uni-regensburg.de/id/eprint/43327 |
Actions (login required)
 |
View Item |
