Finze, Anika and Biechele, Gloria and Rauchmann, Boris-Stephan and Franzmeier, Nicolai and Palleis, Carla and Katzdobler, Sabrina and Weidinger, Endy and Guersel, Selim and Schuster, Sebastian and Harris, Stefanie and Schmitt, Julia and Beyer, Leonie and Gnoerich, Johannes and Lindner, Simon and Albert, Nathalie L. and Wetzel, Christian H. and Rupprecht, Rainer and Rominger, Axel and Danek, Adrian and Burow, Lena and Kurz, Carolin and Tato, Maia and Utecht, Julia and Papazov, Boris and Zaganjori, Mirlind and Trappmann, Lena-Katharina and Goldhardt, Oliver and Grimmer, Timo and Haeckert, Jan and Janowitz, Daniel and Buerger, Katharina and Keeser, Daniel and Stoecklein, Sophia and Dietrich, Olaf and Morenas-Rodriguez, Estrella and Barthel, Henryk and Sabri, Osama and Bartenstein, Peter and Simons, Mikael and Haass, Christian and Hoeglinger, Gunter U. and Levin, Johannes and Perneczky, Robert and Brendel, Matthias (2023) Individual regional associations between Aβ-, tau- and neurodegeneration (ATN) with microglial activation in patients with primary and secondary tauopathies. MOLECULAR PSYCHIATRY, 28. pp. 4438-4450. ISSN 1359-4184, 1476-5578
Full text not available from this repository. (Request a copy)Abstract
& beta;-amyloid (A & beta;) and tau aggregation as well as neuronal injury and atrophy (ATN) are the major hallmarks of Alzheimer's disease (AD), and biomarkers for these hallmarks have been linked to neuroinflammation. However, the detailed regional associations of these biomarkers with microglial activation in individual patients remain to be elucidated. We investigated a cohort of 55 patients with AD and primary tauopathies and 10 healthy controls that underwent TSPO-, A & beta;-, tau-, and perfusion-surrogate-PET, as well as structural MRI. Z-score deviations for 246 brain regions were calculated and biomarker contributions of A & beta; (A), tau (T), perfusion (N1), and gray matter atrophy (N2) to microglial activation (TSPO, I) were calculated for each individual subject. Individual ATN-related microglial activation was correlated with clinical performance and CSF soluble TREM2 (sTREM2) concentrations. In typical and atypical AD, regional tau was stronger and more frequently associated with microglial activation when compared to regional A & beta; (AD: & beta;(T) = 0.412 & PLUSMN; 0.196 vs. & beta;(A) = 0.142 & PLUSMN; 0.123, p < 0.001; AD-CBS: & beta;(T) = 0.385 & PLUSMN; 0.176 vs. & beta;(A) = 0.131 & PLUSMN; 0.186, p = 0.031). The strong association between regional tau and microglia reproduced well in primary tauopathies (& beta;(T) = 0.418 & PLUSMN; 0.154). Stronger individual associations between tau and microglial activation were associated with poorer clinical performance. In patients with 4RT, sTREM2 levels showed a positive association with tau-related microglial activation. Tau pathology has strong regional associations with microglial activation in primary and secondary tauopathies. Tau and A & beta; related microglial response indices may serve as a two-dimensional in vivo assessment of neuroinflammation in neurodegenerative diseases.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | PROGRESSIVE SUPRANUCLEAR PALSY; BLOOD-BRAIN-BARRIER; ALZHEIMERS-DISEASE; NEUROINFLAMMATION; BINDING; ACCUMULATION; PRINCIPLES; DIAGNOSIS; AFFINITY; MOCA |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Psychiatrie und Psychotherapie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 14 May 2024 12:37 |
| Last Modified: | 15 May 2024 04:23 |
| URI: | https://pred.uni-regensburg.de/id/eprint/60644 |
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