PT  - JOURNAL ARTICLE
AU  - Sacher, Christian
AU  - Blume, Tanja
AU  - Beyer, Leonie
AU  - Biechele, Gloria
AU  - Sauerbeck, Julia
AU  - Eckenweber, Florian
AU  - Deussing, Maximilian
AU  - Focke, Carola
AU  - Parhizkar, Samira
AU  - Lindner, Simon
AU  - Gildehaus, Franz-Josef
AU  - von Ungern-Sternberg, Barbara
AU  - Baumann, Karlheinz
AU  - Tahirovic, Sabina
AU  - Kleinberger, Gernot
AU  - Willem, Michael
AU  - Haass, Christian
AU  - Bartenstein, Peter
AU  - Cumming, Paul
AU  - Rominger, Axel
AU  - Herms, Jochen
AU  - Brendel, Matthias
TI  - Asymmetry of Fibrillar Plaque Burden in Amyloid Mouse Models
AID  - 10.2967/jnumed.120.242750
DP  - 2020 Dec 01
TA  - Journal of Nuclear Medicine
PG  - 1825--1831
VI  - 61
IP  - 12
4099  - http://jnm.snmjournals.org/content/61/12/1825.short
4100  - http://jnm.snmjournals.org/content/61/12/1825.full
SO  - J Nucl Med2020 Dec 01; 61
AB  - Asymmetries of amyloid-β (Aβ) burden are well known in Alzheimer disease (AD) but did not receive attention in Aβ mouse models of Alzheimer disease. Therefore, we investigated Aβ asymmetries in Aβ mouse models examined by Aβ small-animal PET and tested if such asymmetries have an association with microglial activation. Methods: We analyzed 523 cross-sectional Aβ PET scans of 5 different Aβ mouse models (APP/PS1, PS2APP, APP-SL70, AppNL-G-F, and APPswe) together with 136 18-kDa translocator protein (TSPO) PET scans for microglial activation. The asymmetry index (AI) was calculated between tracer uptake in both hemispheres. AIs of Aβ PET were analyzed in correlation with TSPO PET AIs. Extrapolated required sample sizes were compared between analyses of single and combined hemispheres. Results: Relevant asymmetries of Aβ deposition were identified in at least 30% of all investigated mice. There was a significant correlation between AIs of Aβ PET and TSPO PET in 4 investigated Aβ mouse models (APP/PS1: R = 0.593, P = 0.001; PS2APP: R = 0.485, P = 0.019; APP-SL70: R = 0.410, P = 0.037; AppNL-G-F: R = 0.385, P = 0.002). Asymmetry was associated with higher variance of tracer uptake in single hemispheres, leading to higher required sample sizes. Conclusion: Asymmetry of fibrillar plaque neuropathology occurs frequently in Aβ mouse models and acts as a potential confounder in experimental designs. Concomitant asymmetry of microglial activation indicates a neuroinflammatory component to hemispheric predominance of fibrillary amyloidosis.