Microglial activation states drive glucose uptake and FDG-PET alterations in neurodegenerative diseases
Xianyuan Xiang, Karin Wind, Thomas Wiedemann, Tanja Blume, Yuan Shi, Nils Briel, Leonie Beyer, Gloria Biechele, Florian Eckenweber, Artem Zatcepin, Sven Lammich, Sara Ribičić, Sabina Tahirović, Michael Willem, Maximilian Deußing, Carla Palleis, Boris‐Stephan Rauchmann, Franz‐Josef Gildehaus, Simon Lindner, Charlotte Spitz, Nicolai Franzmeier, Karlheinz Baumann, Axel Rominger, Peter Bartenstein, Sibylle Ziegler, Alexander Drzezga, Gesine Respondek, Katharina Büerger, Robert Perneczky, Johannes Levin, Günter U. Höglinger, Jochen Herms, Christian Haass, Matthias Brendel
Abstract
F-GE-180 18-kDa translocator protein PET (TSPO-PET) in preserved brain regions, indicating that the cerebral glucose uptake in humans is also strongly influenced by microglial activity. Our findings suggest that microglia activation states are responsible for FDG-PET signal alterations in patients with neurodegenerative diseases and mouse models for amyloidosis. Microglial activation states should therefore be considered when performing FDG-PET.