Longitudinal PET Monitoring of Amyloidosis and Microglial Activation in a Second-Generation Amyloid-β Mouse Model.

ABSTRACT: Nonphysiologic overexpression of amyloid-β (Aβ) precursor protein in common transgenic Aβ mouse models of Alzheimer disease likely hampers their translational potential. The novel App^NL-G-F mouse incorporates a mutated knock-in, potentially presenting an improved model of Alzheimer disease for Aβ-targeting treatment trials. We aimed to establish serial small-animal PET of amyloidosis and neuroinflammation in App^NL-G-F mice as a tool for therapy monitoring. Methods:App^NL-G-F mice (20 homozygous and 21 heterogeneous) and 12 age-matched wild-type mice were investigated longitudinally from 2.5 to 10 mo of age with ¹⁸F-florbetaben Aβ PET and ¹⁸F-GE-180 18-kDa translocator protein (TSPO) PET.

SUBMITTER: Sacher C 

PROVIDER: S-EPMC6894380 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature