Longitudinal [18F]FDG-PET/CT analysis of the glucose metabolism in ApoE-deficient mice

EJNMMI Research

Tobias Lindner¹  Jan Stenzel¹  Bernd J. Krause²  Jens Kurth³  Stefan Teipel⁴  Änne Glass⁵  Guenther Kundt⁵  Angela Kuhla⁶  Lou Meuth⁶  Brigitte Vollmar⁷  Chris Lappe⁸ 

[1] Core Facility Multimodal Small Animal Imaging, Rostock University Medical Center, Rostock, Germany;Core Facility Multimodal Small Animal Imaging, Rostock University Medical Center, Rostock, Germany;Department of Nuclear Medicine, Rostock University Medical Center, Rostock, Germany;Department of Nuclear Medicine, Rostock University Medical Center, Rostock, Germany;German Center for Neurodegenerative Diseases (DZNE), Rostock, Greifswald, Germany;Department of Psychosomatic Medicine, Rostock University Medical Center, Rostock, Germany;Institute for Biostatistics and Informatics in Medicine and Ageing Research, Rostock University Medical Center, Rostock, Germany;Institute for Experimental Surgery, Rostock University Medical Center, Schillingallee 69a, 18057, Rostock, Germany;Institute for Experimental Surgery, Rostock University Medical Center, Schillingallee 69a, 18057, Rostock, Germany;Core Facility Multimodal Small Animal Imaging, Rostock University Medical Center, Rostock, Germany;Institute of Diagnostic and Interventional Radiology, Pediatric and Neuroradiology, Rostock University Medical Center, Rostock, Germany;German Center for Neurodegenerative Diseases (DZNE), Rostock, Greifswald, Germany;

关键词: Cerebral glucose metabolism;    [F]FDG-PET/CT imaging;    Proton magnetic resonance spectroscopy;    Brain stem;    ApoE-;   

DOI  :  10.1186/s13550-020-00711-4

来源: Springer

【 摘 要 】

BackgroundStrong line of evidence suggests that the increased risk to develop AD may at least be partly mediated by cholesterol metabolism. A key regulator of cholesterol transport is the Apolipoprotein E4 (ApoE4), which plays a fundamental role in neuronal maintenance and repair. Impaired function of ApoE4 may contribute to altered cerebral metabolism leading to higher susceptibility to neurodegeneration.MethodsTo determine a possible link between ApoE function and alterations in AD in the brain of Apolipoprotein E-deficient mice (ApoE−/−) in a longitudinal manner metabolic and neurochemical parameters were analyzed. Cortical metabolism was measured by 2-deoxy-2-[18F]fluoroglucose ([18F]FDG)-PET/CT and proton magnetic resonance spectroscopy (1H-MRS) served to record neurochemical status.ResultsBy using [18F]FDG-PET/CT, we showed that brain metabolism declined significantly stronger with age in ApoE−/− versus wild type (wt) mice. This difference was particularly evident at the age of 41 weeks in almost each analyzed brain region. In contrast, the 1H-MRS-measured N-acetylaspartate to creatine ratio, a marker of neuronal viability, did not decline with age and did not differ between ApoE−/− and wt mice.ConclusionIn summary, this longitudinal in vivo study shows for the first time that ApoE−/− mice depict cerebral hypometabolism without neurochemical alterations.

【 授权许可】

CC BY