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Background  Strong 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.    Methods  To 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-[ 18 F]fluoroglucose ([ 18 F]FDG)-PET/CT and proton magnetic resonance spectroscopy ( 1 H-MRS) served to record neurochemical status.    Results  By using [ 18 F]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  1 H-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.    Conclusion  In summary, this longitudinal in vivo study shows for the first time that  ApoE −/− mice depict cerebral hypometabolism without neurochemical alterations.

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