Introduction of APP induces bioenergetic deficits within an aged humanized APOE risk model of Alzheimer's disease: An FDG‐PET analysis

In a mouse cohort at a comparative human age of ∼70 years, lower brain SUVR in APP carriers coupled with lower FBG indicates bioenergetic deficits and the inability to meet energetic demands via glycolysis. This bioenergetic profile is also observed in clinical populations. Greater FKB in APP carriers suggests a shift toward utilizing fatty acids to meet bioenergetic demands. These results highlight the downstream metabolic impact of hAPP in the presence of hAPOE in these aged mice, providing important evidence for the interplay between AD genetic risk factors and bioenergetic dysfunction.