Brain glucose hypometabolism has been observed in Alzheimer’s disease (AD) patients, and is detected with
18F radiolabelled glucose, using positron emission tomography. A pathological hallmark of AD is deposition of brain β-
amyloid plaques that may influence cerebral glucose metabolism. The five times familial AD (5XFAD) mouse is a model
of brain amyloidosis exhibiting AD-like phenotypes. This study examines brain β-amyloid plaque deposition and 18FDG
uptake, to search for an early biomarker distinguishing 5XFAD from wild-type mice. Thus, brain 18FDG uptake and
plaque deposition was studied in these mice at age 2, 5 and 13 months. The 5XFAD mice demonstrated significantly reduced
brain 18FDG uptake at 13 months relative to wild-type controls but not in younger mice, despite substantial β-
amyloid plaque deposition. However, by comparing the ratio of uptake values for glucose in different regions in the same
brain, 5XFAD mice could be distinguished from controls at age 2 months. This method of measuring altered glucose metabolism
may represent an early biomarker for the progression of amyloid deposition in the brain. We conclude that brain
18FDG uptake can be a sensitive biomarker for early detection of abnormal metabolism in the 5XFAD mouse when alternative
relative uptake values are utilized.
Keywords: Alzheimer's disease, β-amyloid, computed tomography, glucose metabolism, magnetic resonance imaging, positron
emission tomography, standardized uptake value, Tg6799.
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