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Updated: Jul 11, 2025
Detecting Amyloid-β Accumulation via Immunofluorescent Staining in a Mouse Model of Alzheimer's Disease
Published on: April 19, 2021
[18F]-FDG uptake in brain slices prepared from an aged mouse model of Alzheimer's disease using a dynamic
Hiroko Maruyama1, Misaki Gomi2, Thet-Thet Lwin3
1Cytopathology, Graduate School of Medical Sciences, School of Allied Health Sciences, Kitasato University, 1-15-1 Kitasato, Minami-ku, Sagamihara, 252-0373, Japan. maruyama@ahs.kitasato-u.ac.jp.
Objective:
2-[18F]fluoro-2-deoxy-D-glucose positron emission tomography ([18F]-FDG-PET) is a imaging modality that has been used to measure of glucose metabolism in the brain in Alzheimer's disease (AD). Clinically, decreased glucose uptake has been reported in the brain of AD, although the precise underlying mechanisms have not yet been elucidated. To elucidate the mechanisms of decreased [18F]-FDG uptake in the AD by PET, [18F]-FDG uptake in the brain of aged model mouse of AD was investigated using a dynamic autoradiography technique "bioradiography". A X-ray phase-contrast imaging (X-PCI) and a histopathological evaluation were also investigated to elucidate the mechanisms underlying the relationships between decreased [18F]-FDG uptake and the pathological changes in the brain of AD mouse.
Methods:
In this study, AD model mouse (5XFAD, APP+/PS1+) were used. [18F]-FDG-bioradiography was conducted in fresh slices of brain tissue under the condition of resting (slices immersed in 5 mM K+ solution) and metabolically active (in 50 mM K+ solution). Amyloid β42 (Aβ42) deposition in the brain of AD mouse was confirmed by X-PCI. In addition, the positive cells of phosphated tau protein (P-tau) and deposition of Aβ42 were also examined by immunohistochemical staining.
Results:
No significant differences were observed between the two groups in the resting condition. In the activate condition of the brain, [18F]-FDG uptake was significantly decreased in AD mice compared to WT mice. In X-PCI showed Aβ deposition in the AD mouse, but not in the WT. The AD mouse also showed increased P-tau, accumulation of Aβ42, increase in neuronal apoptosis, and decrease in the number of neurons than that of the WT mouse.
Conclusion:
Neuronal damage, and induction of neuronal apoptosis, decreased [18F]-FDG uptake, increased Aβ accumulation and P-tau induced neurofibrillary degeneration are observed in AD mouse. In clinical diagnosis, reduction of [18F]-FDG uptake by PET is one of the means of diagnosing the onset of AD. Our results suggest that decreased uptake of [18F]-FDG in the brains of AD may be associated with neuronal dysfunction and cell death in the brain.
