Journal of Alzheimer's disease reports · 2025
Higher cerebellum florbetapir uptake in cerebral amyloid angiopathy compared to Alzheimer's disease: A dual florbetapir and FDG PET study.
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Sha Yuhui, Jia Chenhao, Liang Menglin, Wu Juanjuan, Zhang Tianhao, Zhu Yicheng, Yuan Jing, Li Qijun, Huang Zhaoxia, Cui Ruixue, Ni Jun
Аннотация
BACKGROUND: Amyloid-β (Aβ) is the primary amyloidogenic protein involved in various diseases associated with cognitive dysfunction, including Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA).
OBJECTIVE: This cross-sectional study aimed to investigate the characteristics of 18F-florbetapir PET, which detects Aβ deposition, and 18F-FDG PET, which measures glucose metabolism in patients with CAA and AD.
METHODS: 30 patients with AD, 37 with probable CAA, and 14 control subjects (CSs) underwent 18F-florbetapir and 18F-FDG PET imaging within a one-month period. Region of interest and voxel-wise analyses were performed to compare Aβ deposition and glucose metabolism patterns among the three study groups. Standardized uptake value ratios were calculated using brainstem as the reference region for 18F-florbetapir and 18F-FDG PET, respectively.
RESULTS: Patients with CAA exhibited significantly higher 18F-florbetapir uptake in the cerebellum, global cerebral cortex, and various cortical regions compared to CSs. Compared to patients with AD, those with CAA showed predominantly higher 18F-florbetapir uptake in the cerebellum but lower uptake in the insular cortex and posterior cingulate gyrus. Glucose hypometabolism patterns in CAA did not differ significantly from those observed in AD.
CONCLUSIONS: Distinct Aβ deposition patterns, particularly the increased amyloid burden in the cerebellum, could serve as a valuable biomarker for differentiating CAA from AD.
OBJECTIVE: This cross-sectional study aimed to investigate the characteristics of 18F-florbetapir PET, which detects Aβ deposition, and 18F-FDG PET, which measures glucose metabolism in patients with CAA and AD.
METHODS: 30 patients with AD, 37 with probable CAA, and 14 control subjects (CSs) underwent 18F-florbetapir and 18F-FDG PET imaging within a one-month period. Region of interest and voxel-wise analyses were performed to compare Aβ deposition and glucose metabolism patterns among the three study groups. Standardized uptake value ratios were calculated using brainstem as the reference region for 18F-florbetapir and 18F-FDG PET, respectively.
RESULTS: Patients with CAA exhibited significantly higher 18F-florbetapir uptake in the cerebellum, global cerebral cortex, and various cortical regions compared to CSs. Compared to patients with AD, those with CAA showed predominantly higher 18F-florbetapir uptake in the cerebellum but lower uptake in the insular cortex and posterior cingulate gyrus. Glucose hypometabolism patterns in CAA did not differ significantly from those observed in AD.
CONCLUSIONS: Distinct Aβ deposition patterns, particularly the increased amyloid burden in the cerebellum, could serve as a valuable biomarker for differentiating CAA from AD.