Spatial Patterns of Hypometabolism and Amyloid Deposition in Variants of Alzheimer’s Disease Corresponding to Brain Networks: a Prospective Cohort Study

Abstract

Purpose: To identify the most vulnerable network among typical and three variants of Alzheimer’s disease (AD) and to link amyloid-β (Aβ) deposition and downstream network dysfunction. Procedures: In this study, 38 typical AD, 11 frontal variants, 8 logopenic variants, 6 posterior variants, and 20 normal controls were enrolled. 2-(4′-[ 11 C] Methylaminophenyl)-6-hydroxybenzothiazole ([ 11 C]PIB) and 2-deoxy-2-[ 18 ]fluoro-d-glucose ([ 18 F]FDG) positron emission tomography (PET) imaging were performed. Voxel-wise statistical analysis was used for [ 18 F]FDG analysis, whereas two-sample t test was performed between each AD group and control group. Moreover, the goodness of fit (GOF) of t-maps with brain functional network templates was assessed, and the most vulnerable network in each phenotypic of AD was chosen as volume of interests (VOIs). [ 11 C]PIB binding potential (BP ND ) of VOIs were generated by using PMOD software. In addition, statistical analysis of BP ND among four types of AD in each specific network was calculated by SPSS software. Results: The hypometabolism patterns indicated that in typical and frontal variants of AD, the most vulnerable network was the left executive control network (GOF score = 4.3, 5.0). For the logopenic variant, the highest GOF score (1.9) belonged to the auditory network. For the posterior variant, the higher visual network was the most vulnerable (GOF score = 6.0). The [ 11 C]PIB BP ND showed that there were no significant differences (p > 0.05) among AD groups within the specific networks. Conclusion: The phenotypic diversity of AD correlates with specific functional network failure; however, Aβ plaques do not associate with specific network vulnerability.