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Molecular Imaging and Biology

, Volume 21, Issue 1, pp 140–148 | Cite as

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

  • Ying Wang
  • Zhihong Shi
  • Nan Zhang
  • Li Cai
  • Yansheng Li
  • Hailei Yang
  • Shaobo Yao
  • Xiling Xing
  • Yong Ji
  • Shuo GaoEmail author
Research Article

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′-[11C] Methylaminophenyl)-6-hydroxybenzothiazole ([11C]PIB) and 2-deoxy-2-[18]fluoro-d-glucose ([18F]FDG) positron emission tomography (PET) imaging were performed. Voxel-wise statistical analysis was used for [18F]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). [11C]PIB binding potential (BPND) of VOIs were generated by using PMOD software. In addition, statistical analysis of BPND 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 [11C]PIB BPND 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.

Key words

Alzheimer’s disease Amyloid-β [18F]FDG [11C]PIB Positron-emission tomography 

Notes

Acknowledgements

The study was supported by the National Natural Science Foundation of China (Grant NO. 81571057 and 81501035), Tianjin Science and Technology Project (Grant NO. 16ZXMJSY00010).

Compliance with Ethical Standards

This study was approved by the Ethics Committee of Tianjin Medical University General Hospital (IRB2014–071-01).

Conflict of Interest Statement

The authors declare that they have no conflict of interest.

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Copyright information

© World Molecular Imaging Society 2018

Authors and Affiliations

  • Ying Wang
    • 1
  • Zhihong Shi
    • 2
  • Nan Zhang
    • 3
  • Li Cai
    • 1
  • Yansheng Li
    • 1
  • Hailei Yang
    • 1
  • Shaobo Yao
    • 1
  • Xiling Xing
    • 1
  • Yong Ji
    • 2
  • Shuo Gao
    • 1
    Email author
  1. 1.Department of PET-CT DiagnosticTianjin Medical University General HospitalTianjinChina
  2. 2.Tianjin Key Laboratory of Cerebrovascular and Neurodegenerative DiseasesTianjin Huanhu HospitalTianjinChina
  3. 3.Department of NeurologyTianjin Medical University General Hospital, Tianjin Neurological InstituteTianjinChina

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