11C-PIB PET and 18F-FDG PET in patients with Alzheimer's disease and amnestic mild cognitive impairment

Zhihong Shi, Ying Wang, Shuai Liu, Shuling Liu, Yuying Zhou, Jinhuan Wang, Li Cai, Shuo Gao, Yong Ji

Abstract


Objective The present study investigated the relationship between amyloid deposition and glucose metabolism using Pittsburgh compound B (11C-PIB) and fluorodeoxyglucose (18F-FDG) positron-emission tomography (PET) in patients with Alzheimer's disease (AD) and amnestic mild cognitive impairment (aMCI) and assessed the apolipoprotein E (ApoE) ε4 allele to explore the correlation between aMCI and AD.  Methods Amyloid load in the brain and cerebral glucose metabolism were determined and ApoE genotypes were analyzed in patients with AD (N = 14), aMCI (N = 10), and healthy controls (N = 5).  Results The mean 11C-PIB standardized uptake value ratio (SUVR) was higher in inferior parietal lobe, lateral temporal cortex, frontal cortex, posterior cingulate cortex and precuneus, occipital lobe, and striatum in AD patients compared with controls (P < 0.05). 11C-PIB binding levels in aMCI patients were bimodal. No significant difference in the 11C-PIB SUVR was found between the 11C-PIB + aMCI subgroup and AD group (P > 0.05). 18F-FDG PET revealed hypometabolism in bilateral parietal lobes, temporal lobe, and precuneus in 3 of 5 11C-PIB + aMCI subjects, including two of them with ApoE ε 4 allele converted to AD, and hypometabolism in the bilateral frontal lobe and anterior cingulate in 3 of 5 11C-PIB - aMCI subjects.  Conclusions 11C-PIB PET is a powerful tool for screening aMCI with AD pathology. The aMCI patients with AD pathology who presented hypometabolism in the parietal lobe, lateral temporal cortex, precuneus and with ApoE ε 4 allele are more likely to convert to clinical AD dementia.

 

doi: 10.3969/j.issn.1672-6731.2014.03.013


Keywords


Alzheimer disease; Cognition disorders; Apolipoprotein E4; Radioactive tracers; Positron-emission tomography

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