| Summary: | <p><strong>Objective</strong> The present study investigated the relationship between amyloid deposition and glucose metabolism using Pittsburgh compound B (<sup>11</sup>C-PIB) and fluorodeoxyglucose (<sup>18</sup>F-FDG) positron-emission tomography (PET) in patients with Alzheimer's disease (AD) and amnestic mild cognitive impairment (aMCI) and assessed the apolipoprotein E (<em>ApoE</em>) ε4 allele to explore the correlation between aMCI and AD. <strong>Methods</strong> Amyloid load in the brain and cerebral glucose metabolism were determined and <em>ApoE</em> genotypes were analyzed in patients with AD (N = 14), aMCI (N = 10), and healthy controls (N = 5). <strong>Results </strong>The mean <sup>11</sup>C-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 (<em>P</em> < 0.05). <sup>11</sup>C-PIB binding levels in aMCI patients were bimodal. No significant difference in the <sup>11</sup>C-PIB SUVR was found between the <sup>11</sup>C-PIB + aMCI subgroup and AD group (<em>P</em> > 0.05). <sup>18</sup>F-FDG PET revealed hypometabolism in bilateral parietal lobes, temporal lobe, and precuneus in 3 of 5 <sup>11</sup>C-PIB + aMCI subjects, including two of them with <em>ApoE ε 4</em> allele converted to AD, and hypometabolism in the bilateral frontal lobe and anterior cingulate in 3 of 5 <sup>11</sup>C-PIB - aMCI subjects. <strong>Conclusions</strong> <sup>11</sup>C-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 <em>ApoE ε 4</em> allele are more likely to convert to clinical AD dementia.</p><p> </p><p>doi: 10.3969/j.issn.1672-6731.2014.03.013</p>
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