Background and Purpose
Decreased glucose metabolism in the temporal and parietal lobes on [18F]fluorodeoxyglucose (FDG) PET is recognized as an early imaging marker for the Alzheimer’s disease (AD) pathology. Our objective was to investigate the effects of age on FDG PET findings in aMCI.
25 patients with aMCI at 55–86 years of age (median = 73), and 25 age and gender matched cognitively normal (CN) subjects underwent FDG PET. SPM5 was used to compare the FDG uptake in aMCI-old (>73 years) and aMCI-young (>73 years) patients to CN subjects. The findings in the aMCI-old patients were independently validated in a separate cohort of 10 aMCI and 13 CN subjects older than 73 years of age.
The pattern of decreased glucose metabolism and gray matter atrophy in the medial temporal, posterior cingulate, precuneus, lateral parietal and temporal lobes in aMCI-young subjects was consistent with the typical pattern observed in AD. The pattern of glucose metabolic changes in aMCI-old subjects was different, predominantly involving the frontal lobes and the left parietal lobe. Gray matter atrophy in aMCI-old subjects was less pronounced than the aMCI-young subjects involving the hippocampus and the basal forebrain in both hemispheres
Pathological heterogeneity may be underlying the absence of AD-like glucose metabolic changes in older compared to younger aMCI patients. This may be an important consideration for the clinical use of temporoparietal hypometabolism on FDG PET as a marker for early diagnosis of AD in aMCI.