Glucose Hypometabolism in Hippocampal Subdivisions in Alzheimer's Disease: A Pilot Study Using High-Resolution ¹⁸F-FDG PET and 7.0-T MRI

J Clin Neurol. 2018 Apr;14(2):158-164. doi: 10.3988/jcn.2018.14.2.158.

Abstract

Background and purpose: Atrophy of the hippocampus is an important clinical diagnostic marker of Alzheimer's disease (AD), and so assessments of hippocampal activity and its subdivisions might provide invaluable information. This study compared the glucose metabolism of hippocampal subdivisions in mild-AD patients and healthy controls.

Methods: High-resolution T2*-weighted gradient-echo magnetic resonance imaging (MRI) images and ¹⁸F-fluorodeoxyglucose (FDG) positron-emission tomography (PET) images were acquired using 7.0-T MRI and high-resolution research tomograph FDG-PET, respectively, in 9 early-stage AD patients and 10 healthy subjects. The hippocampal body was divided into three equal parts (anterior, middle, and posterior), and in each part a region of interest (ROI) was drawn over the cornus ammonis (CA)1, CA2/3, CA4/dentate gyrus (DG), and subiculum. The standardized uptake values of the hippocampal subdivisions were calculated for each ROI as ratios relative to the pons standardized uptake value. Statistical analysis was conducted using the Mann-Whitney U test.

Results: Patients with early-stage AD patients showed significantly less metabolic activity than healthy controls focally in the middle (p=0.050) and posterior (p=0.034) CA2/3 regions of the right hippocampus, and significantly less activity throughout the left hippocampal body in the anterior CA2/3 (p=0.027) and CA4/DG (p=0.027) regions, the middle CA1 region (p=0.011), and the posterior CA1 (p=0.034), CA2/3 (p=0.007), and CA4/DG (p=0.014) regions.

Conclusions: It was possible to use high-resolution PET-MRI fusion images to identify hippocampus subdivisions and assess glucose metabolism in the subfields. Reductions in metabolic activity were found to vary along the hippocampal axis in early-stage AD patients.

Keywords: Alzheimer's disease; fluorodeoxyglucose; hippocampus; hypometabolism.