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Background: Deficit of memory function is a main symptom found in Alzheimer disease (AD) even in the early stage of disease. Since the hippocampus is a critical area for memory function, hippocampal atrophy can serve as a biomarker of AD. To identify whether the hippocampus connectivity may change as the disease progress in patients with AD, interregional-connectivity analysis were conducted using [18F]fluorodeoxyglucose (FDG)-positron emission tomography (PET) and statistical parametric mapping (SPM). Materials and methods: We examined metabolic correlation of the ippocampus using a sample of 72 AD patients who had undergone FDG-PET. Count normalized regional FDG activities were extracted from left and right hippocampi using the pre-identified region of interest (ROI) by automated anatomical labeling (AAL) and MarsBar toolbox implanted in SPM2. Inter-regional analyses using the left or right hippocampus as seeds were conducted in each CDR group (0.5, 1, and 2/3). Normalized mean radioactive counts from left or right hippocampus were used as independent variables in a general linear model to search for voxels correlated with seed area across the whole brain. Results: In CDR 0.5 group, both left and right hippocampal seeds yielded correlations that were limited to themselves; there was no correlation in contralateral homologous regions or any other cortical/subcortical regions. In CDR 1 group, however, the left and right hippocampal seeds yielded positive correlation in ipsilateral temporal cortex, visual cortex and frontal motor areas. In CDR 2/3 group, distinctive hippocampal metabolic connectivity patterns in each hemisphere were found. Left hippocampal seed yielded correlations that were limited to itself, while right hippocampus showed enlarged correlations in temporal cortex and occipital visual cortex as well as frontal cortex including orbitofrontal cortex and basal ganglia. Conclusions: The changes in the hippocampal communication loop we observed in this study may reflect changes in local neuroplasticity according to the progression of AD. Our results may have implication for understanding the decline and compensation mechanism of memory function in AD patients

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