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Title: β-Amyloid is associated with aberrant metabolic connectivity in subjects with mild cognitive impairment
Authors: Carbonell, F
Charil, A
Zijdenbos, AP
Evans, AC
Bedell, BJ
Keywords: Positron computed tomography
Age hardening
Image processing
Issue Date: 16-Apr-2014
Publisher: SAGE Journals
Citation: Carbonell, F., Charil, A., Zijdenbos, A. P., Evans, A. C., & Bedell, B. J. (2014). β-Amyloid is associated with aberrant metabolic connectivity in subjects with mild cognitive impairment. Journal of Cerebral Blood Flow & Metabolism, 34(7), 1169. doi:10.1038/jcbfm.2014.66
Abstract: Positron emission tomography (PET) studies using [18F]2-fluoro-2-deoxyglucose (FDG) have identified a well-defined pattern of glucose hypometabolism in Alzheimer's disease (AD). The assessment of the metabolic relationship among brain regions has the potential to provide unique information regarding the disease process. Previous studies of metabolic correlation patterns have demonstrated alterations in AD subjects relative to age-matched, healthy control subjects. The objective of this study was to examine the associations between β-amyloid, apolipoprotein E ɛ4 (APOE ɛ4) genotype, and metabolic correlations patterns in subjects diagnosed with mild cognitive impairment (MCI). Mild cognitive impairment subjects from the Alzheimer's Disease Neuroimaging Initiative (ADNI) study were categorized into β-amyloid-low and β-amyloid-high groups, based on quantitative analysis of [18F]florbetapir PET scans, and APOE ɛ4 non-carriers and carriers based on genotyping. We generated voxel-wise metabolic correlation strength maps across the entire cerebral cortex for each group, and, subsequently, performed a seed-based analysis. We found that the APOE ɛ4 genotype was closely related to regional glucose hypometabolism, while elevated, fibrillar β-amyloid burden was associated with specific derangements of the metabolic correlation patterns. © 2014 International Society for Cerebral Blood Flow & Metabolism, Inc. This work is licensed under a Creative Commons Attribution 3.0
Gov't Doc #: 8694
ISSN: 1559-7016
Appears in Collections:Journal Articles

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