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IC‐P‐118: Cerebral blood flow measured with arterial spin–labeled perfusion MRI at 3T and structural brain changes in Alzheimer's disease
Author(s) -
Prins Niels,
Benedictus Marije,
Binnewijzend Maja,
Scheltens Philip,
Barkhof Frederik,
Flier Wiesje
Publication year - 2012
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2012.05.152
Subject(s) - cerebral blood flow , atrophy , arterial spin labeling , medicine , cardiology , hyperintensity , magnetic resonance imaging , white matter , perfusion , neurodegeneration , pathology , nuclear medicine , disease , radiology
drawn around these voxels, and glucose metabolism (measured using FDG-PET) and amyloid deposition (PIB-PET) values were extracted for each ROI. Multiple regressions were performed in SPM to assess where glucose metabolism and amyloid deposition across the brain correlates with FDG and PIB uptake, respectively, in each ROI. Analyses were conducted with all subjects pooled together, adjusting for age, gender, education and mini-mental state examination (MMSE) score. Results: FDG in the three ROIs produced distinct patterns of covariance (Figure top), greatly overlapping with regions and functional networks typically associated with each syndrome used to generate the ROIs. Regions where glucose hypometabolism correlated with FDG in the EOAD region were found bilaterally in temporoparietal and frontal areas, whilst FDG uptake in the AD-LANG ROI mainly correlated with hypometabolism in left hemisphere temporoparietal regions, and FDG in the AD-VIS ROI correlated with bilateral occipitoparietal regions. In contrast, PIB uptake in the three ROIs showed diffuse covariance patterns across the brain, with great overlap between the three correlation maps (Figure bottom). Conclusions: Regions targeted in AD clinical variants showed distinct FDG covariance patterns that corresponded with expected functional networks. In contrast, PIB uptake covaried diffusely across the brain. We hypothesize that AD syndromes are associated with degeneration of specific networks, and that anatomic differences between AD variants are not explained by distinctions in the regional deposition of amyloid.