| Literature DB >> 29431005 |
Jens Göttler1,2, Christine Preibisch1,2,3, Isabelle Riederer1,2, Lorenzo Pasquini2,4, Panagiotis Alexopoulos5, Karl Peter Bohn6, Igor Yakushev2,6, Ebba Beller7, Stephan Kaczmarz1,2, Claus Zimmer1, Timo Grimmer2,5, Alexander Drzezga6,8, Christian Sorg1,2,5.
Abstract
Functional connectivity of blood oxygenation level dependent signal fluctuations (BOLD-FC) is decreased in Alzheimer's disease (AD), and suggested to reflect reduced coherence in neural population activity; however, as both neuronal and vascular-hemodynamic processes underlie BOLD signals, impaired perfusion might also contribute to reduced BOLD-FC; 42 AD patients and 27 controls underwent simultaneous PET/MR imaging. Resting-state functional MRI assessed BOLD co-activity to quantify BOLD-FC, pulsed arterial spin labeling (pASL) assessed cerebral blood flow (CBF) as proxy for vascular hemodynamics, and 18F-fluorodeoxyglucose PET assessed glucose metabolism (GluMet) to index neuronal activity. Patients' BOLD-FC, CBF, and GluMet were reduced within the same precuneal parietal regions. BOLD-FC was positively associated with mean CBF, specifically in patients and controlled for GluMet levels, suggesting that BOLD-FC reductions correlate with pASL-derived hypoperfusion in AD, independently from 18F-fluorodeoxyglucose PET-derived hypometabolism. Data indicate that impaired vascular hemodynamic processes contribute to reduced BOLD connectivity in AD.Entities:
Keywords: Alzheimer’s disease; F-fluorodeoxyglucose-positron emission tomography; arterial spin labeling; blood oxygenation level dependent-functional connectivity; resting-state fMRI
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Year: 2018 PMID: 29431005 PMCID: PMC6668525 DOI: 10.1177/0271678X18759182
Source DB: PubMed Journal: J Cereb Blood Flow Metab ISSN: 0271-678X Impact factor: 6.200