Reduced blood oxygenation level dependent connectivity is related to hypoperfusion in Alzheimer's disease. Issue 7 (July 2019)

• Record Type: Journal Article
• Authors: Göttler, Jens; Preibisch, Christine; Riederer, Isabelle; Pasquini, Lorenzo; Alexopoulos, Panagiotis; Bohn, Karl Peter; Yakushev, Igor; Beller, Ebba; Kaczmarz, Stephan; Zimmer, Claus; Grimmer, Timo; Drzezga, Alexander; Sorg, Christian
• Is Part Of: Journal of cerebral blood flow & metabolism. Volume 39:Issue 7(2019)
• Page Start: 1314
• Page End: 1325
• Publication Date: 2019-07
• Subjects: Alzheimer's disease -- resting-state fMRI -- blood oxygenation level dependent-functional connectivity -- arterial spin labeling -- 18F-fluorodeoxyglucose-positron emission tomography; Cerebral circulation -- Periodicals; Brain -- Metabolism -- Periodicals; Brain -- Blood-vessels -- Periodicals; Cerebrovascular disease -- Periodicals; 612.824
• DOI: 10.1177/0271678X18759182
• Languages: English
• ISSNs: 0271-678X

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 18 F-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 18 F-fluorodeoxyglucose PET-derived hypometabolism. Data indicate that impaired vascular hemodynamic processes contribute to reduced BOLD connectivity in AD.