Increased cerebral blood volume in small arterial vessels is a correlate of amyloid-β-related cognitive decline.
Journal article

Increased cerebral blood volume in small arterial vessels is a correlate of amyloid-β-related cognitive decline.

  • Hua J Neurosection, Division of MRI Research, Department of Radiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute, Baltimore, MD, USA.
  • Lee S Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD, USA.
  • Blair NIS Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD, USA.
  • Wyss M Institute for Biomedical Engineering, University of Zurich and ETH Zurich, Zurich, Switzerland.
  • van Bergen JMG Institute for Regenerative Medicine (IREM), University of Zurich, Schlieren, Switzerland.
  • Schreiner SJ Institute for Regenerative Medicine (IREM), University of Zurich, Schlieren, Switzerland; Hospital for Psychogeriatric Medicine, Psychiatric University Hospital Zurich (PUK), Zurich, Switzerland.
  • Kagerer SM Institute for Regenerative Medicine (IREM), University of Zurich, Schlieren, Switzerland; Hospital for Psychogeriatric Medicine, Psychiatric University Hospital Zurich (PUK), Zurich, Switzerland.
  • Leh SE Institute for Regenerative Medicine (IREM), University of Zurich, Schlieren, Switzerland.
  • Gietl AF Institute for Regenerative Medicine (IREM), University of Zurich, Schlieren, Switzerland.
  • Treyer V Institute for Regenerative Medicine (IREM), University of Zurich, Schlieren, Switzerland; Department of Nuclear Medicine, University Hospital Zurich, Switzerland.
  • Buck A Department of Nuclear Medicine, University Hospital Zurich, Switzerland.
  • Nitsch RM Institute for Regenerative Medicine (IREM), University of Zurich, Schlieren, Switzerland.
  • Pruessmann KP Institute for Biomedical Engineering, University of Zurich and ETH Zurich, Zurich, Switzerland.
  • Lu H Neurosection, Division of MRI Research, Department of Radiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute, Baltimore, MD, USA.
  • Van Zijl PCM Neurosection, Division of MRI Research, Department of Radiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute, Baltimore, MD, USA.
  • Albert M Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  • Hock C Institute for Regenerative Medicine (IREM), University of Zurich, Schlieren, Switzerland.
  • Unschuld PG Institute for Regenerative Medicine (IREM), University of Zurich, Schlieren, Switzerland; Hospital for Psychogeriatric Medicine, Psychiatric University Hospital Zurich (PUK), Zurich, Switzerland. Electronic address: Paul.unschuld@uzh.ch.
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  • 2019-02-10
Published in:
  • Neurobiology of aging. - 2019
English The protracted accumulation of amyloid-β (Aβ) is a major pathologic hallmark of Alzheimer's disease and may trigger secondary pathological processes that include neurovascular damage. This study was aimed at investigating long-term effects of Aβ burden on cerebral blood volume of arterioles and pial arteries (CBVa), possibly present before manifestation of dementia. Aβ burden was assessed by 11C Pittsburgh compound-B positron emission tomography in 22 controls and 18 persons with mild cognitive impairment (MCI), [ages: 75(±6) years]. After 2 years, inflow-based vascular space occupancy at ultra-high field strength of 7-Tesla was administered for measuring CBVa, and neuropsychological testing for cognitive decline. Crushing gradients were incorporated during MR-imaging to suppress signals from fast-flowing blood in large arteries, and thereby sensitize inflow-based vascular space occupancy to CBVa in pial arteries and arterioles. CBVa was significantly elevated in MCI compared to cognitively normal controls and regional CBVa related to local Aβ deposition. For both MCI and controls, Aβ burden and follow-up CBVa in several brain regions synergistically predicted cognitive decline over 2 years. Orbitofrontal CBVa was positively associated with apolipoprotein E e4 carrier status. Increased CBVa may reflect long-term effects of region-specific pathology associated with Aβ deposition. Additional studies are needed to clarify the role of the arteriolar system and the potential of CBVa as a biomarker for Aβ-related vascular downstream pathology.
Language
  • English
Open access status
hybrid
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https://sonar.ch/global/documents/122013
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