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J Stroke Cerebrovasc Dis. 2014 May-Jun;23(5):958-66. doi: 10.1016/j.jstrokecerebrovasdis.2013.08.004. Epub 2014 Feb 28.

Blood viscosity in subcortical vascular mild cognitive impairment with versus without cerebral amyloid burden.

Author information

  • 1Department of Neurology, Sungkyunkwan University School of Medicine, Samsung Medical Center, Seoul, Korea.
  • 2Department of Neurology, Sungkyunkwan University School of Medicine, Samsung Medical Center, Seoul, Korea. Electronic address: sangwonseo@empal.com.
  • 3Department of Bio and Brain Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Korea.
  • 4Department of Cardiology, Sungkyunkwan University School of Medicine, Samsung Medical Center, Seoul, Korea.
  • 5Department of Neurology, Inha University School of Medicine, Incheon, Korea.
  • 6Department of Neurology, Gachon University Gil Medical Center, Incheon, Korea.
  • 7Department of Brain Repair and Rehabilitation, University College of London Institute of Neurology, Queen Square, London, UK.

Abstract

BACKGROUND:

Subcortical vascular dementia (SVaD) is a common form of dementia, attributed to ischemic small-vessel disease. Blood viscosity (BV) may contribute to the pathophysiology of SVaD. However, SVaD patients with coexisting amyloid deposition may not show differences in BV because their small-vessel disease may result from amyloid angiopathy independently of BV. We, therefore, hypothesized that BV might show different changes compared with control subjects in subcortical vascular mild cognitive impairment (svMCI) that refers to the prodromal stage of SVaD according to cerebral amyloid burden detected by the [(11)C] Pittsburgh compound B (PiB) PET (positron emission tomography), and apolipoprotein 4 (ApoE4) genotype (a known risk factor for vascular and parenchymal amyloid).

METHODS:

Our subjects consisted of 33 healthy normal controls (NC), 28 patients with PiB(-) svMCI, and 12 with PiB(+) svMCI. They underwent scanning capillary tube viscometer measuring BV during systolic and diastolic phases.

RESULTS:

Compared with the NC group, the PiB(-) svMCI group showed increased diastolic blood viscosity (DBV) but no difference in systolic blood viscosity (SBV). By contrast, there was no significant difference in SBV and DBV between the NC and PiB(+) svMCI groups. Within the PiB(+) svMCI group, ApoE4(-) subgroup showed increased DBV compared with the ApoE4(+) subgroup.

CONCLUSIONS:

Increased DBV is an important contributor to the development of "pure" svMCI (ie, without cerebral amyloid deposition). The relationship between BV and PiB(+) svMCI differed according to ApoE genotype, suggesting that the pathogenesis of PiB(+) svMCI might also be heterogeneous.

Copyright © 2014 National Stroke Association. Published by Elsevier Inc. All rights reserved.

KEYWORDS:

Hemodynamic; MRI; amyloid; artherosclerosis; vascular dementia

PMID:
24589034
[PubMed - indexed for MEDLINE]
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