1. Cerebral hypoperfusion is not associated with an increase in amyloid β pathology in middle-aged or elderly people.
- Author
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Hansson O, Palmqvist S, Ljung H, Cronberg T, van Westen D, and Smith R
- Subjects
- Aged, Aged, 80 and over, Alzheimer Disease diagnostic imaging, Alzheimer Disease epidemiology, Aniline Compounds pharmacokinetics, Benzothiazoles pharmacokinetics, Brain drug effects, Carbolines pharmacokinetics, Cerebrovascular Circulation drug effects, Female, Humans, Image Processing, Computer-Assisted, Magnetic Resonance Imaging, Male, Middle Aged, Positron-Emission Tomography, Sweden epidemiology, Tomography, X-Ray Computed, Alzheimer Disease metabolism, Alzheimer Disease pathology, Amyloid beta-Peptides metabolism, Brain diagnostic imaging, Cerebrovascular Circulation physiology
- Abstract
Introduction: It is hypothesized that cerebral hypoperfusion promotes the development of Alzheimer pathology. We therefore studied whether longstanding cerebral hypoperfusion is associated with Alzheimer pathology in nondemented humans., Methods: Cerebral blood flow and amyloid β (
18 F-Flutemetamol) positron emission tomography retention were assessed in eleven patients with unilateral occlusion of precerebral arteries resulting in chronic and uneven hypoperfusion. A subset of patients underwent tau (18 F-AV-1451) positron emission tomography., Results: The blood flow was significantly reduced on the affected side of the brain in patients with unilateral occlusion of the internal carotid artery or stenosis of the middle cerebral artery. However, the cortical uptake of18 F-Flutemetamol or18 F-AV-1451 was not altered., Discussion: Our results suggest that longstanding cerebral hypoperfusion in humans does not result in accumulation of amyloid β fibrils or tau aggregates., (Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.)- Published
- 2018
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