Cerebral hypoperfusion is not associated with an increase in amyloid β pathology in middle‐aged or elderly people
Open Access
- 15 July 2017
- journal article
- research article
- Published by Wiley in Alzheimer's & Dementia
- Vol. 14 (1), 54-61
- https://doi.org/10.1016/j.jalz.2017.06.2265
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 (18F‐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 (18F‐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 of 18F‐Flutemetamol or 18F‐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.Funding Information
- H2020 European Research Council
- Vetenskapsrådet
- Hjärnfonden
- Marianne and Marcus Wallenberg Foundation
- Greta och Johan Kocks stiftelser
- Torsten Söderbergs Stiftelse
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