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Cerebral hypoperfusion is not associated with an increase in amyloid β pathology in middle-aged or elderly people

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)...

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Autores principales: Hansson, Oskar, Palmqvist, Sebastian, Ljung, Hanna, Cronberg, Tobias, van Westen, Danielle, Smith, Ruben
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier, Inc 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5766833/
https://www.ncbi.nlm.nih.gov/pubmed/28719802
http://dx.doi.org/10.1016/j.jalz.2017.06.2265
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author Hansson, Oskar
Palmqvist, Sebastian
Ljung, Hanna
Cronberg, Tobias
van Westen, Danielle
Smith, Ruben
author_facet Hansson, Oskar
Palmqvist, Sebastian
Ljung, Hanna
Cronberg, Tobias
van Westen, Danielle
Smith, Ruben
author_sort Hansson, Oskar
collection PubMed
description 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 of (18)F-Flutemetamol or (18)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.
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spelling pubmed-57668332018-01-18 Cerebral hypoperfusion is not associated with an increase in amyloid β pathology in middle-aged or elderly people Hansson, Oskar Palmqvist, Sebastian Ljung, Hanna Cronberg, Tobias van Westen, Danielle Smith, Ruben Alzheimers Dement Article 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 of (18)F-Flutemetamol or (18)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. Elsevier, Inc 2018-01 /pmc/articles/PMC5766833/ /pubmed/28719802 http://dx.doi.org/10.1016/j.jalz.2017.06.2265 Text en © 2017 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Article
Hansson, Oskar
Palmqvist, Sebastian
Ljung, Hanna
Cronberg, Tobias
van Westen, Danielle
Smith, Ruben
Cerebral hypoperfusion is not associated with an increase in amyloid β pathology in middle-aged or elderly people
title Cerebral hypoperfusion is not associated with an increase in amyloid β pathology in middle-aged or elderly people
title_full Cerebral hypoperfusion is not associated with an increase in amyloid β pathology in middle-aged or elderly people
title_fullStr Cerebral hypoperfusion is not associated with an increase in amyloid β pathology in middle-aged or elderly people
title_full_unstemmed Cerebral hypoperfusion is not associated with an increase in amyloid β pathology in middle-aged or elderly people
title_short Cerebral hypoperfusion is not associated with an increase in amyloid β pathology in middle-aged or elderly people
title_sort cerebral hypoperfusion is not associated with an increase in amyloid β pathology in middle-aged or elderly people
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5766833/
https://www.ncbi.nlm.nih.gov/pubmed/28719802
http://dx.doi.org/10.1016/j.jalz.2017.06.2265
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