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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)...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier, Inc
2018
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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. |
format | Online Article Text |
id | pubmed-5766833 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Elsevier, Inc |
record_format | MEDLINE/PubMed |
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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