Cerebral hypoperfusion is not associated with an increase in amyloid β pathology in middle-aged or elderly people
(2018) In Alzheimer's and Dementia 14(1). p.54-61- 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... (More)
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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- author
- Hansson, Oskar LU ; Palmqvist, Sebastian LU ; Ljung, Hanna LU ; Cronberg, Tobias LU ; van Westen, Danielle LU and Smith, Ruben LU
- organization
-
- MultiPark: Multidisciplinary research focused on Parkinson´s disease
- Clinical Memory Research (research group)
- Neurobiology (research group)
- Clinical Sciences, Helsingborg
- Neurology, Lund
- Neuroradiology (research group)
- Diagnostic Radiology, (Lund)
- BioCARE: Biomarkers in Cancer Medicine improving Health Care, Education and Innovation
- Regeneration in Movement Disorders (research group)
- publishing date
- 2018
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Alzheimer's and Dementia
- volume
- 14
- issue
- 1
- pages
- 54 - 61
- publisher
- Wiley
- external identifiers
-
- scopus:85027115618
- pmid:28719802
- ISSN
- 1552-5279
- DOI
- 10.1016/j.jalz.2017.06.2265
- language
- English
- LU publication?
- yes
- id
- f6991fb2-95c3-4258-aa60-1acd18cfdc42
- date added to LUP
- 2017-08-14 13:54:59
- date last changed
- 2024-03-17 18:56:08
@article{f6991fb2-95c3-4258-aa60-1acd18cfdc42, abstract = {{<p>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.</p><p>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.</p><p>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.</p><p>DISCUSSION: Our results suggest that longstanding cerebral hypoperfusion in humans does not result in accumulation of amyloid β fibrils or tau aggregates.</p>}}, author = {{Hansson, Oskar and Palmqvist, Sebastian and Ljung, Hanna and Cronberg, Tobias and van Westen, Danielle and Smith, Ruben}}, issn = {{1552-5279}}, language = {{eng}}, number = {{1}}, pages = {{54--61}}, publisher = {{Wiley}}, series = {{Alzheimer's and Dementia}}, title = {{Cerebral hypoperfusion is not associated with an increase in amyloid β pathology in middle-aged or elderly people}}, url = {{http://dx.doi.org/10.1016/j.jalz.2017.06.2265}}, doi = {{10.1016/j.jalz.2017.06.2265}}, volume = {{14}}, year = {{2018}}, }