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

Hansson, Oskar LU ; Palmqvist, Sebastian LU ; Ljung, Hanna LU ; Cronberg, Tobias LU ; van Westen, Danielle LU and Smith, Ruben LU (2017) In Alzheimer's and Dementia
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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organization
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Contribution to journal
publication status
epub
subject
keywords
Journal Article
in
Alzheimer's and Dementia
publisher
Elsevier
external identifiers
  • scopus:85027115618
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
2017-09-20 04:00:30
@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},
  keyword      = {Journal Article},
  language     = {eng},
  month        = {07},
  publisher    = {Elsevier},
  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},
  year         = {2017},
}