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

Oskar Hansson; Sebastian Palmqvist; Hanna Ljung; Tobias Cronberg; Danielle van Westen; Ruben Smith

doi:10.1016/j.jalz.2017.06.2265

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

Oskar Hansson, Sebastian Palmqvist, Hanna Ljung, Tobias Cronberg, Danielle van Westen, Ruben Smith

Skåne University Hospital

Research output: Contribution to journal › Article › peer-review

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 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.

Original language	English
Pages (from-to)	54-61
Journal	Alzheimer's and Dementia
Volume	14
Issue number	1
Early online date	2017 Jul 15
DOIs	https://doi.org/10.1016/j.jalz.2017.06.2265
Publication status	Published - 2018

Subject classification (UKÄ)

Neurology

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10.1016/j.jalz.2017.06.2265

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

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 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.",

author = "Oskar Hansson and Sebastian Palmqvist and Hanna Ljung and Tobias Cronberg and {van Westen}, Danielle and Ruben Smith",

year = "2018",

doi = "10.1016/j.jalz.2017.06.2265",

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pages = "54--61",

journal = "Alzheimer's and Dementia",

issn = "1552-5279",

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T1 - Cerebral hypoperfusion is not associated with an increase in amyloid β pathology in middle-aged or elderly people

AU - Hansson, Oskar

AU - Palmqvist, Sebastian

AU - Ljung, Hanna

AU - Cronberg, Tobias

AU - van Westen, Danielle

AU - Smith, Ruben

PY - 2018

Y1 - 2018

N2 - 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.

AB - 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.

U2 - 10.1016/j.jalz.2017.06.2265

DO - 10.1016/j.jalz.2017.06.2265

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SN - 1552-5279

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JO - Alzheimer's and Dementia

JF - Alzheimer's and Dementia

IS - 1

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

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