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Alzheimers Dement. 2018 Jan;14(1):54-61. doi: 10.1016/j.jalz.2017.06.2265. Epub 2017 Jul 15.

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

Author information

1
Department of Clinical Sciences Malmö, Clinical Memory Research Unit, Lund University, Malmö, Sweden; Memory Clinic, Skåne University Hospital, Malmö, Sweden. Electronic address: Oskar.Hansson@med.lu.se.
2
Department of Clinical Sciences Malmö, Clinical Memory Research Unit, Lund University, Malmö, Sweden; Department of Neurology, Skåne University Hospital, Lund, Sweden.
3
Department of Neurology, Skåne University Hospital, Lund, Sweden; Department of Clinical Sciences, Neurology, Skåne University Hospital, Lund University, Lund, Sweden.
4
Department of Clinical Sciences Lund, Diagnostic radiology, Skåne University Hospital, Lund University, Lund, Sweden.
5
Department of Clinical Sciences Malmö, Clinical Memory Research Unit, Lund University, Malmö, Sweden; Department of Neurology, Skåne University Hospital, Lund, Sweden; Department of Clinical Sciences, Neurology, Skåne University Hospital, Lund University, Lund, Sweden. Electronic address: Ruben.Smith@med.lu.se.

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 (18F-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 (18F-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 18F-Flutemetamol or 18F-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.

KEYWORDS:

Alzheimer's disease; Cerebral hypoperfusion; Pathogenesis; Tau; amyloid β

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