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

Research output: Contribution to journalArticle


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.


External organisations
  • Skåne University Hospital
Research areas and keywords

Subject classification (UKÄ) – MANDATORY

  • Neurology
Original languageEnglish
Pages (from-to)54-61
JournalAlzheimer's and Dementia
Issue number1
Early online date2017 Jul 15
Publication statusPublished - 2018
Publication categoryResearch