Work

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

Year: 2017

Type: article

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.

Source: Alzheimer s & Dementia

DOI: 10.1016/j.jalz.2017.06.2265

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

Institutions: Lund University, Skåne University Hospital

Language: English

Topic: Alzheimer's disease research and treatments

Subfield: Physiology

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: hybrid

Estimated APC paid: $4,200