Paul Préfontaine
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Paul Préfontaine has a total of 3 co-authors. Here are the top co-authors by number of shared publications:
- Ayman ElAli
Neuroscience Laboratory, CHU de Québec Research Center and Department of Molecular Medicine, Faculty of Medicine, Laval University, 2705 Laurier boul., Québec City, QC G1V 4G2, Canada
1 shared publication - Peter Thériault
Neuroscience Laboratory, CHU de Québec Research Center and Department of Molecular Medicine, Faculty of Medicine, Laval University, 2705 Laurier boul., Québec City, QC G1V 4G2, Canada
1 shared publication - Serge Rivest
Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Department of Molecular Medicine, Faculty of Medicine, Laval University, Quebec City, QC, Canada
1 shared publication
Latest Publications
- Open Access
- 13 November 2013
- Published by Springer Nature in Acta Neuropathologica Communications
- Vol. 1 (1) , 75
Mild chronic cerebral hypoperfusion induces neurovascular dysfunction, triggering peripheral beta-amyloid brain entry and aggregation
The Blood–brain barrier (BBB) controls brain supply with oxygen and nutrients, and protects the brain from toxic metabolites, such as beta-amyloid (Aβ) peptides. The neurovascular unit (NVU) couples vascular and neuronal functions by controlling BBB parameters based on brain needs. As such, NVU/BBB dysfunction, associated to irregularities in cerebral blood flow (CBF), has been proposed to contribute in the pathogenesis of Alzheimer’s disease (AD), mainly by impairing cerebral Aβ clearance. However, the spatiotemporal contribution of the NVU/BBB in the neurodegenerative cascades remains elusive.
- 13 November 2013
- Published by Springer Nature in Acta Neuropathologica Communications
- Vol. 1 (1) , 75
Open AccessMild chronic cerebral hypoperfusion induces neurovascular dysfunction, triggering peripheral beta-amyloid brain entry and aggregation
The Blood–brain barrier (BBB) controls brain supply with oxygen and nutrients, and protects the brain from toxic metabolites, such as beta-amyloid (Aβ) peptides. The neurovascular unit (NVU) couples vascular and neuronal functions by controlling BBB parameters based on brain needs. As such, NVU/BBB dysfunction, associated to irregularities in cerebral blood flow (CBF), has been proposed to contribute in the pathogenesis of Alzheimer’s disease (AD), mainly by impairing cerebral Aβ clearance. However, the spatiotemporal contribution of the NVU/BBB in the neurodegenerative cascades remains elusive.