152434 - Neurovascular coupling.pdf (1.62 MB)
Download fileNeurovascular coupling mechanisms in health and neurovascular uncoupling in Alzheimer's disease
journal contribution
posted on 2023-05-21, 12:05 authored by Zhu, W, Neuhaus, A, Beard, DJ, Brad SutherlandBrad Sutherland, DeLuca, GCTo match the metabolic demands of the brain, mechanisms have evolved to couple neuronal activity to vasodilation, thus increasing local cerebral blood flow and delivery of oxygen and glucose to active neurons. Rather than relying on metabolic feedback signals such as the consumption of oxygen or glucose, the main signalling pathways rely on the release of vasoactive molecules by neurons and astrocytes, which act on contractile cells. Vascular smooth muscle cells and pericytes are the contractile cells associated with arterioles and capillaries, respectively, which relax and induce vasodilation. Much progress has been made in understanding the complex signalling pathways of neurovascular coupling, but issues such as the contributions of capillary pericytes and astrocyte calcium signal remain contentious. Study of neurovascular coupling mechanisms is especially important as cerebral blood flow dysregulation is a prominent feature of Alzheimer's disease. In this article we will discuss developments and controversies in the understanding of neurovascular coupling and finish by discussing current knowledge concerning neurovascular uncoupling in Alzheimer's disease.
Funding
National Health & Medical Research Council
History
Publication title
Brain: A Journal of NeurologyVolume
145Issue
7Pagination
2276-2292ISSN
0006-8950Department/School
Tasmanian School of MedicinePublisher
Oxford Univ PressPlace of publication
Great Clarendon St, Oxford, England, Ox2 6DpRights statement
Copyright 2022 The Author(s). This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly citedRepository Status
- Open