From the earliest stages of development, when cerebral angiogenesis and neurogenesis are entwined, to the end of life, the interplay between vascular and neural systems of the brain is critical in health and disease. Cerebral microvascular endothelial cells constitute the blood–brain barrier and in concert with pericytes or smooth muscle cells, glia and neurons, integrate into a functional neurovascular unit (NVU). This multicellular NVU maintains homoeostasis of the brain’s microenvironment by restricting the entry of systemic pathogens and neurotoxins as well as meeting the metabolic demands of neural activity. Recent evidence of cerebral microvascular pathologies in vascular diseases and dementia, including Alzheimer’s disease, has challenged the notion that vascular events are merely the consequence of neuronal pathology. This review focuses on molecular mechanisms of neurovascular dysfunction in dementia and outlines currently employed in vitro models to decode such mechanisms. Deciphering neurovascular crosstalk is likely to be more important in understanding the molecular mechanisms of disease than previously anticipated and may offer novel therapeutic opportunities for dementia and related conditions.
Skip Nav Destination
Article navigation
February 2018
-
Cover Image
Cover Image
A representative image of an airway from a mouse sensitized and challenged with an allergen. The histological image was captured 24 hours after allergen exposure at which point airway hyperresponsiveness persists without any discernible change to wall structure. In Clinical Science volume 132, issue 3, Wang et al. report on the effects of airway remodelling and allergy on airway responsiveness; for details see pages 327–338. Image kindly provided by Kimberley C.W. Wang (The University of Western Australia).
Review Article|
February 14 2018
Neurovascular dysfunction in dementia – human cellular models and molecular mechanisms
Isobel Parkes;
Isobel Parkes
*
1Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, U.K.
Search for other works by this author on:
Satyan Chintawar;
Satyan Chintawar
*
1Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, U.K.
Search for other works by this author on:
M. Zameel Cader
1Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, U.K.
Correspondence: M. Zameel Cader ([email protected])
Search for other works by this author on:
Publisher: Portland Press Ltd
Received:
July 17 2017
Revision Received:
January 15 2018
Accepted:
January 19 2018
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© 2018 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society
2018
Clin Sci (Lond) (2018) 132 (3): 399–418.
Article history
Received:
July 17 2017
Revision Received:
January 15 2018
Accepted:
January 19 2018
Citation
Isobel Parkes, Satyan Chintawar, M. Zameel Cader; Neurovascular dysfunction in dementia – human cellular models and molecular mechanisms. Clin Sci (Lond) 14 February 2018; 132 (3): 399–418. doi: https://doi.org/10.1042/CS20160720
Download citation file:
Sign in
Don't already have an account? Register
Sign in to your personal account
You could not be signed in. Please check your email address / username and password and try again.
Could not validate captcha. Please try again.
Biochemical Society Member Sign in
Sign InSign in via your Institution
Sign in via your InstitutionGet Access To This Article
Open Access for all
We offer compliant routes for all authors from 2025. With library support, there will be no author nor reader charges in 5 journals. Check here |
![]() |