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      The blood–brain barrier in health and disease: Important unanswered questions

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          Abstract

          The blood vessels of the central nervous system tightly control the movement of ions, molecules, and cells between the blood and tissue. This “blood–brain barrier” is vital for neural homeostasis and protection. This review discusses current knowledge of the blood–brain barrier, emphasizing key unanswered questions.

          Abstract

          The blood vessels vascularizing the central nervous system exhibit a series of distinct properties that tightly control the movement of ions, molecules, and cells between the blood and the parenchyma. This “blood–brain barrier” is initiated during angiogenesis via signals from the surrounding neural environment, and its integrity remains vital for homeostasis and neural protection throughout life. Blood–brain barrier dysfunction contributes to pathology in a range of neurological conditions including multiple sclerosis, stroke, and epilepsy, and has also been implicated in neurodegenerative diseases such as Alzheimer’s disease. This review will discuss current knowledge and key unanswered questions regarding the blood–brain barrier in health and disease.

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          Most cited references167

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          RAGE mediates amyloid-beta peptide transport across the blood-brain barrier and accumulation in brain.

          Rashid Deane, Shi Du Yan, Ram Submamaryan … (2003)
          Amyloid-beta peptide (Abeta) interacts with the vasculature to influence Abeta levels in the brain and cerebral blood flow, providing a means of amplifying the Abeta-induced cellular stress underlying neuronal dysfunction and dementia. Systemic Abeta infusion and studies in genetically manipulated mice show that Abeta interaction with receptor for advanced glycation end products (RAGE)-bearing cells in the vessel wall results in transport of Abeta across the blood-brain barrier (BBB) and expression of proinflammatory cytokines and endothelin-1 (ET-1), the latter mediating Abeta-induced vasoconstriction. Inhibition of RAGE-ligand interaction suppresses accumulation of Abeta in brain parenchyma in a mouse transgenic model. These findings suggest that vascular RAGE is a target for inhibiting pathogenic consequences of Abeta-vascular interactions, including development of cerebral amyloidosis.
          Article 0 comments Cited 407 times – based on 0 reviews     Review now
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            Central nervous system pericytes in health and disease.

            Ethan Winkler, Robert D Bell, Berislav Zlokovic (2011)
            Pericytes are uniquely positioned within the neurovascular unit to serve as vital integrators, coordinators and effectors of many neurovascular functions, including angiogenesis, blood-brain barrier (BBB) formation and maintenance, vascular stability and angioarchitecture, regulation of capillary blood flow and clearance of toxic cellular byproducts necessary for proper CNS homeostasis and neuronal function. New studies have revealed that pericyte deficiency in the CNS leads to BBB breakdown and brain hypoperfusion resulting in secondary neurodegenerative changes. Here we review recent progress in understanding the biology of CNS pericytes and their role in health and disease.
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              Phenotypic heterogeneity of the endothelium: II. Representative vascular beds.

              William C. Aird (2007)
              Endothelial cells, which form the inner cellular lining of blood vessels and lymphatics, display remarkable heterogeneity in structure and function. This is the second of a 2-part review on the phenotypic heterogeneity of blood vessel endothelial cells. The first part discusses the scope, the underlying mechanisms, and the diagnostic and therapeutic implications of phenotypic heterogeneity. Here, these principles are applied to an understanding of organ-specific phenotypes in representative vascular beds including arteries and veins, heart, lung, liver, and kidney. The goal is to underscore the importance of site-specific properties of the endothelium in mediating homeostasis and focal vascular pathology, while at the same time emphasizing the value of approaching the endothelium as an integrated system.
              Article 0 comments Cited 319 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Caterina P. Profaci:
                ORCID: https://orcid.org/0000-0002-4073-2164
                Role: ConceptualizationRole: VisualizationRole: Writing – original draftRole: Writing – review & editing
                Roeben N. Munji:
                ORCID: https://orcid.org/0000-0003-1313-8968
                Role: ConceptualizationRole: InvestigationRole: VisualizationRole: Writing – original draftRole: Writing – review & editing
                Robert S. Pulido: Role: ConceptualizationRole: Writing – original draftRole: Writing – review & editing
                Richard Daneman:
                ORCID: https://orcid.org/0000-0002-7749-6353
                Role: ConceptualizationRole: ResourcesRole: SupervisionRole: ValidationRole: VisualizationRole: Writing – original draftRole: Writing – review & editing
                Journal
                Journal ID (nlm-ta): J Exp Med
                Journal ID (iso-abbrev): J. Exp. Med
                Journal ID (publisher-id): jem
                Title: The Journal of Experimental Medicine
                Publisher: Rockefeller University Press
                ISSN (Print): 0022-1007
                ISSN (Electronic): 1540-9538
                Publication date Collection: 06 April 2020
                Publication date (Electronic): 25 March 2020
                Volume: 217
                Issue: 4
                Electronic Location Identifier: e20190062
                Affiliations
                [1 ]Department of Neurosciences, University of California, San Diego, San Diego, CA
                [2 ]Department of Pharmacology, University of California, San Diego, San Diego, CA
                Author notes
                Correspondence to Caterina P. Profaci: cprofaci@ 123456ucsd.edu
                Richard Daneman: rdaneman@ 123456ucsd.edu

                Disclosures: The authors declare no competing interests exist.

                Author information
                https://orcid.org/0000-0002-4073-2164
                https://orcid.org/0000-0003-1313-8968
                https://orcid.org/0000-0002-7749-6353
                Article
                Publisher ID: jem.20190062
                DOI: 10.1084/jem.20190062
                PMC ID: 7144528
                PubMed ID: 32211826
                SO-VID: 5a21a2d7-4d21-454a-a3cd-7df5165620dc
                Copyright © © 2020 Profaci et al.
                License:

                This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

                History
                Date received : 02 July 2019
                Date revision received : 21 September 2019
                Date accepted : 21 November 2019
                Page count
                Pages: 16
                Categories
                Subject: Review
                Subject: Neuroscience
                Subject: Neuroinflammation

                ScienceOpen disciplines: Medicine
                Data availability:
                ScienceOpen disciplines: Medicine

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