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      Role of Thrombin in Central Nervous System Injury and Disease

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          Abstract

          Thrombin is a Na +-activated allosteric serine protease of the chymotrypsin family involved in coagulation, inflammation, cell protection, and apoptosis. Increasingly, the role of thrombin in the brain has been explored. Low concentrations of thrombin are neuroprotective, while high concentrations exert pathological effects. However, greater attention regarding the involvement of thrombin in normal and pathological processes in the central nervous system is warranted. In this review, we explore the mechanisms of thrombin action, localization, and functions in the central nervous system and describe the involvement of thrombin in stroke and intracerebral hemorrhage, neurodegenerative diseases, epilepsy, traumatic brain injury, and primary central nervous system tumors. We aim to comprehensively characterize the role of thrombin in neurological disease and injury.

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          Experimental autoimmune encephalomyelitis (EAE) as a model for multiple sclerosis (MS).

          Cris Constantinescu, Nasr Farooqi, Kate O'Brien … (2011)
          Experimental autoimmune encephalomyelitis (EAE) is the most commonly used experimental model for the human inflammatory demyelinating disease, multiple sclerosis (MS). EAE is a complex condition in which the interaction between a variety of immunopathological and neuropathological mechanisms leads to an approximation of the key pathological features of MS: inflammation, demyelination, axonal loss and gliosis. The counter-regulatory mechanisms of resolution of inflammation and remyelination also occur in EAE, which, therefore can also serve as a model for these processes. Moreover, EAE is often used as a model of cell-mediated organ-specific autoimmune conditions in general. EAE has a complex neuropharmacology, and many of the drugs that are in current or imminent use in MS have been developed, tested or validated on the basis of EAE studies. There is great heterogeneity in the susceptibility to the induction, the method of induction and the response to various immunological or neuropharmacological interventions, many of which are reviewed here. This makes EAE a very versatile system to use in translational neuro- and immunopharmacology, but the model needs to be tailored to the scientific question being asked. While creating difficulties and underscoring the inherent weaknesses of this model of MS in straightforward translation from EAE to the human disease, this variability also creates an opportunity to explore multiple facets of the immune and neural mechanisms of immune-mediated neuroinflammation and demyelination as well as intrinsic protective mechanisms. This allows the eventual development and preclinical testing of a wide range of potential therapeutic interventions. © 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.
          Article 0 comments Cited 327 times – based on 0 reviews     Review now
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            The blood-brain barrier: an overview: structure, regulation, and clinical implications.

            Praveen Ballabh, Alex Braun, Maiken Nedergaard (2004)
            The blood-brain barrier (BBB) is a diffusion barrier, which impedes influx of most compounds from blood to brain. Three cellular elements of the brain microvasculature compose the BBB-endothelial cells, astrocyte end-feet, and pericytes (PCs). Tight junctions (TJs), present between the cerebral endothelial cells, form a diffusion barrier, which selectively excludes most blood-borne substances from entering the brain. Astrocytic end-feet tightly ensheath the vessel wall and appear to be critical for the induction and maintenance of the TJ barrier, but astrocytes are not believed to have a barrier function in the mammalian brain. Dysfunction of the BBB, for example, impairment of the TJ seal, complicates a number of neurologic diseases including stroke and neuroinflammatory disorders. We review here the recent developments in our understanding of the BBB and the role of the BBB dysfunction in CNS disease. We have focused on intraventricular hemorrhage (IVH) in premature infants, which may involve dysfunction of the TJ seal as well as immaturity of the BBB in the germinal matrix (GM). A paucity of TJs or PCs, coupled with incomplete coverage of blood vessels by astrocyte end-feet, may account for the fragility of blood vessels in the GM of premature infants. Finally, this review describes the pathogenesis of increased BBB permeability in hypoxia-ischemia and inflammatory mechanisms involving the BBB in septic encephalopathy, HIV-induced dementia, multiple sclerosis, and Alzheimer disease.
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              Dabigatran for Prevention of Stroke after Embolic Stroke of Undetermined Source

              Hans-Christoph Diener, Ralph Sacco, J. Easton … (2019)
              Cryptogenic strokes constitute 20 to 30% of ischemic strokes, and most cryptogenic strokes are considered to be embolic and of undetermined source. An earlier randomized trial showed that rivaroxaban is no more effective than aspirin in preventing recurrent stroke after a presumed embolic stroke from an undetermined source. Whether dabigatran would be effective in preventing recurrent strokes after this type of stroke was unclear.
              Article 0 comments Cited 208 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Tracey Martin: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Biomolecules
                Journal ID (iso-abbrev): Biomolecules
                Journal ID (publisher-id): biomolecules
                Title: Biomolecules
                Publisher: MDPI
                ISSN (Electronic): 2218-273X
                Publication date (Electronic): 12 April 2021
                Publication date Collection: April 2021
                Volume: 11
                Issue: 4
                Electronic Location Identifier: 562
                Affiliations
                [1 ]Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA
                [2 ]Department of Anatomy and Anthropology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 6997801, Israel
                [3 ]Sylvan Adams Sports Institute, Tel Aviv University, Tel Aviv 6997801, Israel
                [4 ]Department of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 6997801, Israel; Zeev.ItsekzonHayosh@ 123456sheba.health.gov.il
                [5 ]Department of Neurology and Joseph Sagol Neuroscience Center, The Chaim Sheba Medical Center, Tel HaShomer 5262000, Israel
                [6 ]Department of Neurosurgery, Beilinson Hospital, Rabin Medical Center, Tel Aviv University, Petah Tikva 4941492, Israel; sagiha@ 123456clalit.org.il
                [7 ]Sagol School of Neuroscience, Tel Aviv University, Tel Aviv 6997801, Israel
                [8 ]Center for Biology of Addictive Diseases, Tel Aviv University, Tel Aviv 6997801, Israel
                Author notes
                [* ]Correspondence: nathan.shlobin@ 123456northwestern.edu (N.A.S.); meiravhe@ 123456mail.tau.ac.il (M.H.-E.); pickc@ 123456tauex.tau.ac.il (C.G.P.); Tel.: +03-6-409-247 (C.G.P.); Fax: +03-6-408-287 (C.G.P.)
                Author information
                https://orcid.org/0000-0001-7114-339X
                Article
                Publisher ID: biomolecules-11-00562
                DOI: 10.3390/biom11040562
                PMC ID: 8070021
                PubMed ID: 33921354
                SO-VID: 14949d24-ee0d-48fc-8a71-ddabdc468dbc
                Copyright © © 2021 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( https://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 27 February 2021
                Date accepted : 07 April 2021
                Categories
                Subject: Review

                Keywords: blood–brain barrier,glioblastoma,neurodegenerative diseases,neuroinflammation,protease-activated receptor,prothrombin,tbi,thrombin
                Data availability:
                Keywords: blood–brain barrier, glioblastoma, neurodegenerative diseases, neuroinflammation, protease-activated receptor, prothrombin, tbi, thrombin

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