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      Call for Papers: Sex and Gender in Neurodegenerative Diseases

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      About Neurodegenerative Diseases: 3.0 Impact Factor I 4.3 CiteScore I 0.695 Scimago Journal & Country Rank (SJR)

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      Cocktail Blood Biomarkers: Prediction of Clinical Outcomes in Patients with Acute Ischemic Stroke

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          Abstract

          Background: Timely prediction of stroke outcomes is important for proper personalized treatment. In the present study, we aimed to develop cocktail blood biomarkers to increase prediction efficiency using a combination of hemostasis, inflammatory and repair-related biomarkers. Methods: 105 patients suffering from acute ischemic stroke were divided into good outcome group and poor outcome group by modified Rankin Scale (mRS). Cytokines including CD40L, IFN-γ, IL-1α, IL-1β, IL-6, IL-8, IL-17 and TNF-α, as well as hemostasis markers fibrinogen, fibrin degradation products (FDP), D-dimer, tissue plasminogen activator, and plasminogen activation inhibitor-1 in plasma were examined by ELISA. Repair-related biomarker microRNA-210 (miR-210) was measured by real-time PCR. The prediction efficiency was explored by receiver operator characteristic analysis. Results: We demonstrated that FDP, IL-6 and miR-210 levels were closely associated with mRS in stroke patients. The prediction sensitivity of FDP, IL-6 and miR-210 for stroke outcome was 72.0, 86.7 and 82.5%, respectively. Using a combination of biomarkers including FDP, IL-6 and miR-210, the prognostic sensitivity of ischemic stroke increased to 95.2%. Conclusion: The combination of FDP, IL-6 and miR-210 has a high sensitivity for predicting stroke recovery, it serves as a potential cocktail blood biomarker. It provides a novel approach for stroke prognosis.

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          Pivotal role of cerebral interleukin-17-producing gammadeltaT cells in the delayed phase of ischemic brain injury.

          Takashi Shichita, Yuki Sugiyama, Hiroaki Ooboshi … (2009)
          Lymphocyte recruitment and activation have been implicated in the progression of cerebral ischemia-reperfusion (I/R) injury, but the roles of specific lymphocyte subpopulations and cytokines during stroke remain to be clarified. Here we demonstrate that the infiltration of T cells into the brain, as well as the cytokines interleukin-23 (IL-23) and IL-17, have pivotal roles in the evolution of brain infarction and accompanying neurological deficits. Blockade of T cell infiltration into the brain by the immunosuppressant FTY720 reduced I/R-induced brain damage. The expression of IL-23, which was derived mostly from infiltrated macrophages, increased on day 1 after I/R, whereas IL-17 levels were elevated after day 3, and this induction of IL-17 was dependent on IL-23. These data, together with analysis of mice genetically disrupted for IL-17 and IL-23, suggest that IL-23 functions in the immediate stage of I/R brain injury, whereas IL-17 has an important role in the delayed phase of I/R injury during which apoptotic neuronal death occurs in the penumbra. Intracellular cytokine staining revealed that gammadeltaT lymphocytes, but not CD4(+) helper T cells, were a major source of IL-17. Moreover, depletion of gammadeltaT lymphocytes ameliorated the I/R injury. We propose that T lymphocytes, including gammadeltaT lymphocytes, could be a therapeutic target for mitigating the inflammatory events that amplify the initial damage in cerebral ischemia.
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            Mechanisms of ischemic brain damage.

            Kristian Doyle, Roger P. Simon, Mary Stenzel-Poore (2008)
            In the United States stroke is the third leading cause of death and the leading cause of disability. Brain injury following stroke results from the complex interplay of multiple pathways including excitotoxicity, acidotoxicity, ionic imbalance, peri-infarct depolarization, oxidative and nitrative stress, inflammation and apoptosis. There are very few treatments for stroke and the development of new treatments requires a comprehensive understanding of the diverse mechanisms of ischemic brain damage that are responsible for neuronal death. Here, we discuss the underlying pathophysiology of this devastating disease and reveal the intertwined pathways that are the target of therapeutic intervention.
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              MicroRNA-210: a unique and pleiotropic hypoxamir.

              Joseph Loscalzo, David Chan (2010)
              Inadequate oxygen availability or hypoxia induces a complex and still incompletely understood set of adaptations that influence cellular survival and function. Many of these adaptations are directly controlled by a master transcription factor, hypoxia inducible factor-alpha (HIF-α). In response to hypoxia, HIF-α levels increase and directly induce the transcription of > 100 genes, influencing functions ranging from metabolism, survival, proliferation, migration, to angiogenesis, among others. Recently, it has been demonstrated that a specific set of microRNA molecules are upregulated by hypoxia, which we denote here as "hypoxamirs." In particular, the HIF-responsive hypoxamir microRNA-210 (miR-210) is a unique microRNA that is evolutionarily conserved and ubiquitously expressed in hypoxic cell and tissue types. A number of direct targets of miR-210 have been identified by in silico, transcriptional, and biochemical methods, a subset of which have been extensively validated. As a result, miR-210 has been mechanistically linked to the control of a wide range of cellular responses known to influence normal developmental physiology as well as a number of hypoxia-dependent disease states, including tissue ischemia, inflammation, and tumorigenesis. Thus, reflecting the pleiotropic actions of HIF-α, miR-210 appears to function as a "master microRNA" relevant for the control of diverse functions in the hypoxic state.
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                Author and article information

                Journal
                Journal ID (publisher-id): ENE
                Journal ID (nlm-ta): Eur Neurol
                Journal ID (doi): 10.1159/issn.0014-3022
                Title: European Neurology
                Publisher: S. Karger AG
                ISSN (Print): 0014-3022
                ISSN (Electronic): 1421-9913
                Publication date Subscription-year: 2013
                Publication date (Print): February 2013
                Publication date (Electronic): 14 November 2012
                Volume: 69
                Issue: 2
                Pages: 68-75
                Affiliations
                aDepartment of Neurology, Ruijin Hospital, bNeuroscience and Neuroengineering Center, Med-X Research Institute, and cSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China
                Author notes
                *Guo-Yuan Yang, MD, PhD, Neuroscience and Neuroengineering Center, Med-X Research Institute, Shanghai Jiao Tong University, 1954 Hua Shan Road, Shanghai 200030 (China), E-Mail gyyang0626@gmail.com
                Article
                Publisher ID: 342896 Other ID: Eur Neurol 2013;69:68–75
                DOI: 10.1159/000342896
                PubMed ID: 23154383
                SO-VID: 18d7b96e-a298-4932-ab5d-d889c52819b0
                Copyright © © 2012 S. Karger AG, Basel
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Date received : 14 May 2012
                Date accepted : 16 August 2012
                Page count
                Figures: 2, Tables: 1, Pages: 8
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Geriatric medicine,Neurology,Cardiovascular Medicine,Neurosciences,Clinical Psychology & Psychiatry,Public health
                Keywords: Biomarker,Interleukin-6,Stroke,microRNA,Prognosis
                Data availability:
                ScienceOpen disciplines: Geriatric medicine, Neurology, Cardiovascular Medicine, Neurosciences, Clinical Psychology & Psychiatry, Public health
                Keywords: Biomarker, Interleukin-6, Stroke, microRNA, Prognosis

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