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Lactate transport and receptor actions in cerebral malaria

Frontiers in neuroenergetics, 2014-05, Vol.8, p.125-125 [Peer Reviewed Journal]

2014. This work is licensed under http://creativecommons.org/licenses/by/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;info:eu-repo/semantics/openAccess ;Copyright © 2014 Mariga, Kolko, Gjedde and Bergersen. 2014 ;ISSN: 1662-4548 ;ISSN: 1662-453X ;ISSN: 1662-6427 ;EISSN: 1662-453X ;EISSN: 1662-6427 ;DOI: 10.3389/fnins.2014.00125 ;PMID: 24904266

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  • Title:
    Lactate transport and receptor actions in cerebral malaria
  • Author: Mariga, Shelton T ; Kolko, Miriam ; Gjedde, Albert ; Bergersen, Linda H
  • Subjects: Adenylate cyclase ; Biology ; Blood vessels ; Blood-brain barrier ; Brain ; Brain injury ; Cell membranes ; Edema ; Endothelium ; Erythrocytes ; Families & family life ; Homeostasis ; Lactic acid ; Malaria ; Membranes ; Metabolism ; Metabolites ; Neuroscience ; Neurosciences ; Parasites ; Pathogenesis ; Plasmodium falciparum ; Seizures ; Therapeutic applications
  • Is Part Of: Frontiers in neuroenergetics, 2014-05, Vol.8, p.125-125
  • Description: Cerebral malaria (CM), caused by Plasmodium falciparum infection, is a prevalent neurological disorder in the tropics. Most of the patients are children, typically with intractable seizures and high mortality. Current treatment is unsatisfactory. Understanding the pathogenesis of CM is required in order to identify therapeutic targets. Here, we argue that cerebral energy metabolic defects are probable etiological factors in CM pathogenesis, because malaria parasites consume large amounts of glucose metabolized mostly to lactate. Monocarboxylate transporters (MCTs) mediate facilitated transfer, which serves to equalize lactate concentrations across cell membranes in the direction of the concentration gradient. The equalizing action of MCTs is the basis for lactate's role as a volume transmitter of metabolic signals in the brain. Lactate binds to the lactate receptor GPR81, recently discovered on brain cells and cerebral blood vessels, causing inhibition of adenylyl cyclase. High levels of lactate delivered by the parasite at the vascular endothelium may damage the blood-brain barrier, disrupt lactate homeostasis in the brain, and imply MCTs and the lactate receptor as novel therapeutic targets in CM.
  • Publisher: Switzerland: Frontiers Research Foundation
  • Language: English;Norwegian
  • Identifier: ISSN: 1662-4548
    ISSN: 1662-453X
    ISSN: 1662-6427
    EISSN: 1662-453X
    EISSN: 1662-6427
    DOI: 10.3389/fnins.2014.00125
    PMID: 24904266
  • Source: GFMER Free Medical Journals
    NORA Norwegian Open Research Archives
    PubMed Central
    ROAD: Directory of Open Access Scholarly Resources
    ProQuest Central
    DOAJ Directory of Open Access Journals
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