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  • Author: Marta Roldán-Lázaro x
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Davinia Domínguez-González Department of Physiology, Faculty of Medicine and Dentistry, University of Valencia- INCLIVA, Valencia, Spain

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Blanca Romero-Llopis Department of Physiology, Faculty of Medicine and Dentistry, University of Valencia- INCLIVA, Valencia, Spain

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Marta Roldán-Lázaro Department of Physiology, Faculty of Medicine and Dentistry, University of Valencia- INCLIVA, Valencia, Spain
Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Valencia, Spain

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Lorena Baquero Department of Physiology, Faculty of Medicine and Dentistry, University of Valencia- INCLIVA, Valencia, Spain
Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Valencia, Spain

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Rita Noverques Department of Physiology, Faculty of Medicine and Dentistry, University of Valencia- INCLIVA, Valencia, Spain

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Federico V Pallardó Department of Physiology, Faculty of Medicine and Dentistry, University of Valencia- INCLIVA, Valencia, Spain
Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Valencia, Spain

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Juan Antonio Navarro Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Valencia, Spain
Department of Genetics, Universitat de València, Valencia, Spain
INCLIVA Biomedical Research Institute, Unversitat de València, Valencia, Spain

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Pilar Gonzalez-Cabo Department of Physiology, Faculty of Medicine and Dentistry, University of Valencia- INCLIVA, Valencia, Spain
Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Valencia, Spain

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l-glutamate is one of the major neurotransmitters in the central nervous system, directly and indirectly involved in numerous brain functions. In several neurodegenerative diseases, it has been observed that an excess of extracellular glutamate overstimulates glutamate receptors, leading to exacerbated neuronal excitation in a process of excitotoxicity and oxidative damage that promotes neuronal death. A number of l-glutamate transporters have been identified in the membrane of neurons and astrocytes. They are responsible for the reuptake of glutamate released into the synaptic cleft after excitatory neurotransmission concomitantly regulating the extracellular concentration of glutamate, protecting neurons from its excitotoxic action. Among all of them, literature highlights glutamate transporter 1, known as excitatory amino acid transporter type 2 in humans and glutamate transporter type 1 in rodents, also known as solute carrier family 1 member 2. It is the predominant glutamate transporter in the brain and ensures the majority of l-glutamate reuptake. Decreased expression of this transporter along with increased levels of oxidative stress have been observed in several chronic and acute neurodegenerative disorders. For this reason, the use of drugs capable of both increasing the expression of glutamate transporter 1 and mitigating oxidative damage has been proposed as an effective therapeutic strategy for these pathologies. We present in this work an overview of the main drugs displaying such a double effect.

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