Glutamate transporter EAAT2: a new target for the treatment of neurodegenerative diseases



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Future Medicinal Chemistry


Glutamate is the primary excitatory amino acid neurotransmitter in the CNS. The concentration of glutamate in the synaptic cleft is tightly controlled by interplay between glutamate release and glutamate clearance. Abnormal glutamate release and/or dysfunction of glutamate clearance can cause overstimulation of glutamate receptors and result in neuronal injury known as excitotoxicity. The glial glutamate transporter EAAT2 plays a major role in glutamate clearance. Dysfunction or reduced expression of EAAT2 has been documented in many neurodegenerative diseases. In addition, many studies in animal models of disease indicate that increased EAAT2 expression provides neuronal protection. Here, we summarize these studies and suggest that EAAT2 is a potential target for the prevention of excitotoxicity. EAAT2 can be upregulated by transcriptional or translational activation. We discuss current progress in the search for EAAT2 activators, which is a promising direction for the treatment of neurodegenerative diseases.




Copyright 2012 Future Medicinal Chemistry. This is a post-print version of a published paper that is available at: Recommended citation: Lin, Chien-Liang Glenn, Qiongman Kong, Gregory D. Cuny, and Marcie A. Glicksman. "Glutamate transporter EAAT2: a new target for the treatment of neurodegenerative diseases." Future medicinal chemistry 4, no. 13 (2012): 1689-1700. doi: 10.4155/fmc.12.122. This item has been deposited in accordance with publisher copyright and licensing terms and with the author's permission.