Year: 2014
Type: article
Abstract: Glutamate excitotoxicity contributes to the neuronal injury and death associated with many neurodegenerative diseases. The glutamate transporter EAAT2, which is primarily localized on astrocytic processes, facilitates glutamate clearance from synapses, thus preventing neuronal damage. In this issue of the JCI, Kong et al. characterize a compound that upregulates EAAT2 translation, thereby increasing glutamate uptake by glial cells. Furthermore, this strategy for alleviating excitotoxicity was found to be beneficial in mouse models of both amyotrophic lateral sclerosis (ALS) and epilepsy, suggesting that future development in this chemical series may lead to much-needed treatments for these disorders.
DOI: 10.1172/jci74608
Authors: Allison S. Limpert, Nicholas D.P. Cosford
Language: English
Subfield: Cellular and Molecular Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: bronze
Funder: U.S. Department of Defense
Award: G4119534169
OpenAlex ID: W1964756987
