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Novel EAAT2 activators improve motor and cognitive impairment in a transgenic model of Huntington’s disease
Journal article   Open access   Peer reviewed

Novel EAAT2 activators improve motor and cognitive impairment in a transgenic model of Huntington’s disease

Akanksha Bhatnagar, Visha Parmar, Nicholas Barbieri, Frank Bearoff, Felice Elefant and Sandhya Kortagere
Frontiers in behavioral neuroscience, v 17
07 Jun 2023
url
https://doi.org/10.3389/fnbeh.2023.1176777View
CC BY V4.0 Open

Abstract

Allosteric properties Associative learning Cognitive ability Drosophila Excitatory amino acid transporter Excitatory amino acid transporter 2 Excitotoxicity Glutamic acid transporter Huntingtin Huntington's disease Hypotheses Insects Memory Neostriatum Neurodegeneration Neuroprotection Olfactory discrimination learning Proteins Short term memory Therapeutic targets Amino Acids Apoptosis Brain Disease Epigenetics Neurodegenerative Diseases Pathogenesis Pathology Pharmacokinetics
Glutamate excitotoxicity is causal in striatal neurodegeneration underlying motor dysfunction and cognitive deficits in Huntington’s disease (HD). Excitatory amino acid transporter 2 (EAAT2), the predominant glutamate transporter accounting for > 90% of glutamate transport, plays a key role in preventing excitotoxity by clearing excess glutamate from the intrasynaptic cleft. Accordingly, EAAT2 has emerged as a promising therapeutic target for prevention of neuronal excitotoxicity underlying HD and other neurodegenerative diseases.

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Web of Science research areas
Behavioral Sciences
Neurosciences
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