Positive allosteric activation of glial EAAT-2 transporter protein: A novel strategy for Alzheimer's disease.
EAAT-2
Glutamate
Neuroprotection
Positive allosteric site
Synaptic clearance
Journal
Medical hypotheses
ISSN: 1532-2777
Titre abrégé: Med Hypotheses
Pays: United States
ID NLM: 7505668
Informations de publication
Date de publication:
Sep 2020
Sep 2020
Historique:
received:
02
01
2020
revised:
18
03
2020
accepted:
28
04
2020
pubmed:
16
5
2020
medline:
15
5
2021
entrez:
16
5
2020
Statut:
ppublish
Résumé
Excitatory amino acid transporter-2 (EAAT-2) protein localized in the membrane of glial cells are responsible for the clearance of glutamate in synapse and it plays a key role among the five glutamate transporters (EAATs) in regulating synaptic transmission and preventing excitotoxicity in neurons. EAAT-2 dysfunction has been associated with the neuropathology of Alzheimer's disease (AD). Impairment of EAAT-2 transporter function results excess accumulation of glutamate in synaptic cleft that acts on post-synaptic glutaminergic receptors excessively resulting in influx of Na
Identifiants
pubmed: 32413698
pii: S0306-9877(20)30011-6
doi: 10.1016/j.mehy.2020.109794
pii:
doi:
Substances chimiques
Excitatory Amino Acid Transporter 2
0
SLC1A2 protein, human
0
Glutamic Acid
3KX376GY7L
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
109794Informations de copyright
Copyright © 2020 Elsevier Ltd. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.