The role of excitatory amino acid transporter 2 (EAAT2) in epilepsy and other neurological disorders

被引：12

作者：

Alijanpour, Sahar ^{[1
]}

Miryounesi, Mohammad ^{[1
]}

Ghafouri-Fard, Soudeh ^{[1
]}

机构：

[1] Shahid Beheshti Univ Med Sci, Fac Med, Dept Med Genet, Tehran, Iran

来源：

METABOLIC BRAIN DISEASE | 2023年 / 38卷 / 01期

关键词：

SLC1A2; EAAT2; Developmental and epileptic encephalopathy 41; Epilepsy; Neurological disorders; Genetic; GLIAL GLUTAMATE TRANSPORTER; DE-NOVO MUTATIONS; AMYOTROPHIC-LATERAL-SCLEROSIS; FRAGILE-X-SYNDROME; ALZHEIMERS-DISEASE; MOLECULAR PHARMACOLOGY; HIPPOCAMPAL GLUTAMATE; ANTISENSE KNOCKDOWN; NEURONAL DAMAGE; MICE LACKING;

D O I：

10.1007/s11011-022-01091-5

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Glutamate is the major excitatory neurotransmitter in the central nervous system (CNS). Excitatory amino acid transporters (EAATs) have important roles in the uptake of glutamate and termination of glutamatergic transmission. Up to now, five EAAT isoforms (EAAT1-5) have been identified in mammals. The main focus of this review is EAAT2. This protein has an important role in the pathoetiology of epilepsy. De novo dominant mutations, as well as inherited recessive mutation in this gene, have been associated with epilepsy. Moreover, dysregulation of this protein is implicated in a range of neurological diseases, namely amyotrophic lateral sclerosis, alzheimer's disease, parkinson's disease, schizophrenia, epilepsy, and autism. In this review, we summarize the role of EAAT2 in epilepsy and other neurological disorders, then provide an overview of the therapeutic modulation of this protein.

引用

页码：1 / 16

页数：16

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