Contribution of Glial Cells to Polyglutamine Diseases: Observations from Patients and Mouse Models

Cvetanović, Marija; Gray, Michelle

doi:10.1007/s13311-023-01357-5

Cited by 2 publications

(2 citation statements)

References 194 publications

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“…A decreased expression of this transporter has been observed in several chronic and acute neurodegenerative disorders, including Huntington's, epilepsy, stroke and several spinocerebellar ataxias, among many others CNS-related diseases (Miller et al 2008, Bacigaluppi et al 2016, Suto et al 2016, Ramandi et al 2021, Cvetanovic & Gray 2023. Although the underlying mechanism has not been fully elucidated, several reports have suggested that reactive oxygen species reduce glutamate reuptake by either impairing correct expression of transporters (Hayashi et al 2002, Sivasubramanian et al 2020 or by their oxidative-inactivation (Miralles et al 2001, Yun et al 2007.…”

Section: -Introductionmentioning

confidence: 99%

Regulatory drugs of glutamate transporter 1 (EAAT2/GLT-1) expression and activity: role in quenching oxidative damage

Domínguez-González,

Romero-Llopis,

Roldán-Lázaro

et al. 2024

Redox Experimental Medicine

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L-glutamate is one of the major neurotransmitters in the CNS, directly and indirectly involved in numerous brain functions. In several neurodegenerative diseases, it has been observed that an excess of extracellular glutamate overstimulates glutamate receptors, leading to exacerbated neuronal excitation in a process of excitotoxicity and oxidative damage that promotes neuronal death. A number of L-glutamate transporters have been identified in the membrane of neurons and astrocytes. They are responsible for the reuptake of glutamate released into the synaptic cleft after excitatory neurotransmission concomitantly regulating the extracellular concentration of glutamate, protecting neurons from its excitotoxic action. Among all of them, literature highlights Glutamate Transporter 1, known as Excitatory Amino Acid Transporter type 2 (EAAT2) in humans and Glutamate Transporter type 1 (GLT-1) in rodents, also known as solute carrier family 1 member 2 (SLC1A2). It is the predominant glutamate transporter in the brain and ensures the majority of L-glutamate reuptake. Decreased expression of this transporter along with increased levels of oxidative stress have been observed in several chronic and acute neurodegenerative disorders. For this reason, the use of drugs capable of both, increasing the expression of Glutamate Transporter 1 and mitigating oxidative damage, has been proposed as an effective therapeutic strategy for these pathologies. We present in this work an overview of the main drugs displaying such a double effect.

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Section: -Introductionmentioning

confidence: 99%

Regulatory drugs of glutamate transporter 1 (EAAT2/GLT-1) expression and activity: role in quenching oxidative damage

Domínguez-González,

Romero-Llopis,

Roldán-Lázaro

et al. 2024

Redox Experimental Medicine

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“…A major recent contribution of animal models to the understanding of stroke (Carmichael and Llorente [3]) and Huntington's disease (Cvetanovic and Gray [4]) comes from the ability to model the complex role of glial cells, long neglected contributors to pathology.…”

mentioning

confidence: 99%

A New Look at Animal Models of Neurological Disorders

Chesselet

2023

Neurotherapeutics

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Contribution of Glial Cells to Polyglutamine Diseases: Observations from Patients and Mouse Models

Cited by 2 publications

References 194 publications

Regulatory drugs of glutamate transporter 1 (EAAT2/GLT-1) expression and activity: role in quenching oxidative damage

Regulatory drugs of glutamate transporter 1 (EAAT2/GLT-1) expression and activity: role in quenching oxidative damage

A New Look at Animal Models of Neurological Disorders

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