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Modulation of the GABAergic pathway for the treatment of fragile X syndrome
Fragile X syndrome (FXS) is the most common genetic cause of intellectual disability and the most common single-gene cause of autism. It is caused by mutations on the fragile X mental retardation gene (FMR1) and lack of fragile X mental retardation protein, which in turn, leads to decreased inhibiti...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Dove Medical Press
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4172237/ https://www.ncbi.nlm.nih.gov/pubmed/25258535 http://dx.doi.org/10.2147/NDT.S42919 |
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author | Lozano, Reymundo Hare, Emma B Hagerman, Randi J |
author_facet | Lozano, Reymundo Hare, Emma B Hagerman, Randi J |
author_sort | Lozano, Reymundo |
collection | PubMed |
description | Fragile X syndrome (FXS) is the most common genetic cause of intellectual disability and the most common single-gene cause of autism. It is caused by mutations on the fragile X mental retardation gene (FMR1) and lack of fragile X mental retardation protein, which in turn, leads to decreased inhibition of translation of many synaptic proteins. The metabotropic glutamate receptor (mGluR) hypothesis states that the neurological deficits in individuals with FXS are due mainly to downstream consequences of overstimulation of the mGluR pathway. The main efforts have focused on mGluR5 targeted treatments; however, investigation on the gamma-aminobutyric acid (GABA) system and its potential as a targeted treatment is less emphasized. The fragile X mouse models (Fmr1-knock out) show decreased GABA subunit receptors, decreased synthesis of GABA, increased catabolism of GABA, and overall decreased GABAergic input in many regions of the brain. Consequences of the reduced GABAergic input in FXS include oversensitivity to sensory stimuli, seizures, and anxiety. Deficits in the GABA receptors in different regions of the brain are associated with behavioral and attentional processing deficits linked to anxiety and autistic behaviors. The understanding of the neurobiology of FXS has led to the development of targeted treatments for the core behavioral features of FXS, which include social deficits, inattention, and anxiety. These symptoms are also observed in individuals with autism and other neurodevelopmental disorders, therefore the targeted treatments for FXS are leading the way in the treatment of other neurodevelopmental syndromes and autism. The GABAergic system in FXS represents a target for new treatments. Herein, we discuss the animal and human trials of GABAergic treatment in FXS. Arbaclofen and ganaxolone have been used in individuals with FXS. Other potential GABAergic treatments, such as riluzole, gaboxadol, tiagabine, and vigabatrin, will be also discussed. Further studies are needed to determine the safety and efficacy of GABAergic treatments for FXS. |
format | Online Article Text |
id | pubmed-4172237 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-41722372014-09-25 Modulation of the GABAergic pathway for the treatment of fragile X syndrome Lozano, Reymundo Hare, Emma B Hagerman, Randi J Neuropsychiatr Dis Treat Review Fragile X syndrome (FXS) is the most common genetic cause of intellectual disability and the most common single-gene cause of autism. It is caused by mutations on the fragile X mental retardation gene (FMR1) and lack of fragile X mental retardation protein, which in turn, leads to decreased inhibition of translation of many synaptic proteins. The metabotropic glutamate receptor (mGluR) hypothesis states that the neurological deficits in individuals with FXS are due mainly to downstream consequences of overstimulation of the mGluR pathway. The main efforts have focused on mGluR5 targeted treatments; however, investigation on the gamma-aminobutyric acid (GABA) system and its potential as a targeted treatment is less emphasized. The fragile X mouse models (Fmr1-knock out) show decreased GABA subunit receptors, decreased synthesis of GABA, increased catabolism of GABA, and overall decreased GABAergic input in many regions of the brain. Consequences of the reduced GABAergic input in FXS include oversensitivity to sensory stimuli, seizures, and anxiety. Deficits in the GABA receptors in different regions of the brain are associated with behavioral and attentional processing deficits linked to anxiety and autistic behaviors. The understanding of the neurobiology of FXS has led to the development of targeted treatments for the core behavioral features of FXS, which include social deficits, inattention, and anxiety. These symptoms are also observed in individuals with autism and other neurodevelopmental disorders, therefore the targeted treatments for FXS are leading the way in the treatment of other neurodevelopmental syndromes and autism. The GABAergic system in FXS represents a target for new treatments. Herein, we discuss the animal and human trials of GABAergic treatment in FXS. Arbaclofen and ganaxolone have been used in individuals with FXS. Other potential GABAergic treatments, such as riluzole, gaboxadol, tiagabine, and vigabatrin, will be also discussed. Further studies are needed to determine the safety and efficacy of GABAergic treatments for FXS. Dove Medical Press 2014-09-16 /pmc/articles/PMC4172237/ /pubmed/25258535 http://dx.doi.org/10.2147/NDT.S42919 Text en © 2014 Lozano et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. |
spellingShingle | Review Lozano, Reymundo Hare, Emma B Hagerman, Randi J Modulation of the GABAergic pathway for the treatment of fragile X syndrome |
title | Modulation of the GABAergic pathway for the treatment of fragile X syndrome |
title_full | Modulation of the GABAergic pathway for the treatment of fragile X syndrome |
title_fullStr | Modulation of the GABAergic pathway for the treatment of fragile X syndrome |
title_full_unstemmed | Modulation of the GABAergic pathway for the treatment of fragile X syndrome |
title_short | Modulation of the GABAergic pathway for the treatment of fragile X syndrome |
title_sort | modulation of the gabaergic pathway for the treatment of fragile x syndrome |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4172237/ https://www.ncbi.nlm.nih.gov/pubmed/25258535 http://dx.doi.org/10.2147/NDT.S42919 |
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