Cargando…

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...

Descripción completa

Detalles Bibliográficos
Autores principales: Lozano, Reymundo, Hare, Emma B, Hagerman, Randi J
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2014
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
_version_ 1782336021584674816
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
work_keys_str_mv AT lozanoreymundo modulationofthegabaergicpathwayforthetreatmentoffragilexsyndrome
AT hareemmab modulationofthegabaergicpathwayforthetreatmentoffragilexsyndrome
AT hagermanrandij modulationofthegabaergicpathwayforthetreatmentoffragilexsyndrome