ArticleFrontiers in molecular neuroscience2017
Combination Therapy in Fragile X Syndrome; Possibilities and Pitfalls Illustrated by Targeting the mGluR5 and GABA Pathway Simultaneously.
Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- Electrical Synapses Mediate Embryonic Hyperactivity in a Zebrafish Model of Fragile X Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Computing a cure for fragile-X syndrome.Brain communications · 2024Article
- Mouse models of fragile X-related disorders.Disease models & mechanisms · 2023Review
- From bench to bedside: The mGluR5 system in people with and without Autism Spectrum Disorder and animal model systems.Translational psychiatry · 2022Article
- Chloride imbalance in Fragile X syndrome.Frontiers in neuroscience · 2022Article
- Combining Lovastatin and Minocycline for the Treatment of Fragile X Syndrome: Results From the LovaMiX Clinical Trial.Frontiers in psychiatry · 2021Article
- Growing up with Fragile X Syndrome: Concerns and Care Needs of Young Adult Patients and Their Parents.Journal of autism and developmental disorders · 2020Article
- Paradoxical effect of baclofen on social behavior in the fragile X syndrome mouse model.Brain and behavior · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fragile X syndrome (FXS) is the most common monogenetic cause of intellectual disability and autism. The disorder is characterized by altered synaptic plasticity in the brain. Synaptic plasticity is tightly regulated by a complex balance of different synaptic pathways. In FXS, various synaptic pathways are disrupted, including the excitatory metabotropic glutamate receptor 5 (mGluR5) and the inhibitory γ-aminobutyric acid (GABA) pathways. Targeting each of these pathways individually, has demonstrated beneficial effects in animal models, but not in patients with FXS. This lack of translation might be due to oversimplification of the disease mechanisms when targeting only one affected pathway, in spite of the complexity of the many pathways implicated in FXS. In this report we outline the hypothesis that targeting more than one pathway simultaneously, a combination therapy, might improve treatment effects in FXS. In addition, we present a glance of the first results of chronic combination therapy on social behavior in
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