ReviewNature reviews. Neuroscience2015
Dysregulation and restoration of translational homeostasis in fragile X syndrome.
Review in Nature reviews. Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 3 registered trials, which are not on this map. Cited by 164 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Safety and Tolerability of CTH120, First-in-human Phase I Study Encompassing Three Parts: Single and Multiple Ascending Doses and Potential Food Interaction
Assessment of Neural Biomarkers in Adult Subjects With Fragile X Syndrome and Typically Developing Subjects
Evaluation of the Safety, Tolerability, and Effectiveness of CTH120 in Adult Males With Fragile X Syndrome
Who cites it
164 citing papers in PubMed, 1 synthesis or guideline pooled it, 278 citations in OpenAlex.
- Brain volumes in genetic syndromes associated with mTOR dysregulation: a systematic review and meta-analysis.Molecular psychiatry · 2025Pooled it
- Targeting autophagy for postsynaptic organization and cognitive rescue in Fragile X syndrome.Neural regeneration research · 2026Article
- Unraveling in vitro phase separation and aggregation properties of the structured region of FMRP and the impact of Fragile X syndrome-linked mutations.The FEBS journal · 2026Article
- Article
- Review
- FMR1 gene therapy restores translationally relevant phenotypes in a mouse model for fragile X syndrome.Gene therapy · 2026Article
- GABA as an Overlooked Mediator of Metformin Action: GABA-mediated Neuropsychiatric and Hepatoprotective Activities of Metformin.Annals of neurosciences · 2026Review
- The mMolecular psychiatry · 2026Article
- FMRP regulates neuronal RNA granules containing stalled ribosomes, not where ribosomes stall.eLife · 2026Article
- Article
- FMRP regulation of STAT3-MYC signaling is critical for adult hippocampal neurogenesis and cognitive flexibility.Cell death and differentiation · 2026Article
- Autophagy controls the hippocampal postsynaptic organization and affects cognition in a mouse model of Fragile X syndrome.Molecular psychiatry · 2026Article
- Multiplexed smFISH Reveals the Spatial Organization of Neuropil Localized mRNAs Is Linked to Abundance.eNeuro · 2025Article
- Autophagy controls the hippocampal postsynaptic organization and affects cognition in a mouse model of Fragile X syndrome.Research square · 2025Article
- FMRP-dependent translational control negatively regulates adapter protein complex 2-mediated endocytosis.iScience · 2025Article
- Shank3 modulates Rpl3 expression and protein synthesis via mGlu5: implications for Phelan McDermid syndrome.Molecular psychiatry · 2025Article
- Article
- Neuronal potassium channel activity triggers initiation of mRNA translation through binding of translation regulators.Science advances · 2025Article
- The Unified Theory of Neurodegeneration Pathogenesis Based on Axon Deamidation.International journal of molecular sciences · 2025Review
- From Discovery to Innovative Translational Approaches in 80 Years of Fragile X Syndrome Research.Biomedicines · 2025Review
104 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Fragile X syndrome (FXS), the most-frequently inherited form of intellectual disability and the most-prevalent single-gene cause of autism, results from a lack of fragile X mental retardation protein (FMRP), an RNA-binding protein that acts, in most cases, to repress translation. Multiple pharmacological and genetic manipulations that target receptors, scaffolding proteins, kinases and translational control proteins can rescue neuronal morphology, synaptic function and behavioural phenotypes in FXS model mice, presumably by reducing excessive neuronal translation to normal levels. Such rescue strategies might also be explored in the future to identify the mRNAs that are critical for FXS pathophysiology.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.