ReviewTrends in neurosciences2013
Meeting at the crossroads: common mechanisms in Fragile X and Down syndrome.
Review in Trends in neurosciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Distinct Defects in Spine Formation or Pruning in Two Gene Duplication Mouse Models of Autism.Neuroscience bulletin · 2017Article
- A brain proteomic investigation of rapamycin effects in theMolecular autism · 2017Article
- Division of labor in the growth cone by DSCR1.The Journal of cell biology · 2016Article
- DSCR1 is required for both axonal growth cone extension and steering.The Journal of cell biology · 2016Article
- Where Environment Meets Cognition: A Focus on Two Developmental Intellectual Disability Disorders.Neural plasticity · 2016Review
- Dendritic spine dysgenesis in autism related disorders.Neuroscience letters · 2015Review
- Teaching reading to youth with fragile X syndrome: Should phonemic awareness and phonics instruction be used?EBP briefs · 2015Article
- Inter-Dependent Mechanisms Behind Cognitive Dysfunction, Vascular Biology and Alzheimer's Dementia in Down Syndrome: Multi-Faceted Roles of APP.Frontiers in behavioral neuroscience · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Intellectual disability is characterized by significantly impaired cognitive abilities and is due to various etiological factors, including both genetic and non-genetic causes. Two of the most common genetic forms of intellectual disability are Fragile X syndrome (FXS) and Down syndrome (DS). Recent studies have shown that proteins altered in FXS and DS can physically interact and participate in common signaling pathways regulating dendritic spine development and local protein synthesis, thus supporting the notion that spine dysmorphogenesis and abnormal local protein synthesis may be molecular underpinnings of intellectual disability. Here we review the molecular constituents regulating local protein synthesis and spine morphology and their alterations in FXS and DS. We argue that these changes might ultimately affect synaptic homeostasis and alter cognitive performance.
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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.