ReviewNeurogenetics2024
Understanding pathophysiology in fragile X syndrome: a comprehensive review.
Review in Neurogenetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fragile X syndrome (FXS) is the leading hereditary cause of intellectual disability and the most commonly associated genetic cause of autism. Historically, research into its pathophysiology has focused predominantly on neurons; however, emerging evidence suggests involvement of additional cell types and systems. The objective of this study was to review and synthesize current evidence regarding the pathophysiology of Fragile X syndrome. A comprehensive literature review was conducted using databases such as PubMed and Google Scholar, employing MeSH terms including "Fragile X Syndrome," "FMR1 gene," and "FMRP." Studies on both human and animal models, from inception to 2022, published in recognized journals were included. The evidence supports those neurons, glial cells, stem cells, the immune system, and lipid metabolism pathways contribute to the pathophysiology of Fragile X syndrome. Further research is necessary to explore these fields independently and to elucidate their interactions.
Indexed as
Identifiers
39585476What Socratic 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 Socratic graph.