Evidence map›Paper›PMID 33215285›Full record

ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2021

Overlapping Molecular Pathways Leading to Autism Spectrum Disorders, Fragile X Syndrome, and Targeted Treatments.

Maria Jimena Salcedo-Arellano, Ana Maria Cabal-Herrera, Ruchi Harendra Punatar, Courtney Jessica Clark, Christopher Allen Romney, Randi J Hagerman

Open access · bronzeAbstract readReview
In one paragraph

Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 10% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Epigenetic insights into Fragile X Syndrome.Frontiers in cell and developmental biology · 2024
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Targeted Treatments for Fragile X Syndrome.Advances in neurobiology · 2023
    Article
  15. Article
  16. Fragile X Syndrome: From Molecular Aspect to Clinical Treatment.International journal of molecular sciences · 2022
    Review
  17. Article
  18. Article
  19. Review
  20. Local Translation in Nervous System Pathologies.Frontiers in integrative neuroscience · 2021
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Maria Jimena Salcedo-Arellano *Department of Pediatrics, University of California Davis School of Medicine, Sacramento, CA, 95817, USA. mjsalcedo@ucdavis.edu.ORCID http://orcid.org/0000-0002-2412-9146
Ana Maria Cabal-Herrera *Group on Congenital Malformations and Dysmorphology, Faculty of Health, Universidad del Valle, Cali, 00000, Colombia.
Ruchi Harendra PunatarDepartment of Pediatrics, University of California Davis School of Medicine, Sacramento, CA, 95817, USA.
Courtney Jessica ClarkDepartment of Pediatrics, University of California Davis School of Medicine, Sacramento, CA, 95817, USA.
Christopher Allen RomneyDepartment of Pediatrics, University of California Davis School of Medicine, Sacramento, CA, 95817, USA.
Randi J HagermanDepartment of Pediatrics, University of California Davis School of Medicine, Sacramento, CA, 95817, USA. rjhagerman@ucdavis.edu.
University of California, Davis · USUniversity of California Davis Medical Center · USUniversidad del Valle · CO

Funding

GENOTYPE/PHENOTYPE RELATIONSHIPS IN FRAGILE X FAMILIESR01HD036071 · NICHD · UNIVERSITY OF CALIFORNIA DAVIS · PI PAUL J HAGERMAN, RANDI J. HAGERMAN · 1998 to 2026
$13.8M
Research Project: Pathologic Significance of Maternal AutoantibodiesP50HD103526 · NICHD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI LEONARD J. ABBEDUTO, Melissa Dawn Bauman · 2020 to 2026
$9.7M
NICHD NIH HHS P50 HD103526
6 · The paper itself

Abstract

Autism spectrum disorders (ASD) are subdivided into idiopathic (unknown) etiology and secondary, based on known etiology. There are hundreds of causes of ASD and most of them are genetic in origin or related to the interplay of genetic etiology and environmental toxicology. Approximately 30 to 50% of the etiologies can be identified when using a combination of available genetic testing. Many of these gene mutations are either core components of the Wnt signaling pathway or their modulators. The full mutation of the fragile X mental retardation 1 (FMR1) gene leads to fragile X syndrome (FXS), the most common cause of monogenic origin of ASD, accounting for ~ 2% of the cases. There is an overlap of molecular mechanisms in those with idiopathic ASD and those with FXS, an interaction between various signaling pathways is suggested during the development of the autistic brain. This review summarizes the cross talk between neurobiological pathways found in ASD and FXS. These signaling pathways are currently under evaluation to target specific treatments in search of the reversal of the molecular abnormalities found in both idiopathic ASD and FXS.

Indexed as

Molecular Targeted TherapyAutism Spectrum DisorderFragile X Messenger Ribonucleoprotein 1Fragile X SyndromeHumansMetabolic Networks and PathwaysSignal TransductionFMR1 protein, humanFragile X Messenger Ribonucleoprotein 1Autism spectrum disordersendocannabinoid systemERK/MAPKfragile X syndromemTORneurodevelopmental disordersretinoic acidsignaling cross talktargeted treatmentsWnt

Identifiers

PMID33215285
PMCPMC8116395
OpenAlexW3098728977

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.