Evidence map›Paper›PMID 24605182›Full record

ReviewCommunicative & integrative biology2014

Glutamate receptor mutations in psychiatric and neurodevelopmental disorders.

David Soto, Xavier Altafaj, Carlos Sindreu, Alex Bayés

Open access · goldAbstract readReview
In one paragraph

Review in Communicative & integrative biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Disruption ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Protein quality control ofFrontiers in cellular neuroscience · 2022
    Review
  12. Review
  13. Translational medicine of the glutamate AMPA receptor.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2021
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Distinct roles ofF1000Research · 2019
    Review
  19. Article
  20. 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

4 authors at 4 institutions in 3 countries.

David SotoLaboratori de Neurobiologia; Institut d'Investigació Biomèdica de Bellvitge (IDIBELL) Feixa Llarga; L'Hospitalet de Llobregat; Barcelona, Spain.
Xavier AltafajInstitut de Neuropatologia; Institut d'Investigació Biomèdica de Bellvitge (IDIBELL); L'Hospitalet de Llobregat, Barcelona, Spain.
Carlos SindreuDepartment of Pharmacology; Universitat de Barcelona; Barcelona, Spain.
Alex BayésMolecular Physiology of the Synapse Laboratory; Biomedical Research Institute Sant Pau (IIB Sant Pau); Barcelona, Spain ; Universitat Autònoma de Barcelona; Bellaterra (Cerdanyola del Vallès), Spain.
Ajuntament de L’Hospitalet · ESBiomedical Research Institute · USManufacturas Serviplast (Spain) · ESUniversitat de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alterations in glutamatergic neurotransmission have long been associated with psychiatric and neurodevelopmental disorders (PNDD), but only recent advances in high-throughput DNA sequencing have allowed interrogation of the prevalence of mutations in glutamate receptors (GluR) among afflicted individuals. In this review we discuss recent work describing GluR mutations in the context of PNDDs. Although there are no strict relationships between receptor subunit or type and disease, some interesting preliminary conclusions have arisen. Mutations in genes coding for ionotropic glutamate receptor subunits, which are central to synaptic transmission and plasticity, are mostly associated with intellectual disability and autism spectrum disorders. In contrast, mutations of metabotropic GluRs, having a role on modulating neural transmission, are preferentially associated with psychiatric disorders. Also, the prevalence of mutations among GluRs is highly heterogeneous, suggesting a critical role of certain subunits in PNDD pathophysiology. The emerging bias between GluR subtypes and specific PNDDs may have clinical implications.

Indexed as

Glutamate receptorsintellectual disabilityneurodevelopmental disorderspsychiatric disorders

Identifiers

PMID24605182
PMCPMC3937208
OpenAlexW1998295234

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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 OpenQuestion graph.