Evidence map›Paper›PMID 24851087›Full record

ArticleCurrent neuropharmacology2014

The glutamatergic aspects of schizophrenia molecular pathophysiology: role of the postsynaptic density, and implications for treatment.

Felice Iasevoli, Carmine Tomasetti, Elisabetta F Buonaguro, Andrea de Bartolomeis

Open access · bronzeAbstract read
In one paragraph

Article in Current neuropharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
3.3field-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

26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Alpha psychiatry · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. The Effects of Antipsychotics on the Synaptic Plasticity GeneInternational journal of molecular sciences · 2020
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Altered expression of schizophrenia-related genes in mice lacking mGlu5 receptors.European archives of psychiatry and clinical neuroscience · 2018
    Article
  18. Article
  19. New Targets for Schizophrenia Treatment beyond the Dopamine Hypothesis.International journal of molecular sciences · 2017
    Review
  20. Article
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 1 institution in 1 country.

Felice IasevoliDepartment of Neuroscience, Reproductive and Odontostomatological Sciences - University "Federico II", Naples, Italy.
Carmine TomasettiDepartment of Neuroscience, Reproductive and Odontostomatological Sciences - University "Federico II", Naples, Italy.
Elisabetta F BuonaguroDepartment of Neuroscience, Reproductive and Odontostomatological Sciences - University "Federico II", Naples, Italy.
Andrea de BartolomeisDepartment of Neuroscience, Reproductive and Odontostomatological Sciences - University "Federico II", Naples, Italy.
Federico II University Hospital · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schizophrenia is one of the most debilitating psychiatric diseases with a lifetime prevalence of approximately 1%. Although the specific molecular underpinnings of schizophrenia are still unknown, evidence has long linked its pathophysiology to postsynaptic abnormalities. The postsynaptic density (PSD) is among the molecular structures suggested to be potentially involved in schizophrenia. More specifically, the PSD is an electron-dense thickening of glutamatergic synapses, including ionotropic and metabotropic glutamate receptors, cytoskeletal and scaffolding proteins, and adhesion and signaling molecules. Being implicated in the postsynaptic signaling of multiple neurotransmitter systems, mostly dopamine and glutamate, the PSD constitutes an ideal candidate for studying dopamine-glutamate disturbances in schizophrenia. Recent evidence suggests that some PSD proteins, such as PSD-95, Shank, and Homer are implicated in severe behavioral disorders, including schizophrenia. These findings, further corroborated by genetic and animal studies of schizophrenia, offer new insights for the development of pharmacological strategies able to overcome the limitations in terms of efficacy and side effects of current schizophrenia treatment. Indeed, PSD proteins are now being considered as potential molecular targets against this devastating illness. The current paper reviews the most recent hypotheses on the molecular mechanisms underlying schizophrenia pathophysiology. First, we review glutamatergic dysfunctions in schizophrenia and we provide an update on postsynaptic molecules involvement in schizophrenia pathophysiology by addressing both human and animal studies. Finally, the possibility that PSD proteins may represent potential targets for new molecular interventions in psychosis will be discussed.

Indexed as

DopaminehomerkalirinNMDAPSD-95psychosisshanksynaptic plasticity.

Identifiers

PMID24851087
PMCPMC4023453
OpenAlexW2031405035

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.