Evidence map›Paper›PMID 22251963›Full record

ReviewNature reviews. Neuroscience2012

Interneuron dysfunction in psychiatric disorders.

Oscar Marín

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 716 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
716citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

716 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
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  6. A compact GAD67 promoter enables inhibitory neuron-targeted AAV gene therapy for seizure suppression.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
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656 more citing papers are in PubMed but not listed here.

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

1 author.

Oscar MarínInstituto de Neurociencias, Consejo Superior de Investigaciones Científicas y Universidad Miguel Hernández, 03550 Sant Joan d'Alacant, Spain. o.marin@umh.es

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schizophrenia, autism and intellectual disabilities are best understood as spectrums of diseases that have broad sets of causes. However, it is becoming evident that these conditions also have overlapping phenotypes and genetics, which is suggestive of common deficits. In this context, the idea that the disruption of inhibitory circuits might be responsible for some of the clinical features of these disorders is gaining support. Recent studies in animal models demonstrate that the molecular basis of such disruption is linked to specific defects in the development and function of interneurons - the cells that are responsible for establishing inhibitory circuits in the brain. These insights are leading to a better understanding of the causes of schizophrenia, autism and intellectual disabilities, and may contribute to the development of more-effective therapeutic interventions.

Indexed as

InterneuronsAnimalsBrainDisease Models, AnimalEnvironmentHumansMental DisordersModels, Neurological

Identifiers

PMID22251963

What OpenQuestion 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 OpenQuestion graph.