Evidence map›Paper›PMID 35930223›Full record

ArticleAdvances in experimental medicine and biology2022

What Can We Learn from Animal Models to Study Schizophrenia?

Fernanda Crunfli, Caroline Brandão-Teles, Giuliana S Zuccoli, Adriano J M Chaves Filho, Gabriela Maciel Vieira, Danyelle Silva-Amaral, José Alexandre Crippa, João F C Pedrazzi, Danielle S Macêdo, Elaine Del-Bel and 1 more

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In one paragraph

Article in Advances in experimental medicine and biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

1 citing paper in PubMed, 5 citations in OpenAlex.

  1. 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

11 authors at 3 institutions in 1 country.

Fernanda Crunfli *Laboratory of Neuroproteomics, Department of Cell and Tissue Biology, Institute of Biology, State University of Campinas, Campinas, SP, Brazil. fernandacrunfli@gmail.com.
Caroline Brandão-Teles *Laboratory of Neuroproteomics, Department of Cell and Tissue Biology, Institute of Biology, State University of Campinas, Campinas, SP, Brazil.
Giuliana S ZuccoliLaboratory of Neuroproteomics, Department of Cell and Tissue Biology, Institute of Biology, State University of Campinas, Campinas, SP, Brazil.
Adriano J M Chaves FilhoNeuropharmacology Laboratory, Department of Physiology and Pharmacology, Universidade Federal do Ceará, NPDM, Fortaleza, CE, Brazil.
Gabriela Maciel VieiraLaboratory of Neuroproteomics, Department of Cell and Tissue Biology, Institute of Biology, State University of Campinas, Campinas, SP, Brazil.
Danyelle Silva-AmaralDepartment of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.
José Alexandre CrippaDepartment of Neurosciences and Behavioral Sciences, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.
João F C PedrazziDepartment of Neurosciences and Behavioral Sciences, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.
Danielle S MacêdoNeuropharmacology Laboratory, Department of Physiology and Pharmacology, Universidade Federal do Ceará, NPDM, Fortaleza, CE, Brazil.
Elaine Del-BelDepartment of Basic and Oral Biology, School of Dentistry of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.
Felipe V GomesDepartment of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.
Universidade de São Paulo · BRUniversidade Estadual de Campinas (UNICAMP) · BRUniversidade Federal do Ceará · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schizophrenia is a complex and heterogeneous neurodevelopmental psychiatric disorder characterized by a variety of symptoms classically grouped into three main domains: positive (hallucinations, delusions, and thought disorder) and negative symptoms (social withdrawal, lack of affect) and cognitive dysfunction (attention, working and episodic memory functions, and processing speed). This disorder places an immense emotional and economic pressure on the individual and society-at-large. Although the etiology of schizophrenia is not completely known, it is proposed to involve abnormalities in neurodevelopmental processes and dysregulation in the signaling mediated by several neurotransmitters, such as dopamine, glutamate, and GABA. Preclinical research using animal models are essential in our understanding of disease development and pathology as well as the discovery and advance of novel treatment choices. Here we describe rodent models for studying schizophrenia, including those based on the effects of drugs (pharmacological models), neurodevelopmental disruption, demyelination, and genetic alterations. The advantages and limitations of such models are highlighted. We also discussed the great potential of proteomic technologies in unraveling the molecular mechanism of schizophrenia through animal models.

Indexed as

SchizophreniaAnimalsAttentionDisease Models, AnimalDopamineHumansModels, AnimalProteomicsDopamineAnimal modelsDopamineGlutamateProteomicPsychosisSchizophrenia

Identifiers

PMID35930223
OpenAlexW4289886514

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.