Evidence map›Paper›PMID 35930230›Full record

ArticleAdvances in experimental medicine and biology2022

Modulating Specific Pathways In Vitro to Understand the Synaptic Dysfunction of Schizophrenia.

Verônica M Saia-Cereda

Abstract read
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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. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 79% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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 at 1 institution in 1 country.

Verônica M Saia-CeredaLaboratory of Neuroproteomics, Department of Biochemistry and Tissue Biology, Institute of Biology, University of Campinas (UNICAMP), Campinas, Brazil. vecereda@gmail.com.
Universidade Estadual de Campinas (UNICAMP) · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schizophrenia is an incurable mental disorder that affects 1% of the world population and is among the most disabling human diseases. On average, 70% of patients abandon medication due to its low efficacy and the presence of severe side effects. To change these conditions, it is necessary to understand the pathophysiology of schizophrenia at the molecular level. Besides the long-established neurodevelopmental hypothesis, works based on neuroimaging, postmortem brain proteomics, and pharmacological, genetic, and animal model studies have shown dysfunction and deficits in synaptic transmission. Currently, genetic editing has been growing, and the use of this technique has been improved in the discovery of protein functions; in addition to that, some recent studies have attributed a path to the use of genetic engineering in the treatment of diseases with a genetic nature.

Indexed as

SchizophreniaAnimalsBrainHumansNeuroimagingProteomicsSynaptic TransmissionEmbryonic stem cellsNeural cellsNeurodevelopmental diseases

Identifiers

PMID35930230
OpenAlexW4289922008

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.