Evidence map›Paper›PMID 41142167›Full record

ReviewBehavioural neurology2025

Biomarkers in Schizophrenia: Current Approaches and New Developments-A Literature Review.

Alicja Sierakowska, Ewa Niewiadomska, Sebastian Łabuda, Anna Bieniasiewicz, Mateusz Roszak, Beata Łabuz-Roszak

Abstract readReview
In one paragraph

Review in Behavioural neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. 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

6 authors.

Alicja SierakowskaInstitute of Medical Sciences, University of Opole, Opole, Poland, uni.opole.pl.ORCID https://orcid.org/0000-0003-2057-8734
Ewa NiewiadomskaDepartment of Epidemiology and Biostatistics, Faculty of Public Health in Bytom, Medical University of Silesia, Katowice, Poland, sum.edu.pl.ORCID https://orcid.org/0000-0003-0612-1949
Sebastian ŁabudaDepartment of Psychiatry, St. Jadwiga Provincial Specialist Hospital, Opole, Poland.ORCID https://orcid.org/0009-0007-9433-9935
Anna BieniasiewiczDepartment of Neurology, St. Jadwiga Provincial Specialist Hospital, Institute of Medical Sciences, University of Opole, Opole, Poland, uni.opole.pl.ORCID https://orcid.org/0000-0002-6113-8092
Mateusz RoszakStudent Scientific Association at the Department of Neurology, Institute of Medical Sciences, University of Opole, Opole, Poland, uni.opole.pl.ORCID https://orcid.org/0000-0001-5550-6568
Beata Łabuz-RoszakDepartment of Neurology, St. Jadwiga Provincial Specialist Hospital, Institute of Medical Sciences, University of Opole, Opole, Poland, uni.opole.pl.ORCID https://orcid.org/0000-0002-9835-8240

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schizophrenia (SZ) is categorized as a chronic severe highly heritable brain disease. Symptoms include positive, negative, and cognitive symptoms. Despite numerous theories concerning the etiopathogenesis of SZ, the symptoms, although characteristic in their phenomenology, manifest themselves in a rather heterogeneous manner, which makes them subject to clinical assessment and, at the same time, prone to errors resulting from diverse interpretations of the context of the patient's statements. Therefore, current research is focusing on identifying more subtle and stable features of SZ, such as the phenotype, endophenotype, and assessable abnormalities devoid of human clinical observation. The various biomarker developments focus on the role of transmitters and their corresponding receptors, in particular: glutamate, acetylcholine, dopamine, or serotonin. Also important in terms of etiopathogenesis remain growth factors such as brain-derived neurotrophic factor (BDNF), nerve growth factor receptor (NGFR), or vascular endothelial growth factor (VEGF). More recently, research has emphasized the role of inflammatory processes and secreted pro- as well as anti-inflammatory cytokines, included in the class of interleukins, chemokines, and tumor necrosis factors, as well as on inflammatory markers-C-reactive protein (CRP) or glutathione (GSH). Increasingly, changes at the genetic level have been implicated as the cause of diseases, and it is now believed that noncoding RNAs (micro-RNA [miRNA], long noncoding RNA [lnc-RNA], and circular RNA [circRNA]) are involved in the development of SZ. Among the genes that may prove to be potential biomarkers in SZ belong SEDT1A, FOXP2, GRIN2A, GRIA3, NRN1, BDNF, CACNA1C, and ZNF8A4. The peptide group molecules, Phospholipase A2, Klotho protein, and soluble urokinase plasminogen activator receptor (suPAR), also remain consistently important. From the perspective of SZ as a disease associated with neuronal damage, biomarkers correlating with brain injury, neuron-specific enolase (NSE), and S100B protein should be considered.

Indexed as

BiomarkersSchizophreniaBrain-Derived Neurotrophic FactorCytokinesHumansBiomarkersBrain-Derived Neurotrophic FactorCytokinesbiomarkersetiopathogenesisschizophrenia

Identifiers

PMID41142167
PMCPMC12539668

What OpenQuestion holds

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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.