OSCR

Peripheral Transcriptomic Signatures Reveal Convergent Neuroinflammatory, Metabolic, and miRNA Dysregulation in Major Psychiatric Disorders.

Overview

Authors: Ron Jacob B. Avila1,2, Jhyme Lou O. De La Cerna1,2, Lemmuel L. Tayo3
  1. School of Chemical, Biological, and Materials Engineering and Sciences, Mapúa University, Manila 1002, Philippines; (R.J.B.A.); (J.L.O.D.L.C.)
  2. School of Graduate Studies, Mapúa University, Manila 1002, Philippines
  3. Department of Biology, School of Health Sciences, Mapúa University, Makati 1203, Philippines
Institutions: Mapúa University (Philippines)
Journal: Biology, volume 15, issue 9, article 673
Dates: received 6 March 2026; accepted 22 April 2026; published online 24 April 2026
Type: Research article · Language: English
License: CC BY
Identifiers: DOI 10.3390/biology15090673 · PMID 42117812 · PMCID PMC13162896 · OpenAlex W7155530013
Open access: gold, a free copy (OpenAlex)
Status: data only
Categories: genetics / omics (modality), cellular / molecular (subfield)
Methods: Statistics, Smoothing, state filtering, decompositions, Connectivity, Graphs, Spectral & time-frequency
Keywords: neuropsychiatric disorders, WGCNA, hub genes, neuroinflammation, microRNA, dendritic pruning
Topic: Tryptophan and brain disorders (Biological Psychiatry, Neuroscience), according to OpenAlex
Citations: not cited yet (Europe PMC); 194 references in the paper

Abstract

Background/Objectives: Although clinically distinct, bipolar disorder (BP), schizophrenia (SZ), major depressive disorder (MDD), and social anxiety disorder (SAD) share fundamental biology. We mapped these transdiagnostic systemic mechanisms. Methods: Weighted Gene Co-Expression Network Analysis (WGCNA) of peripheral blood RNA-Seq datasets evaluated module preservation, hub gene disruption, and microRNA (miRNA) networks. Results: Seven modules showed robust cross-disease preservation. Overall, 56 of 105 candidate hub genes exhibited altered expression, with 22 passing the false discovery rate (FDR) correction. Hubs like IL1B, TLR2, and MMP9 dominated networks linked to altered inflammatory signaling and structural remodeling. Downregulated ribosomal hubs characterized systemic metabolic stress. Discussion: These signatures capture extensive systemic dysregulation. Inflammation and metabolic shifts correlate strongly with pathways regulating chronic neuroinflammation, epigenetic control, and dendritic pruning. Computational models suggest these cascades evade miRNA controls, potentially compromising structural neural plasticity. Conclusions: This shared transcriptomic architecture challenges rigid diagnostic boundaries. Identifying systemic immune dysregulation and translational alterations as core pathogenic denominators provides a rationale for transdiagnostic therapies targeting upstream systemic networks to mitigate neural vulnerabilities.

Reproduced under the paper's license (CC BY), from the paper cited above.

Code

The paper links to its data, not to its authors' code: see the Data section.

Tracing map

A tracing map links a paper to the code its authors published: this paper has none, so it has no map.

Data

Data links

Data Availability Statement

The transcriptomic datasets analyzed in this study are publicly available from the Gene Expression Omnibus (GEO) database (https://www.ncbi.nlm.nih.gov/geo/ (accessed on 3 January 2026)). The datasets include SZ (GSE243841), BP (GSE124326), MDD (GSE251778), and SAD (GSE228702).

Reproduced under the paper's license (CC BY), from the paper cited above.

Versions

The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.

Version 1, 29 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 3 authors, 6 keywords, 194 references.

Cite

This paper

Avila, R. J. B., De La Cerna, J. L. O., & Tayo, L. L. (2026). Peripheral Transcriptomic Signatures Reveal Convergent Neuroinflammatory, Metabolic, and miRNA Dysregulation in Major Psychiatric Disorders. Biology, 15(9), 673. https://doi.org/10.3390/biology15090673

BibTeX

@article{avila2026peripheral,
author = {Avila, Ron Jacob B. and De La Cerna, Jhyme Lou O. and Tayo, Lemmuel L.},
title = {{Peripheral Transcriptomic Signatures Reveal Convergent Neuroinflammatory, Metabolic, and miRNA Dysregulation in Major Psychiatric Disorders}},
journal = {Biology},
year = {2026},
month = apr,
volume = {15},
number = {9},
pages = {673},
publisher = {Multidisciplinary Digital Publishing Institute (MDPI)},
issn = {2079-7737},
doi = {10.3390/biology15090673},
url = {https://doi.org/10.3390/biology15090673},
pmid = {42117812},
pmcid = {PMC13162896}
}

RIS

TY - JOUR
AU - Avila, Ron Jacob B.
AU - De La Cerna, Jhyme Lou O.
AU - Tayo, Lemmuel L.
TI - Peripheral Transcriptomic Signatures Reveal Convergent Neuroinflammatory, Metabolic, and miRNA Dysregulation in Major Psychiatric Disorders
T2 - Biology
J2 - Biology (Basel)
PY - 2026
DA - 2026/04/24
VL - 15
IS - 9
SP - 673
SN - 2079-7737
PB - Multidisciplinary Digital Publishing Institute (MDPI)
DO - 10.3390/biology15090673
UR - https://doi.org/10.3390/biology15090673
LA - en
ER -

CSL-JSON

{
"id": "10.3390/biology15090673",
"type": "article-journal",
"title": "Peripheral Transcriptomic Signatures Reveal Convergent Neuroinflammatory, Metabolic, and miRNA Dysregulation in Major Psychiatric Disorders",
"container-title": "Biology",
"author": [
{
"family": "Avila",
"given": "Ron Jacob B."
},
{
"family": "De La Cerna",
"given": "Jhyme Lou O."
},
{
"family": "Tayo",
"given": "Lemmuel L."
}
],
"container-title-short": "Biology (Basel)",
"volume": "15",
"issue": "9",
"page": "673",
"DOI": "10.3390/biology15090673",
"PMID": "42117812",
"PMCID": "PMC13162896",
"ISSN": "2079-7737",
"publisher": "Multidisciplinary Digital Publishing Institute (MDPI)",
"URL": "https://doi.org/10.3390/biology15090673",
"language": "en",
"issued": {
"date-parts": [
[
2026,
4,
24
]
]
}
}

Similar papers

The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.

[1] doi:10.1038/s41386-026-02406-1 [code]
Functional genomic profiling of schizophrenia-associated genes reveals key microglial regulators.
Journal: Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
In common: genetics / omics, cellular / molecular, 5 references
[2] doi:10.1038/s41380-026-03571-x [code]
Convergent coexpression reveals shared biological mechanisms underlying common and rare variant risk in six neuropsychiatric disorders.
Journal: Molecular psychiatry
In common: genetics / omics, cellular / molecular, 4 references
[3] doi:10.1038/s41467-026-71542-5 [code]
Astrocyte fatty acid metabolism as a driver of risk for major depressive disorder.
Journal: Nature communications
In common: genetics / omics, cellular / molecular, 4 references
[4] doi:10.1177/09727531261420619
A Meta-analysis to Identify Common Key Genes Across Ageing, Alzheimer's and Parkinson's Diseases.
Journal: Annals of neurosciences
In common: genetics / omics, cellular / molecular, 3 references
[5] doi:10.3390/biomedicines14030610
Magnesium Transporter SLC41A1 Links Magnesium Homeostasis to NMDA Receptor-Related Synaptic Dysfunction: A Transdiagnostic Therapeutic Target for Neuropsychiatric Disorders.
Journal: Biomedicines
In common: genetics / omics, cellular / molecular, 3 references
[6] doi:10.1007/s10571-026-01726-6
Gene Expression Analysis of Mitochondria-Associated Membrane (MAM)-Related Genes in ER Stress and Alzheimer's Disease.
Journal: Cellular and molecular neurobiology
In common: genetics / omics, cellular / molecular, 4 references
[7] doi:10.1371/journal.pcbi.1014422 [code]
Deciphering cell type-specific causal genetic effects on brain imaging-derived phenotypes and disorders with single-cell Mendelian randomization.
Journal: PLoS computational biology
In common: genetics / omics, cellular / molecular, 3 references
[8] doi:10.1038/s41588-026-02646-3 [code]
Co-expression-based models improve eQTL predictions for transcriptome-wide association studies and highlight new schizophrenia-associated genes.
Journal: Nature genetics
In common: genetics / omics, cellular / molecular, 3 references
[9] doi:10.1002/ejp.70277 [code]
Proximity Labelling Reveals the Compartmental Proteome of Murine Sensory Neurons.
Journal: European journal of pain (London, England)
In common: genetics / omics, cellular / molecular, 4 references
[10] doi:10.1002/advs.77453 [code]
Tau Aggregate Imaging and Transcriptomics of Alzheimer's Disease Brain at Different Stages of Disease.
Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)
In common: genetics / omics, cellular / molecular, 3 references

Contribute

The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.

Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.

Request its removal

To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).

Discussion, reproductions, activity

Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.

Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.

Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.