Evidence map›Paper›PMID 41090786›Full record

ReviewCells2025

Inflammatory and Immune Biomarkers in Mood Disorders: From Mechanistic Pathways to Clinical Translation.

Mario Pinzi, Andrea Fagiolini, Despoina Koukouna, Giacomo Gualtieri, Maria Beatrice Rescalli, Caterina Pierini, Simone Pardossi, Benjamin Patrizio, Alessandro Cuomo

Abstract readReview
In one paragraph

Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

9 authors.

Mario PinziDepartment of Molecular Medicine, School of Medicine, University of Siena, 53100 Siena, Italy.
Andrea FagioliniDepartment of Molecular Medicine, School of Medicine, University of Siena, 53100 Siena, Italy.ORCID 0000-0001-5827-0853
Despoina KoukounaDepartment of Molecular Medicine, School of Medicine, University of Siena, 53100 Siena, Italy.ORCID 0009-0009-5200-1148
Giacomo GualtieriDepartment of Molecular Medicine, School of Medicine, University of Siena, 53100 Siena, Italy.ORCID 0009-0004-1008-9915
Maria Beatrice RescalliDepartment of Molecular Medicine, School of Medicine, University of Siena, 53100 Siena, Italy.
Caterina PieriniDepartment of Molecular Medicine, School of Medicine, University of Siena, 53100 Siena, Italy.
Simone PardossiDepartment of Molecular Medicine, School of Medicine, University of Siena, 53100 Siena, Italy.ORCID 0009-0004-3002-529X
Benjamin PatrizioDepartment of Molecular Medicine, School of Medicine, University of Siena, 53100 Siena, Italy.
Alessandro CuomoDepartment of Molecular Medicine, School of Medicine, University of Siena, 53100 Siena, Italy.ORCID 0000-0002-9211-5248

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over the past two decades, immune-inflammatory dysregulation has emerged as a central paradigm in the biology of mood disorders. Patients with major depression (MDD) and bipolar disorder (BD) frequently display low-grade systemic inflammation. Elevated C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) identify clinically relevant subgroups of patients characterized by greater severity, cognitive impairment, and poor treatment response. Changes in the gut microbiota and disruptions of the blood-brain barrier (BBB) act as important gateways through which systemic immune activity can influence the brain. At the intracellular level, pattern-recognition receptors activate convergent hubs including NF-κB, JAK/STAT, and MAPK cascades, while the NLRP3 inflammasome integrates mitochondrial dysfunction and oxidative stress with IL-1β release and pyroptosis. These pathways converge on glial dysregulation, impaired BDNF/TrkB signaling, and kynurenine pathway (KP) alterations, fostering excitotoxicity and synaptic deficits. Translational studies demonstrate that elevated CRP and IL-6 predict poor antidepressant outcomes. Anti-inflammatory agents such as infliximab and celecoxib show efficacy in specific subgroups of patients. Emerging multi-omics approaches identify immuno-metabolic biotypes, supporting the rationale for biomarker-guided stratification. These findings define an 'inflammatory biotype' of mood disorders and highlight the need for biomarkers and precision-based trials to guide treatment.

Indexed as

BiomarkersImmune SystemMood DisordersNeuroinflammatory DiseasesC-Reactive ProteinHumansImmunomodulationInterleukin-6MicrobiotaSignal TransductionTumor Necrosis Factor-alphaBiomarkersC-Reactive ProteinInterleukin-6Tumor Necrosis Factor-alphabiomarkersmood disordersneuroinflammationprecision psychiatry

Identifiers

PMID41090786
PMCPMC12524191

What OpenQuestion holds

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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.