Evidence map›Paper›PMID 33859358›Full record

ReviewMolecular psychiatry2022

A unified model of the pathophysiology of bipolar disorder.

Paola Magioncalda, Matteo Martino

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Molecular psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07785167 (Characterization of Chemokine Receptor Expression in CD8+ T Lymphocytes in Bipolar Disorder), which is not on this map. Cited by 47 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 6 pooled it
7.5field-weighted citation impact, top 2% 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.

NCT07785167 not yet recruitingnot on this mapstarted 2026, after this paper: background citation

Characterization of Chemokine Receptor Expression in CD8+ T Lymphocytes in Bipolar Disorder

TypeobservationalSponsorUniversity of CataniaRan2026 to 2028Enrolled172ConditionsBipolar Affective DisordersArmsCD8+ T-Cell Gene Expression Analysis
3 · Its place in the literature

Who cites it

47 citing papers in PubMed, 6 syntheses or guidelines pooled it, 74 citations in OpenAlex.

  1. Pooled it
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  4. Associations between structural brain measures and cognitive function in bipolar disorder: a systematic review and meta-analysis.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
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  7. Polarisation of brain dynamics in mania and depression.Dialogues in clinical neuroscience · 2026
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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

2 authors at 1 institution in 1 country.

Paola Magioncalda *Graduate Institute of Mind Brain and Consciousness, Taipei Medical University, Taipei, Taiwan. paola.magioncalda@gmail.com.ORCID http://orcid.org/0000-0003-4985-4819
Matteo Martino *Graduate Institute of Mind Brain and Consciousness, Taipei Medical University, Taipei, Taiwan. matteomartino9@gmail.com.ORCID http://orcid.org/0000-0002-3783-707X
Taipei Medical University-Shuang Ho Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This work provides an overview of the most consistent alterations in bipolar disorder (BD), attempting to unify them in an internally coherent working model of the pathophysiology of BD. Data on immune-inflammatory changes, structural brain abnormalities (in gray and white matter), and functional brain alterations (from neurotransmitter signaling to intrinsic brain activity) in BD were reviewed. Based on the reported data, (1) we hypothesized that the core pathological alteration in BD is a damage of the limbic network that results in alterations of neurotransmitter signaling. Although heterogeneous conditions can lead to such damage, we supposed that the main pathophysiological mechanism is traceable to an immune/inflammatory-mediated alteration of white matter involving the limbic network connections, which destabilizes the neurotransmitter signaling, such as dopamine and serotonin signaling. Then, (2) we suggested that changes in such neurotransmitter signaling (potentially triggered by heterogeneous stressors onto a structurally-damaged limbic network) lead to phasic (and often recurrent) reconfigurations of intrinsic brain activity, from abnormal subcortical-cortical coupling to changes in network activity. We suggested that the resulting dysbalance between networks, such as sensorimotor networks, salience network, and default-mode network, clinically manifest in combined alterations of psychomotricity, affectivity, and thought during the manic and depressive phases of BD. Finally, (3) we supposed that an additional contribution of gray matter alterations and related cognitive deterioration characterize a clinical-biological subgroup of BD. This model may provide a general framework for integrating the current data on BD and suggests novel specific hypotheses, prompting for a better understanding of the pathophysiology of BD.

Indexed as

Bipolar DisorderWhite MatterBrainBrain MappingHumansMagnetic Resonance Imaging

Identifiers

PMID33859358
OpenAlexW3155246096

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.