Lupus & antiphospholipid syndrome
Salience network dysfunction in SLE: convergent roles of complement activation and altered serotonergic signaling
Authors' conclusion
Our study identifies a convergent mechanism in which complement-mediated inflammation, and serotonergic signalling alterations may collectively contribute to SN dysregulation in SLE.
Study context
- Population
- SLE patients and healthy controls
- Participants
- 76 vs 68
- Comparison
- SLE patients vs healthy controls
- SLEn = 76
- Healthy controlsn = 68reference
- Outcome
- SN abnormalities (functional gradients, dFC and sFC with SMN and DMN, gene enrichment, neurotransmitter mapping)
Methodological detailsresting-state fMRI, multimodal, case-control
- Resting-state fMRI
- Multimodal
- Case-control
Main finding
As reported in the abstract
SN abnormalities in SLE vs controls
- Reduced gradient values in salience network (SN) and frontoparietal control network in SLE
- Compressed gradient distance between SN and SMN in SLE
- Decreased static functional connectivity (sFC) between SN and DMN; enhanced sFC between SN and SMN
- Significantly higher fractional occupations in states with lower information integration in SLE (dynamic functional connectivity (dFC))
- Network abnormalities correlated with C3 complement levels
- SN gradient abnormalities associated with enrichment in synaptic and protein-binding genes, WFDC1 strongest predictor
- SN gradient abnormalities significantly related to 5-HT2A receptor expression patterns
Original publication
Salience network dysfunction in SLE: convergent roles of complement activation and altered serotonergic signaling. Rheumatology (Oxford). Published 27 November 2025. doi:10.
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