Sustained hippocampal neuroinflammation and subsequent glutamatergic dysfunction in juvenile idiopathic arthritis: evidence from proton magnetic resonance spectroscopy (1H-MRS)
Authors' conclusion
Sustained hippocampal neuroinflammation (indicated by elevated mI/tCr) and the subsequent glutamatergic synaptic dysfunction (indicated by reduced Glu/tCr and Glx/tCr) were identified in JIA patients.
Study context
- Population
- Juvenile idiopathic arthritis (JIA) patients across active and inactive disease phases and healthy controls248 JIA patients
- Participants
- 61 / 187 / 57
- Exposure
- Active JIA and inactive JIA vs healthy controls
- Active JIAn = 61
- Inactive JIAn = 187
- Healthy controls (HCs)n = 57reference
- Outcome
- Right hippocampal metabolite ratios (tNAA, tCho, mI, Glu, Glx relative to tCr)
Methodological details1H-MRS of the right hippocampus
- 1H-MRS of the right hippocampus
Main finding
As reported in the abstract
Hippocampal metabolite ratios vs HCs
- Both JIA groups showed elevated myo-inositol (mI)/total creatine (tCr) vs HCs (all P < 0.05)
- Reduced glutamate (Glu)/tCr and Glx/tCr in the inactive JIA group vs HCs (all P < 0.05)
Observational data: associations, not effects.
Further findings
Correlation of mI/tCr with systemic inflammation in active JIA
- mI/tCr vs ESR, rho
- 0.269
- mI/tCr vs CRP, rho
- 0.287
- Did not survive the rigid multiple correction
tNAA/tCr, total choline (tCho)/tCr, Glu/tCr and Glx/tCr vs systemic inflammation and clinical indices
- No significant correlations in treatment-naïve and inactive JIA
Original publication
Sustained hippocampal neuroinflammation and subsequent glutamatergic dysfunction in juvenile idiopathic arthritis: evidence from proton magnetic resonance spectroscopy (1H-MRS). Arthritis Res Ther. Published 30 December 2025. doi:10.
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