ArticleArthritis research & therapy2025
Sustained hippocampal neuroinflammation and subsequent glutamatergic dysfunction in juvenile idiopathic arthritis: evidence from proton magnetic resonance spectroscopy (
Article in Arthritis research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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7 authors.
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Abstract
backgroundChronic pain and psychiatric comorbidities in juvenile idiopathic arthritis (JIA) persist even during disease remission, suggesting central nervous system (CNS) alterations. This study used proton magnetic resonance spectroscopy (
methodsA cohort of 248 JIA patients (61 treatment-naïve patients with active JIA and 187 patients with inactive JIA) and 57 healthy controls (HCs) underwent
resultsCompared with HCs, both JIA groups showed elevated mI/tCr and reduced Glu/tCr and Glx/tCr in the inactive JIA group (all, P < 0.05). mI/tCr was positively correlated with ESR (rho = 0.269) and CRP (rho = 0.287) in active JIA patients. However, the results did not survive the rigid multiple correction. Notably, tNAA/tCr, tCho/tCr, Glu/tCr and Glx/tCr showed no significant correlations with systemic inflammation and clinical indices for treatment-naïve and inactive JIA patients.
conclusionsSustained 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. Peripheral inflammation may drive microglial activation during active disease, highlighting the hippocampus as a vulnerable CNS target in chronic inflammatory states.
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