ArticlePediatric rheumatology online journal2022
Evidence of persistent glial cell dysfunction in the anterior cingulate cortex of juvenile idiopathic arthritis children: a proton MRS study.
Article in Pediatric rheumatology online journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Sustained hippocampal neuroinflammation and subsequent glutamatergic dysfunction in juvenile idiopathic arthritis: evidence from proton magnetic resonance spectroscopy (Arthritis research & therapy · 2025Article
- Blood brain barrier permeability and astrocyte-derived extracellular vesicles in children with juvenile idiopathic arthritis: a cross-sectional study.Pediatric rheumatology online journal · 2024Article
- Neurovascular protection of alisol A on cerebral ischemia mice through activating the AKT/GSK3β pathway.Aging · 2023Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThis study aims to investigate whether the neurometabolites of the anterior cingulate cortex (ACC) were distinct in patients with active and inactive juvenile idiopathic arthritis (JIA) using the proton magnetic resonance spectroscopy.
methodsWe measured the levels of total N-acetylaspartate (tNAA), choline (Cho), myo-inositol (ml), glutamate (Glu) and the complex of glutamate and glutamine (Glx) relative to total creatine (tCr) in ACC of each participant.
resultsCompared with the healthy controls, a significant decrease of total Cho/tCr and Glx/tCr ratio in ACC occurred in active and inactive JIA group. The tCho/Cr level was negatively associated with the serum level of ESR in active JIA patients. There was no difference in NAA/tCr ratio among the three groups, which may imply that no neuron and axonal losses occurred in either active or inactive JIA patients.
conclusionsThe abnormal neurometabolites in tCho/tCr and Glx/tCr in ACC may indicate that persistent dysfunction of glial cell, while neither neuron nor axonal losses occurred in active and inactive JIA patients.
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Registered trials
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