Journal
ANNALS OF NEUROLOGY
Volume 88, Issue 6, Pages 1244-1250Publisher
WILEY
DOI: 10.1002/ana.25908
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Funding
- Association of British Neurologists
- Guarantors of Brain
- Wellcome Trust [104079/Z/14/Z]
- UCB-Oxford University Alliance
- BMA
- Epilepsy Research UK [P1201]
- Fulbright UK-US commission (MS-Research Society Award)
- UK NMO commissioning group
- National Institute for Health Research (NIHR) Oxford Biomedical Research Centre (BRC)
- ANR [CE17001002]
- Wellcome Trust [104079/Z/14/Z] Funding Source: Wellcome Trust
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This study aimed to characterise both neuronal autoantibodies and levels of interferon alpha, two proposed causative agents in neuropsychiatric systemic lupus erythematosus (NPSLE). Cerebrospinal fluid (CSF) and plasma from 35 patients with systemic lupus erythematosus (SLE; 15 with NPSLE) showed no antibodies against natively expressed N-methyl-D-aspartate receptors (NMDARs), or the surface of live hippocampal neurons. By comparison to controls (n = 104), patients with SLE had antibodies that bound to a peptide representing the extracellular domain of NMDARs (p< 0.0001), however, binding was retained against both rearranged peptides and no peptide (r = 0.85 and r = 0.79, respectively,p< 0.0001). In summary, neuronal-surface reactive antibodies were not detected in NPSLE. Further, while interferon alpha levels were higher in SLE (p< 0.0001), they lacked specificity for NPSLE. Our findings mandate a search for novel biomarkers in this condition. ANN NEUROL 2020
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