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Interferon (IFN)-\u03b1 is a key immunopathogenic driver of SLE, being persistently overexpressed in the majority of patients. This longitudinal study aimed to investigate whether disease activity and serum IFN-\u03b1 levels over time were associated with objective findings of neuronal impairment regarding (i) higher plasma neurofilament light (NfL) concentrations, (ii) structural alterations on MRI, and (iii) cognitive dysfunction upon testing.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods<\/jats:title>\n            <jats:p>Sixty-six consecutive female SLE outpatients were enrolled in a cross-sectional study. Retrospectively, prior visits with concomitant blood samples (<jats:italic>n<\/jats:italic>\u2009=\u2009199) were selected from the Lund Lupus Cohort database and biobank. Serum IFN-\u03b1 concentrations were measured using an electrochemiluminescence immunoassay. IFN-\u03b1 lupus phenotypes were defined as high (<jats:italic>n<\/jats:italic>\u2009=\u200924) or low (<jats:italic>n<\/jats:italic>\u2009=\u200933) by considering persistent elevations in serum IFN-\u03b1 concentrations despite low SLE Disease Activity Index-2000 (SLEDAI-2\u00a0K) scores. SLEDAI-2\u00a0K lupus phenotypes were defined as moderate-high (<jats:italic>n<\/jats:italic>\u2009=\u200931) or low (<jats:italic>n<\/jats:italic>\u2009=\u200935) based on SLEDAI-2\u00a0K scores from all 576 available visits prior to the study. Ongoing neuronal damage was assessed by plasma NfL concentration measurements using Simoa at the 199 visits. Structural MRI alterations and cognitive dysfunction according to the CNS-Vital Signs test battery were the additional outcomes. Multivariate linear mixed-effect, linear regression, and logistic regression models were used for the statistical analyses.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>Visits with higher disease activity were associated with higher plasma NfL concentrations (e.g. SLEDAI-2\u00a0K total: <jats:italic>p<\/jats:italic>\u2009=\u20091.5*10<jats:sup>\u2212\u20096<\/jats:sup>). High compared with low IFN-\u03b1 lupus phenotype patients displayed more cognitive dysfunction (odds ratio 11.0, <jats:italic>p<\/jats:italic>\u2009=\u20090.004), and smaller volumes of total grey matter, caudate nucleus, and thalamus (<jats:italic>p<\/jats:italic>\u2009=\u20090.036; <jats:italic>p<\/jats:italic>\u2009=\u20090.038; <jats:italic>p<\/jats:italic>\u2009=\u20090.023). Moderate-high compared with low SLEDAI-2\u00a0K lupus phenotype patients displayed larger white matter lesion volumes and smaller total grey matter and thalamus volumes (<jats:italic>p<\/jats:italic>\u2009=\u20090.011; <jats:italic>p<\/jats:italic>\u2009=\u20090.041; <jats:italic>p<\/jats:italic>\u2009=\u20090.005).<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>The study suggests that disease activity and IFN-\u03b1 may drive neuronal affliction in SLE, also in the absence of overt neuropsychiatric symptoms, and that controlling disease activity could improve the cerebral outcome.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/s13075-025-03539-2","type":"journal-article","created":{"date-parts":[[2025,3,20]],"date-time":"2025-03-20T07:19:40Z","timestamp":1742455180000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["The impact of disease activity and interferon-\u03b1 on the nervous system in systemic lupus erythematosus"],"prefix":"10.1186","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4311-1635","authenticated-orcid":false,"given":"Kristoffer A.","family":"Zervides","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elsa","family":"Grenmyr","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shorena","family":"Janelidze","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Petrus","family":"Linge","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jessika","family":"Nystedt","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Petra C.","family":"Nilsson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pia C.","family":"Sundgren","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oskar","family":"Hansson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anders A.","family":"Bengtsson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreas","family":"J\u00f6nsen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,3,20]]},"reference":[{"issue":"9","key":"3539_CR1","doi-asserted-by":"publisher","first-page":"515","DOI":"10.1038\/s41584-021-00668-1","volume":"17","author":"MRW Barber","year":"2021","unstructured":"Barber MRW, Drenkard C, Falasinnu T, Hoi A, Mak A, Kow NY, et al. 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