The following are selected presentations from the 12th Congress of the European Academy of Neurology, held June 27-30, 2026 in Geneva, Switzerland
Ocrelizumab discontinuation
Role of fluid biomarkers in practice
Cyclophosphamide vs. siponimod in SPMS
Relapse during pregnancy in MOGAD, NMOSD
GLP-1 signalling in NMOSD
Ocrelizumab discontinuation
A propensity score-matched study (N=290) reported that ocrelizumab discontinuation was not associated with a significantly increased risk of inflammatory activity (relapse and/or T2 lesions) or progression independent of relapse activity (PIRA) after a median of 28.5 months (Konen et al. EAN 2026;OPR-118). The risk of disease reactivation appeared to increase after 30-32 months off treatment. The authors recommended careful monitoring after two years of treatment cessation.
Role of fluid biomarkers in practice
Two groups in Switzerland and the U.S. examined the value of neurofilament-light (NfL) and glial fibrillary acidic protein (GFAP) in prognosis (Einsiedler et al. EAN 2026;OPR-021). The study compared data from the Swiss MS Cohort (SMSC) (n=1709) and the EPIC cohort (n=620) at the University of California-San Francisco. An elevated baseline NfL Z-score (>1.5) was associated with a significantly higher risk of relapse in the next year; odds ratio was 2.0 for the SMSC cohort and 1.69 for the EPIC cohort. An elevated baseline GFAP Z-score (>1.0) was prognostic of a higher risk of PIRA at the next visit (SMSC 45% higher, EPIC 36% higher). A Z-score unit reduction in GFAP during the first two years of treatment was associated with a lower risk of PIRA (54% lower with fingolimod, 67% lower with anti-CD20).
A separate study in PPMS patients also reported that a higher baseline sNfL was prognostic of early EDSS worsening at one year (OR 1.83) and two years (OR 1.67) but not at three years (Klein Kranenbarg et al. EAN 2026;EPO-0466).
A meta-analysis of 18 biomarker studies (n=15,944) found a higher risk of PIRA with elevated baseline GFAP (pooled hazard ratio 1.85) or baseline NfL (pooled HR 1.51) (Biswas et al. EAN 2026;EPO-0673). The effect size was similar for the two biomarkers, although PIRA was more strongly associated with GFAP.
A study of 177 consecutive MS patients treated at Milan examined the differing effect of dimethyl fumarate (DMF) and ocrelizumab on NfL and GFAP (Mingione et al. EAN 2026;EPO-0506). Both biomarkers showed a decrease after one year of DMF. With ocrelizumab, NfL levels were rapidly normalized in the first year but GFAP levels decreased only after two years of treatment.
Cyclophosphamide vs. siponimod in SPMS
An Italian MS registry analysis compared the effectiveness of pulsed cyclophosphamide (n=123) with siponimod (n=81) on disability worsening in patients with secondary-progressive MS (Mazzeo et al. EAN 2026;OPR-017). Over the first three years of the study, the rate of worsening-free survival was greater with pulsed cyclophosphamide versus siponimod. Cyclophosphamide treatment was also associated with a prolonged time to first relapse and a higher likelihood of achieving NEDA-2.
Relapse during pregnancy in MOGAD, NMOSD
A retrospective study in the U.K. examined peripartum relapse rates in patients with myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) and neuromyelitis optica spectrum disorder (NMOSD) (Dal Bo et al. EAN 2026;EPO-0625). In MOGAD patients, the mean annualized relapse rate in the two years prior to pregnancy was 0.23. ARR decreased significantly during pregnancy, increased numerically in the first few months postpartum (ARR 0.39), then declined by 12 months. ARR was not statistically different for the pre- and postpartum periods. In NMOSD patients, the mean ARR was 0.36 before pregnancy and was significantly lower in the first and third trimesters. ARR returned to the pre-pregnancy rate (ARR 0.37) in the second trimester. During the postpartum period, ARR increased in months 0-3 (ARR 0.74) then declined thereafter.
GLP-1 signalling in NMOSD
A new study examined the effect of GLP-1R antagonists on area postrema syndrome in the AQP4-IgG+ EAE model of NMOSD (Yang et al. EAN 2026;EPO-0341). The goal was to investigate the role of the glucagon-like peptide-1 (GLP-1) receptor in driving area postrema neuronal hyperactivity. Area postrema neurons demonstrated significant upregulation of GLP-1 and GLP-1 receptors, increased glycolysis, lactate accumulation and increased neuronal hyperexcitability. The GLP-1 receptor activated the cAMP-protein kinase A (PKA) pathway and triggered mitochondrial dysfunction. Use of a GLP-1 agonist (Exendin-4) replicated these effects whereas a GLP-1 antagonist (Exendin-(9-39) or satralizumab reversed these changes, restoring normal neuronal excitability, improving mitochondrial function and relieving area postrema-like symptoms.