Blood test spots rare neurological diseases missed by standard screening
Researchers have identified a simple blood marker—calprotectin—that reliably distinguishes two rare neurological disorders from multiple sclerosis, potentially accelerating diagnosis and treatment. The finding could reshape how clinicians screen for conditions that mimic MS but require fundamentally different therapies.
Originaltitel: Calprotectin reveals distinct innate immune signatures in NMOSD, MOGAD, and multiple sclerosis
BACKGROUND: Granulocyte-mediated injury contributes to the immunopathology of aquaporin-4 neuromyelitis optica spectrum disease (AQP4-NMOSD) and myelin oligodendrocyte glycoprotein-associated disease (MOGAD), yet calprotectin, a myeloid-derived inflammatory marker, has not been evaluated in these disorders. OBJECTIVE: To assess the diagnostic and activity-related potential of cerebrospinal fluid (CSF) and serum calprotectin concentrations in AQP4-NMOSD, MOGAD, seronegative or double-negative NMOSD (DNNMOSD) and RRMS. METHODS: In this observational study, CSF and serum calprotectin were measured using a turbidimetric assay in patients with AQP4-NMOSD (n = 10), DNNMOSD (n = 6), MOGAD (n = 9), RRMS (n = 10), and healthy controls (HC; n = 8). Group comparisons, correlations with clinical and laboratory variables, and relapse analyses were performed. RESULTS: Serum calprotectin was markedly elevated in AQP4-NMOSD, DNNMOSD, and MOGAD (p < 0.001), separating these disorders from RRMS and HCs (AUC = 1.0 at 1.18 mg/L). CSF calprotectin was detectable in all samples (range; 0.18-0.82 mg/L) and was significantly lower in patients with MOGAD compared with other groups (p = 0.025). In RRMS, serum and CSF calprotectin concentrations inversely correlated with time since last relapse, whereas no such relationship was observed in NMOSD or MOGAD. CONCLUSION: Serum calprotectin shows promise as a diagnostic biomarker distinguishing NMOSD and MOGAD from RRMS and supports predominant systemic myeloid activation in these disorders.