Contributions
Abstract: P1126
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 25 Biomarkers
Background: Neurofilament light chain protein (NFL) in cerebrospinal fluid (CSF) is considered a marker for axonal injury.
Objective: To investigate the association of NFL levels in CSF with radiologic and clinical parameters of disease activity and severity as well as with findings from standard CSF examinations in patients with clinically isolated syndrome (CIS) or early relapsing-remitting MS (RRMS).
Methods: Patients with CIS or early RRMS (n=43) underwent lumbar punctures for routine diagnostic purposes and were subsequently enrolled in a longitudinal observational study. Patients were assessed by the expanded disability status scale (EDSS) score as well as 3 Tesla cerebral magnetic resonance imaging (MRI) at baseline and follow-up (n=38). NFL was measured in CSF with a commercial ELISA kit.
Results: NFL in CSF was associated with baseline T2-weighted (T2w) lesion number (r=0.412, p=0.006) and volume (r=0.517, p< 0.001) as well as the number of contrast enhancing lesions (CEL; r=0.401, p=0.02). However, we found no association of NFL with baseline whole or segmented brain volumes. At a median of 38.6 months of follow-up, NFL correlated with T2w lesion number (r=0.404, p=0.012) and volume (r=0.488, p=0.002) as well as with the number of new T2w lesions (r=0.381, p=0.018), but not with volume change of T2w lesions (r=0.140, p>0.05). No correlation was found for CEL number and volume at follow-up. Additionally, there was an association of NFL with the CSF/serum albumin quotient (r=0.352, p=0.02), immunoglobulin (Ig)G quotient (r=0.307, p=0.04) and IgA quotient (r=0.350, p=0.020). NFL was not associated with the EDSS score at baseline.
Conclusion: CSF levels of NFL correlate with MRI markers of disease activity and severity in patients with early MS, suggesting that inflammation is associated with axonal damage already early during the course of MS.
Disclosure: Aurelian Ungureanu was supported by a Du Pré Grant from Multiple Sclerosis International Federation.
Johannes Piepgras has nothing to disclose.
Sebastian Papazoglou has nothing to disclose.
Catherina Pfuhl has nothing to disclose.
Johanna Oechtering has nothing to disclose.
Janina R. Behrens has nothing to disclose.
René M. Gieß has nothing to disclose.
Ludwig Rasche nothing to disclose.
Harald Prüß has nothing to disclose.
Jens Wuerfel has nothing to disclose.
Hanna Zimmermann has nothing to disclose.
Ella Maria Kadas has nothing to disclose.
Michael Scheel has nothing to disclose.
Alexander U. Brandt reports consulting or speaker honoraria for Motognosis, Biogen, Teva, Novartis, Bayer, and Nexus not related to the presented work.
Friedemann Paul has received research support from the German Ministry for Education and Research (BMBF/KKNMS; Competence Network Multiple Sclerosis), the Guthy Jackson Charitable Foundation, and National Multiple Sclerosis Society, research grants and speaker honoraria from Bayer, Teva, Genzyme, Merck, Novartis, MedImmune and is member of the steering committee of the OCTIMS study (Novartis), not related to the presented work. Friedemann Paul has received research support from the Deutsche Forschungsgemeinschaft (DFG) (grant Exc. 257) related to the presented work.
Judith Bellmann-Strobl has received travel grants and speaking honoraria from TEVA,SanofiGenyzme and MerckSerono not related to the presented work.
Klemens Ruprecht has received research support from Novartis and Merck Serono and the German Ministry for Education and Research (BMBF/KKNMS; Competence Network Multiple Sclerosis), as well as speaking fees or travel grants from Bayer Healthcare, Biogen Idec, Merck Serono, Sanofi-Aventis/Genzyme, Teva Pharmaceuticals, Roche, Novartis, and the Guthy-Jackson Charitable Foundation.
Abstract: P1126
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 25 Biomarkers
Background: Neurofilament light chain protein (NFL) in cerebrospinal fluid (CSF) is considered a marker for axonal injury.
Objective: To investigate the association of NFL levels in CSF with radiologic and clinical parameters of disease activity and severity as well as with findings from standard CSF examinations in patients with clinically isolated syndrome (CIS) or early relapsing-remitting MS (RRMS).
Methods: Patients with CIS or early RRMS (n=43) underwent lumbar punctures for routine diagnostic purposes and were subsequently enrolled in a longitudinal observational study. Patients were assessed by the expanded disability status scale (EDSS) score as well as 3 Tesla cerebral magnetic resonance imaging (MRI) at baseline and follow-up (n=38). NFL was measured in CSF with a commercial ELISA kit.
Results: NFL in CSF was associated with baseline T2-weighted (T2w) lesion number (r=0.412, p=0.006) and volume (r=0.517, p< 0.001) as well as the number of contrast enhancing lesions (CEL; r=0.401, p=0.02). However, we found no association of NFL with baseline whole or segmented brain volumes. At a median of 38.6 months of follow-up, NFL correlated with T2w lesion number (r=0.404, p=0.012) and volume (r=0.488, p=0.002) as well as with the number of new T2w lesions (r=0.381, p=0.018), but not with volume change of T2w lesions (r=0.140, p>0.05). No correlation was found for CEL number and volume at follow-up. Additionally, there was an association of NFL with the CSF/serum albumin quotient (r=0.352, p=0.02), immunoglobulin (Ig)G quotient (r=0.307, p=0.04) and IgA quotient (r=0.350, p=0.020). NFL was not associated with the EDSS score at baseline.
Conclusion: CSF levels of NFL correlate with MRI markers of disease activity and severity in patients with early MS, suggesting that inflammation is associated with axonal damage already early during the course of MS.
Disclosure: Aurelian Ungureanu was supported by a Du Pré Grant from Multiple Sclerosis International Federation.
Johannes Piepgras has nothing to disclose.
Sebastian Papazoglou has nothing to disclose.
Catherina Pfuhl has nothing to disclose.
Johanna Oechtering has nothing to disclose.
Janina R. Behrens has nothing to disclose.
René M. Gieß has nothing to disclose.
Ludwig Rasche nothing to disclose.
Harald Prüß has nothing to disclose.
Jens Wuerfel has nothing to disclose.
Hanna Zimmermann has nothing to disclose.
Ella Maria Kadas has nothing to disclose.
Michael Scheel has nothing to disclose.
Alexander U. Brandt reports consulting or speaker honoraria for Motognosis, Biogen, Teva, Novartis, Bayer, and Nexus not related to the presented work.
Friedemann Paul has received research support from the German Ministry for Education and Research (BMBF/KKNMS; Competence Network Multiple Sclerosis), the Guthy Jackson Charitable Foundation, and National Multiple Sclerosis Society, research grants and speaker honoraria from Bayer, Teva, Genzyme, Merck, Novartis, MedImmune and is member of the steering committee of the OCTIMS study (Novartis), not related to the presented work. Friedemann Paul has received research support from the Deutsche Forschungsgemeinschaft (DFG) (grant Exc. 257) related to the presented work.
Judith Bellmann-Strobl has received travel grants and speaking honoraria from TEVA,SanofiGenyzme and MerckSerono not related to the presented work.
Klemens Ruprecht has received research support from Novartis and Merck Serono and the German Ministry for Education and Research (BMBF/KKNMS; Competence Network Multiple Sclerosis), as well as speaking fees or travel grants from Bayer Healthcare, Biogen Idec, Merck Serono, Sanofi-Aventis/Genzyme, Teva Pharmaceuticals, Roche, Novartis, and the Guthy-Jackson Charitable Foundation.