Markers of glial processes and axonal damage in CSF and serum help to differentiate between relapsing-remitting and progressive forms of MS
ECTRIMS Online Library. Huss A. 09/13/19; 279548; 286
André Huss
André Huss
Contributions
Abstract

Abstract: 286

Type: Scientific Session

Abstract Category: Pathology and pathogenesis of MS - Biomarkers

A. Huss1, A. Abdelhak1,2, F. Bachhuber1, M. Senel1, M. Otto1, H. Tumani1,3

1Neurology, University Hospital Ulm, Ulm, 2Neurology, University Hospital Tuebingen, Tuebingen, 3Specialty Hospital of Neurology Dietenbronn, Schwendi, Germany

Background: The investigation of central nervous system (CNS) markers in body fluids of multiple sclerosis (MS) patients is a promising approach to monitor different pathophysiological aspects of the disease. We previously reported higher CSF and serum levels of glial fibrillary acidic protein (GFAP) but not Neurofilament light chain (NfL) in progressive (PMS) compared to relapsing-remitting (RMS) MS patients.
Objectives: To evaluate the proportion of glial processes and extent of axonal damage in different subtypes of MS we analyzed the glial markers GFAP and CHI3L1 in comparison to NfL as a marker for axonal damage in the CSF and serum from patients with RMS and PMS.
Methods: For this study we included 86 MS patients (47 RMS and 39 PMS) and 20 patients with other neurological diseases (OND) as controls.
NfL and GFAP levels were determined by the Single molecule array (Simoa) and CHI3L1 levels were measured with conventional ELISA. A score was calculated based on glial markers to axonal markers (CHI3L1*GFAP/NfL, referred to as 'Glia-score') to capture the extent of glial processes in relation to axonal damage in each individual patient.
Results: GFAP levels were higher in the CSF and serum of PMS patients in comparison to RMS and controls (p< 0.01 and p< 0.05, respectively). Likewise, CSF and serum NfL levels were higher in RMS and PMS patients than in controls (CSF p< 0.0001 for both comparisons, serum p< 0.001 and 0.0001, respectively), but no significant difference between the PMS and RMS was observed. CHI3L1 showed higher CSF levels in PMS vs. RMS and controls (p< 0.001 and p< 0.0001), RMS vs. controls (p< 0.01) and higher serum levels for PMS vs. controls (p< 0.05).
The Glia-score was higher in the CSF of PMS patients compared to RMS and controls (p< 0.01 and p< 0.001, respectively) and in the serum of PMS patients compared to RMS and controls (p< 0.0001 for both comparisons).
Furthermore, the Glia-score in serum but not CSF correlated with the disability as detected by EDSS in the PMS group but not in the RMS group (Spearman ρ= 0.56 and 0.09, p= 0.003 and 0.56, respectively).
Conclusions: Our data indicate the involvement of glial mechanisms during the pathogenesis of PMS. Moreover, a calculated score helps to differentiate between PMS and RMS especially in the serum making it an easily accessible and promising marker.
Disclosure: A. Huss: nothing to disclose.
A. Abdelhak: nothing to disclose.
F. Bachhuber: nothing to disclose.
M. Senel: has received consulting and speaker honoraria as well as travel reimbursements from Bayer, Biogen, Sanofi Genzyme and TEVA and research funding from the Hertha-Nathorff-Program and University of Ulm, none related to this study.
M. Otto: served as scientific advisor for Roche, Fujirebio and Axon neuroscience. He received funding from the BMBF, DFG and ALS association, Thierry Latran foundation and foundation of the state Baden-Wuerttemberg
H. Tumani: received funding for research projects, lectures and travel from Bayer, Biogen, Genzyme, Fresenius, Merck, Novartis, Roche, Teva, and received research support from the German MS Society (DMSG) and the German Federal Ministry of Education and Research (BMBF).

Abstract: 286

Type: Scientific Session

Abstract Category: Pathology and pathogenesis of MS - Biomarkers

A. Huss1, A. Abdelhak1,2, F. Bachhuber1, M. Senel1, M. Otto1, H. Tumani1,3

1Neurology, University Hospital Ulm, Ulm, 2Neurology, University Hospital Tuebingen, Tuebingen, 3Specialty Hospital of Neurology Dietenbronn, Schwendi, Germany

Background: The investigation of central nervous system (CNS) markers in body fluids of multiple sclerosis (MS) patients is a promising approach to monitor different pathophysiological aspects of the disease. We previously reported higher CSF and serum levels of glial fibrillary acidic protein (GFAP) but not Neurofilament light chain (NfL) in progressive (PMS) compared to relapsing-remitting (RMS) MS patients.
Objectives: To evaluate the proportion of glial processes and extent of axonal damage in different subtypes of MS we analyzed the glial markers GFAP and CHI3L1 in comparison to NfL as a marker for axonal damage in the CSF and serum from patients with RMS and PMS.
Methods: For this study we included 86 MS patients (47 RMS and 39 PMS) and 20 patients with other neurological diseases (OND) as controls.
NfL and GFAP levels were determined by the Single molecule array (Simoa) and CHI3L1 levels were measured with conventional ELISA. A score was calculated based on glial markers to axonal markers (CHI3L1*GFAP/NfL, referred to as 'Glia-score') to capture the extent of glial processes in relation to axonal damage in each individual patient.
Results: GFAP levels were higher in the CSF and serum of PMS patients in comparison to RMS and controls (p< 0.01 and p< 0.05, respectively). Likewise, CSF and serum NfL levels were higher in RMS and PMS patients than in controls (CSF p< 0.0001 for both comparisons, serum p< 0.001 and 0.0001, respectively), but no significant difference between the PMS and RMS was observed. CHI3L1 showed higher CSF levels in PMS vs. RMS and controls (p< 0.001 and p< 0.0001), RMS vs. controls (p< 0.01) and higher serum levels for PMS vs. controls (p< 0.05).
The Glia-score was higher in the CSF of PMS patients compared to RMS and controls (p< 0.01 and p< 0.001, respectively) and in the serum of PMS patients compared to RMS and controls (p< 0.0001 for both comparisons).
Furthermore, the Glia-score in serum but not CSF correlated with the disability as detected by EDSS in the PMS group but not in the RMS group (Spearman ρ= 0.56 and 0.09, p= 0.003 and 0.56, respectively).
Conclusions: Our data indicate the involvement of glial mechanisms during the pathogenesis of PMS. Moreover, a calculated score helps to differentiate between PMS and RMS especially in the serum making it an easily accessible and promising marker.
Disclosure: A. Huss: nothing to disclose.
A. Abdelhak: nothing to disclose.
F. Bachhuber: nothing to disclose.
M. Senel: has received consulting and speaker honoraria as well as travel reimbursements from Bayer, Biogen, Sanofi Genzyme and TEVA and research funding from the Hertha-Nathorff-Program and University of Ulm, none related to this study.
M. Otto: served as scientific advisor for Roche, Fujirebio and Axon neuroscience. He received funding from the BMBF, DFG and ALS association, Thierry Latran foundation and foundation of the state Baden-Wuerttemberg
H. Tumani: received funding for research projects, lectures and travel from Bayer, Biogen, Genzyme, Fresenius, Merck, Novartis, Roche, Teva, and received research support from the German MS Society (DMSG) and the German Federal Ministry of Education and Research (BMBF).

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