Contributions
Abstract: P1172
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Biomarkers
Levels of two potential biomarkers, glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) in the cerebrospinal fluid (CSF) have been shown to be associated with MS disease progression. Now, both biomarkers can be detected reliably in serum and importantly, their serum levels correlate well with their CSF levels. The purpose of this study was to evaluate whether serum GFAP is associated with MS disease severity and progression, and with NfL.
Forty-seven relapsing-remitting (RRMS) and 32 secondary progressive (SPMS) MS patients were reviewed for this cross-sectional hospital-based study. In addition, 13 healthy age matched controls were included (HC). The expanded disability status scale (EDSS) score was assessed for each patient. The serum levels of GFAP and NfL were measured using single molecule array (Simoa) assay. MRI including 3DT1 and 3DFLAIR sequences was used to determine the T1 and T2 lesion loads. For correlation analyses the Spearman´s rank correlation coefficient was determined. The differences between patient groups were assessed using the Kruskal-Wallis test. Pairwise differences were assessed using the Wilcoxon rank-sum test.
In line with previous studies, the levels of both biomarkers were associated with patient age (GFAP r=0.400 p< 0.001, NfL r=0.486 p< 0.001). The levels of GFAP and NfL strongly associated with each other (r=0.535 p< 0.001). The level of GFAP in MS patients was elevated compared to healthy controls (p=0.031). The GFAP and NfL levels in RRMS did not differ significantly from healthy controls, but GFAP measured in SPMS was significantly elevated compared to both healthy controls (p= 0.001) and RRMS (p< 0.001) while the increase in NfL level in SPMS differed only when compared to RRMS (vs HC p= 0.221, vs RRMS p< 0.001). The low level of NfL in RRMS was likely accountable for benign disease and small T1 and T2 lesion loads. Both EDSS (GFAP r=0.468 p< 0.001, NfL r=0.432 p< 0.001) and disease duration (GFAP r=0.450 p< 0.001, NfL r=0.414 p< 0.001) were strongly associated with the GFAP and NfL levels.
Earlier studies have demonstrated that CSF GFAP, unlike NfL, is not increased in association with acute focal inflammation-related nervous system damage during relapses. Our work demonstrates that serum GFAP level is strongly associated with MS disease progression, and has potential to serve as reliable and easily measurable biomarker of CNS pathology related to MS progression.
Disclosure: Heidi Högel has nothing to disclose. Eero Rissanen has received speaker honoraria from Teva, Biogen, and Roche, a consultational fee for Merck and personal research grants from Turku University Hospital and the Finnish MS Foundation. Christian Barro received travel support by Teva and Novartis. Markus Matilainen has nothing to disclose. Marjo Nylund has nothing to disclose. Jens Kuhle received speaker fees, research support, travel support, and/or served on advisory boards by ECTRIMS, Swiss MS Society, Swiss National Research Foundation, (320030_160221), University of Basel, Bayer, Biogen, Genzyme, Merck, Novartis, Protagen AG, Roche, Teva. Laura Airas has received honoraria from Biogen, F. Hoffmann-La Roche Ltd, Genzyme, Merck Serono and Teva, and institutional research grant support from Biogen, Genzyme, Merck Serono and Novartis.
Abstract: P1172
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Biomarkers
Levels of two potential biomarkers, glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) in the cerebrospinal fluid (CSF) have been shown to be associated with MS disease progression. Now, both biomarkers can be detected reliably in serum and importantly, their serum levels correlate well with their CSF levels. The purpose of this study was to evaluate whether serum GFAP is associated with MS disease severity and progression, and with NfL.
Forty-seven relapsing-remitting (RRMS) and 32 secondary progressive (SPMS) MS patients were reviewed for this cross-sectional hospital-based study. In addition, 13 healthy age matched controls were included (HC). The expanded disability status scale (EDSS) score was assessed for each patient. The serum levels of GFAP and NfL were measured using single molecule array (Simoa) assay. MRI including 3DT1 and 3DFLAIR sequences was used to determine the T1 and T2 lesion loads. For correlation analyses the Spearman´s rank correlation coefficient was determined. The differences between patient groups were assessed using the Kruskal-Wallis test. Pairwise differences were assessed using the Wilcoxon rank-sum test.
In line with previous studies, the levels of both biomarkers were associated with patient age (GFAP r=0.400 p< 0.001, NfL r=0.486 p< 0.001). The levels of GFAP and NfL strongly associated with each other (r=0.535 p< 0.001). The level of GFAP in MS patients was elevated compared to healthy controls (p=0.031). The GFAP and NfL levels in RRMS did not differ significantly from healthy controls, but GFAP measured in SPMS was significantly elevated compared to both healthy controls (p= 0.001) and RRMS (p< 0.001) while the increase in NfL level in SPMS differed only when compared to RRMS (vs HC p= 0.221, vs RRMS p< 0.001). The low level of NfL in RRMS was likely accountable for benign disease and small T1 and T2 lesion loads. Both EDSS (GFAP r=0.468 p< 0.001, NfL r=0.432 p< 0.001) and disease duration (GFAP r=0.450 p< 0.001, NfL r=0.414 p< 0.001) were strongly associated with the GFAP and NfL levels.
Earlier studies have demonstrated that CSF GFAP, unlike NfL, is not increased in association with acute focal inflammation-related nervous system damage during relapses. Our work demonstrates that serum GFAP level is strongly associated with MS disease progression, and has potential to serve as reliable and easily measurable biomarker of CNS pathology related to MS progression.
Disclosure: Heidi Högel has nothing to disclose. Eero Rissanen has received speaker honoraria from Teva, Biogen, and Roche, a consultational fee for Merck and personal research grants from Turku University Hospital and the Finnish MS Foundation. Christian Barro received travel support by Teva and Novartis. Markus Matilainen has nothing to disclose. Marjo Nylund has nothing to disclose. Jens Kuhle received speaker fees, research support, travel support, and/or served on advisory boards by ECTRIMS, Swiss MS Society, Swiss National Research Foundation, (320030_160221), University of Basel, Bayer, Biogen, Genzyme, Merck, Novartis, Protagen AG, Roche, Teva. Laura Airas has received honoraria from Biogen, F. Hoffmann-La Roche Ltd, Genzyme, Merck Serono and Teva, and institutional research grant support from Biogen, Genzyme, Merck Serono and Novartis.