ECTRIMS eLearning

The link between epigenetic regulators, neurotrophins and treatment efficacy in patients with multiple sclerosis
Author(s): ,
C. Irkec
Affiliations:
Neurology
,
F. Yekeler Ozdemir
Affiliations:
Neurology
T. Altı
,
T. Altı
Affiliations:
,
parmak
Affiliations:
Neurology
,
R. Tural
Affiliations:
Biochemistry, Gazi University Medical Faculty, Ankara, Turkey
,
N. Altan
Affiliations:
Biochemistry, Gazi University Medical Faculty, Ankara, Turkey
F. Söke
Affiliations:
Biochemistry, Gazi University Medical Faculty, Ankara, Turkey
ECTRIMS Learn. Söke F. 10/10/18; 229418; EP1581
Fatih Söke
Fatih Söke
Contributions
Abstract

Abstract: EP1581

Type: Poster Sessions

Abstract Category: Therapy - Immunomodulation/Immunosuppression

Multiple Sclerosis (MS) is an neuroinflammatory and neurodegenerative autoimmune disease of the central nervous system (CNS) with considerable heterogenity in all aspects, including response to therapy. A number of disease modifying drugs (DMD), such as interferon beta (IFN- β), glatiramer acetate (GA) and Fingolimod (FTY) available for disease management. However, a considerable number of patients to achieve adequate response at therapeutic doses of IFN-β, GA and FTY.
Epigenetic regulators such as sirtuin 1 (SIRT1) is member of the histone deactylase (HDAC) family. SIRT1 can regulate transcription, energy metabolism, DNA repair, aging and the functions of T helper 17 (Th17) cells. SIRT 1 was found significantly decreased during relapses and increased levels were seen in responders to GA treatment. In literature there haven' t been any study about the effects of IFNβ and FTY according to serum levels of SIRT1.
On the other hand, investigations on neurotrophins, specifically brain derived neurotrophic factor (BDNF) concentration in patients undergoing GA and IFNβ treatment have conflicting results. Levels in GA and IFNβ treated patients have been reported as decreased, increased and unchanged when compared to controls. There haven't been any study about FTY treatment.
In this study we investigated the effects of different therapies on SIRT1 and BDNF serum levels and their subsequent neuroprotective outcomes. In addition, we undertook the analysis of serum SIRT 1 and BDNF levels in responder and non-responder MS patients. For this reason; IFNβ, GA, FTY responder and non responder MS patients serum samples were collected and measured with enzyme linked immunosorbent assay (ELISA) method.
IFNβ treated responder group had significantly higher BDNF serum levels than all other groups. Levels of SIRT1 in GA treated responder group is remarkably higher than all other groups. Consequently our findings suggest that SIRT1 and BDNF could be a possible biomarker to evaluate responsiveness to GA and IFNβ treatments.
Although experimental studies support BDNF mediated neuroprotection of GA in demyelinating conditions, we could not find similar results in vivo. Further studies, on the protective roles of SIRT1 and BDNF in MS patients and their therapy responsiveness are required.
Disclosure: C. İrkec: Nothing to disclosure
F. Yekeler: Nothing to disclosure
T. Altıparmak: Nothing to disclosure
R. Tural: Nothing to disclosure
N. Altan: Nothing to disclosure

Abstract: EP1581

Type: Poster Sessions

Abstract Category: Therapy - Immunomodulation/Immunosuppression

Multiple Sclerosis (MS) is an neuroinflammatory and neurodegenerative autoimmune disease of the central nervous system (CNS) with considerable heterogenity in all aspects, including response to therapy. A number of disease modifying drugs (DMD), such as interferon beta (IFN- β), glatiramer acetate (GA) and Fingolimod (FTY) available for disease management. However, a considerable number of patients to achieve adequate response at therapeutic doses of IFN-β, GA and FTY.
Epigenetic regulators such as sirtuin 1 (SIRT1) is member of the histone deactylase (HDAC) family. SIRT1 can regulate transcription, energy metabolism, DNA repair, aging and the functions of T helper 17 (Th17) cells. SIRT 1 was found significantly decreased during relapses and increased levels were seen in responders to GA treatment. In literature there haven' t been any study about the effects of IFNβ and FTY according to serum levels of SIRT1.
On the other hand, investigations on neurotrophins, specifically brain derived neurotrophic factor (BDNF) concentration in patients undergoing GA and IFNβ treatment have conflicting results. Levels in GA and IFNβ treated patients have been reported as decreased, increased and unchanged when compared to controls. There haven't been any study about FTY treatment.
In this study we investigated the effects of different therapies on SIRT1 and BDNF serum levels and their subsequent neuroprotective outcomes. In addition, we undertook the analysis of serum SIRT 1 and BDNF levels in responder and non-responder MS patients. For this reason; IFNβ, GA, FTY responder and non responder MS patients serum samples were collected and measured with enzyme linked immunosorbent assay (ELISA) method.
IFNβ treated responder group had significantly higher BDNF serum levels than all other groups. Levels of SIRT1 in GA treated responder group is remarkably higher than all other groups. Consequently our findings suggest that SIRT1 and BDNF could be a possible biomarker to evaluate responsiveness to GA and IFNβ treatments.
Although experimental studies support BDNF mediated neuroprotection of GA in demyelinating conditions, we could not find similar results in vivo. Further studies, on the protective roles of SIRT1 and BDNF in MS patients and their therapy responsiveness are required.
Disclosure: C. İrkec: Nothing to disclosure
F. Yekeler: Nothing to disclosure
T. Altıparmak: Nothing to disclosure
R. Tural: Nothing to disclosure
N. Altan: Nothing to disclosure

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