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Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...

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Siponimod treatment response shows partial BDNF dependency in multiple sclerosis models.

Hasan Hüseyin Hendek1, Alina Blusch1, Neele Heitmann1

  • 1Department of Neurology, Ruhr-University Bochum, St. Josef-Hospital, Gudrunstr. 56, 44791, Bochum, Germany.

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Siponimod reduces disease activity in progressive multiple sclerosis (MS) by impacting immune cells and the central nervous system (CNS). Its therapeutic effects are partially linked to brain-derived neurotrophic factor (BDNF) expression in immune cells.

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Area of Science:

  • Neuroimmunology
  • Pharmacology
  • Neuroscience

Background:

  • Progressive multiple sclerosis (MS) has limited effective treatment options.
  • Siponimod, a sphingosine-1-phosphate receptor (S1PR) modulator, is approved for progressive MS and acts within the peripheral immune system and central nervous system (CNS).
  • The role of brain-derived neurotrophic factor (BDNF) in siponimod's therapeutic effects remains unclear.

Purpose of the Study:

  • To investigate the hypothesis that BDNF in immune cells is crucial for siponimod's efficacy in reducing disease activity and neurotoxicity in experimental autoimmune encephalomyelitis (EAE).
  • To elucidate the mechanisms underlying siponimod's anti-inflammatory and neuroprotective effects in the context of BDNF expression.

Main Methods:

  • Used MOG35-55-immunized wild-type (WT) and BDNF knockout (BDNFko) mice treated with siponimod or vehicle.
  • Assessed clinical EAE scores, immune cell phenotyping via flow cytometry, and spinal cord infiltration/demyelination via immunohistochemistry.
  • Conducted in vitro studies using dorsal root ganglion cells with EAE splenocyte supernatant to evaluate neurotoxicity and gene expression changes.

Main Results:

  • Siponimod dose-dependently reduced EAE scores in WT mice.
  • A suboptimal siponimod dose reduced EAE clinical signs, infiltration, and demyelination independently of immune cell BDNF expression.
  • Siponimod modulated T cell populations (Th, Tc, Treg) and demonstrated partial neuroprotective effects in vitro, reversing elevated neuroinflammatory gene expression (CCL2, CX3CL1) in WT but not BDNFko cells.

Conclusions:

  • Siponimod exhibits both anti-inflammatory and neuroprotective effects in EAE.
  • These effects are partially dependent on BDNF expression in immune cells, suggesting a complex interplay.
  • The findings may help explain siponimod's effectiveness in progressive MS and highlight BDNF as a potential therapeutic target.