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Hyperhomocysteinemia and Endothelial Dysfunction in Multiple Sclerosis.

Ekaterina Dubchenko1,2, Alexander Ivanov3, Natalia Spirina4

  • 1Department of Neuroimmunology of Federal Center of Brain and Neurotechnology of the Federal Medical-Biological Agency of Russia, 117997 Moscow, Russia.

Brain Sciences
|September 19, 2020
PubMed
Summary
This summary is machine-generated.

High homocysteine levels contribute to endothelial dysfunction and neurodegeneration, playing a key role in the progression of multiple sclerosis (MS) by damaging the blood-brain barrier and neurons.

Keywords:
endothelial dysfunctionhomocysteinehyperhomocysteinemiamultiple sclerosis

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Area of Science:

  • Neuroscience
  • Pathology
  • Biochemistry

Background:

  • Endothelial dysfunction is a primary factor in central nervous system diseases.
  • Hyperhomocysteinemia is linked to endothelial dysfunction and a prothrombogenic state.
  • Blood-brain barrier (BBB) dysregulation and leukocyte migration are critical in multiple sclerosis (MS) pathogenesis.

Purpose of the Study:

  • To review the multifaceted effects of homocysteine on neurological disease processes.
  • To elucidate the specific role of homocysteine in the pathogenesis of multiple sclerosis.

Main Methods:

  • Literature review of studies on homocysteine, endothelial function, BBB integrity, and neurodegeneration.
  • Analysis of mechanisms including excitotoxicity and apoptosis induction by homocysteine.
  • Synthesis of evidence linking homocysteine to MS progression.

Main Results:

  • Homocysteine contributes to endothelial dysfunction and BBB breakdown.
  • Homocysteine exacerbates neuroinflammation and neurodegeneration through excitotoxicity and apoptosis.
  • These actions of homocysteine are implicated in the progressive nature of MS.

Conclusions:

  • Homocysteine exerts pleiotropic detrimental effects relevant to MS pathogenesis.
  • Targeting homocysteine metabolism may offer therapeutic strategies for multiple sclerosis.
  • Understanding homocysteine's role is crucial for addressing neurodegenerative aspects of MS.