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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.
Insights
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.
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.
Abstract:
Endothelial dysfunction is recognized as one of the leading factors in the pathogenesis of diseases of the central nervous system of various etiologies. Numerous studies have shown the role of hyperhomocysteinemia in the development of endothelial dysfunction and the prothrombogenic state. The most important condition in the development of multiple sclerosis (MS) is a dysregulation of the blood-brain barrier (BBB) and transendothelial leukocyte migration. It has been proven that homocysteine also contributes to the damage of neurons by the mechanism of excitotoxicity and the induction of the apoptosis of neurons. These processes can be one of the factors of neurodegenerative brain damage, which plays a leading role in the progression of MS. This review describes the pleiotropic effect of homocysteine on these processes and its role in MS pathogenesis.
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