Hyperhomocysteinemia and Endothelial Dysfunction in Multiple Sclerosis

Brain Sciences

Natalia Spirina¹  Ekaterina Dubchenko²  Mikhail Melnikov²  Nina Smirnova²  Alexey Boyko²  Evgeniy Gusev³  Aslan Kubatiev⁴  Alexander Ivanov⁴ 

[1] Department of Nervous Diseases with Medical Genetics and Neurosurgery Yaroslavl State Medical University, 150000 Yaroslavl, Russia;Department of Neuroimmunology of Federal Center of Brain and Neurotechnology of the Federal Medical-Biological Agency of Russia, 117997 Moscow, Russia;Department of Neurology, Neurosurgery and Medical Genetic of Pirogov Russian National Research Medical University, 117997 Moscow, Russia;Federal State Budgetary Scientific Institution “Institute of General Pathology and Pathophysiology”, 125315 Moscow, Russia;

关键词: multiple sclerosis;    endothelial dysfunction;    homocysteine;    hyperhomocysteinemia;   

DOI  :  10.3390/brainsci10090637

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown