[Hyperhomocysteinemia and endothelial dysfunction in patients with cerebral vascular and autoimmune diseases]

Area of Science:

• Neuroscience
• Pathophysiology
• 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) development.

Purpose of the Study:

• To review the multifaceted effects of homocysteine on central nervous system disease pathogenesis.
• To elucidate the role of homocysteine in the development and progression of multiple sclerosis (MS).

Main Methods:

• Literature review of studies on homocysteine, endothelial dysfunction, and MS.
• Analysis of homocysteine's impact on BBB integrity and neuronal function.
• Examination of homocysteine's role in excitotoxicity and apoptosis.

Main Results:

• Homocysteine contributes to endothelial dysfunction and BBB disruption.
• Homocysteine induces neuronal excitotoxicity and apoptosis, promoting neurodegeneration.
• These actions highlight homocysteine's significant role in MS pathogenesis.

Conclusions:

• Homocysteine exerts pleiotropic effects contributing to MS progression.
• Targeting homocysteine may offer therapeutic strategies for multiple sclerosis.
• Understanding homocysteine's role is crucial for managing neurodegenerative processes in MS.