[Oxidative stress and inflammation as links in a chain in patients with chronic cerebrovascular diseases]

Area of Science:

• Neurology
• Vascular Biology
• Geriatrics

Background:

• Cerebrovascular diseases (CVD) represent a significant global health challenge, leading to mortality and long-term disability.
• The aging population contributes to an increasing prevalence of chronic CVD, often comorbid with other somatic conditions.
• Microangiopathy, particularly affecting small cerebral vessels, is a primary cause of CVD.

Purpose of the Study:

• To explore the etiopathogenetic factors underlying chronic cerebrovascular diseases.
• To identify molecular mechanisms contributing to small blood vessel dysfunction in CVD.
• To evaluate potential therapeutic strategies for CVD management.

Main Methods:

• Review of current literature on CVD pathogenesis.
• Analysis of molecular factors implicated in cerebral microangiopathy.
• Discussion of therapeutic interventions targeting pathochemical disorders.

Main Results:

• Endothelial dysfunction, systemic inflammation, and oxidative stress are key factors in small cerebral vessel damage.
• A unified pathogenetic mechanism may link CVD with comorbid somatic diseases.
• Dipyridamole exhibits pleiotropic effects, suggesting its potential in complex CVD therapy.

Conclusions:

• Understanding the molecular basis of small vessel damage is crucial for developing pathogenetically justified CVD therapies.
• Therapeutic strategies should be gradual, comprehensive, and address pathochemical imbalances, including neurotransmitter dysfunction.
• Dipyridamole offers a promising option for integrated treatment of patients with cerebrovascular diseases.