Vascular cognitive impairment: pathophysiological mechanisms, insights into structural basis, and perspectives in...

Area of Science:

• Neurology
• Gerontology
• Cardiovascular Medicine

Background:

• Vascular cognitive impairment (VCI) and vascular dementia are leading causes of cognitive decline in older adults, linked to cerebrovascular disease.
• Pathophysiology involves blood-pressure variability, cardiac issues, renin-angiotensin-aldosterone system, endothelial dysfunction, and metabolic disorders.
• S100B protein plays a role in neuronal regulation, affecting cytokine expression, homeostasis, and nervous tissue processes.

Purpose of the Study:

• To review factors contributing to cerebrovascular disease and neurovascular unit alterations in VCI.
• To explore novel therapeutic approaches for cognitive improvement in VCI patients.
• To highlight the potential of a new complex drug for VCI treatment.

Main Methods:

• Literature review focusing on VCI pathophysiology and treatment strategies.
• Analysis of the role of S100B protein and endothelial NO synthase in VCI.
• Examination of a novel complex drug's prospective role in VCI therapy.

Main Results:

• Cerebrovascular disease involves multiple factors impacting the neurovascular unit.
• S100B protein is a key neuronal factor in VCI.
• A novel complex drug targeting S100 and endothelial NO synthase shows therapeutic potential.

Conclusions:

• VCI has a complex and diverse pathological basis requiring multifaceted treatment approaches.
• Targeting specific molecular mechanisms, like S100B and endothelial NO synthase, is crucial for VCI management.
• The novel complex drug presents a promising avenue for future VCI treatment strategies.