Improving Cerebrovascular Function to Increase Neuronal Recovery in Neurodegeneration Associated to Cardiovascular

Lotte Vanherle1,2, Hana Matuskova1,2,3,4, Nicholas Don-Doncow1,2

  • 1Department of Experimental Medical Science, Lund University, Lund, Sweden.

Insights

Cardiovascular disease (CVD) increases cognitive impairment (CI) risk by affecting brain blood flow. Targeting vascular dysfunction may offer new treatments for neurodegeneration linked to CVD.

Area of Science:

  • Neuroscience
  • Cardiology
  • Gerontology

Background:

  • Cardiovascular disease (CVD) and its risk factors are linked to increased cognitive impairment (CI) and dementia.
  • Impaired cardiovascular function in CVD can disrupt cerebral blood flow (CBF), affecting brain oxygen and nutrient supply.
  • Cerebral hypoperfusion and cerebrovascular dysfunction in conditions like hypertension and heart failure are associated with neurodegeneration.

Purpose of the Study:

  • To review the mechanisms linking cerebrovascular dysfunction and CBF deficits to neurodegeneration.
  • To discuss vascular targets that may attenuate neurodegeneration or CI associated with CVD.

Main Methods:

  • Literature review of studies investigating the relationship between CVD, cerebrovascular function, and neurodegeneration.
  • Analysis of evidence for vascular targets in mitigating CVD-related cognitive decline.

Main Results:

  • CVD impairs CBF regulation, leading to reduced oxygen and nutrient supply critical for neuronal function.
  • Hypertension, heart failure, and stroke are associated with cerebral hypoperfusion and impaired cerebrovascular function, contributing to neurodegeneration.
  • Certain vascular targets have shown promise in improving cerebrovascular function and CBF, potentially reducing neurodegeneration.

Conclusions:

  • Understanding the mechanisms linking cerebrovascular dysfunction to neurodegeneration is crucial for developing effective treatments.
  • Improving cerebrovascular function and addressing CBF deficits represent a promising therapeutic strategy for CVD-associated neurodegeneration and CI.

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