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A Study on the Pathogenesis of Vascular Cognitive Impairment and Dementia: The Chronic Cerebral Hypoperfusion

Weiwei Yu1, Yao Li1, Jun Hu1

  • 1Department of Neurology, Peking University Shenzhen Hospital, 1120 Lianhua Road, Futian District, Shenzhen 518036, China.

Journal of Clinical Medicine
|August 26, 2022
PubMed

Insights

Chronic cerebral hypoperfusion (CCH) universally contributes to vascular cognitive impairment and dementia (VCID). This review details CCH-induced pathological mechanisms, including inflammation and oxidative stress, offering insights for prevention.

Area of Science:

  • Neuroscience
  • Pathology
  • Vascular Biology

Background:

  • Vascular cognitive impairment and dementia (VCID) mechanisms are complex and debated.
  • Cerebral blood flow (CBF) dysregulation is a common factor in VCID.
  • Chronic cerebral hypoperfusion (CCH) results from CBF dysregulation, leading to insufficient brain blood supply and VCID.

Purpose of the Study:

  • To review the significant role of CCH in VCID.
  • To illustrate current findings on CCH-induced pathological mechanisms in VCID.
  • To explore molecular pathways contributing to CCH-induced VCID.

Main Methods:

  • Comprehensive literature review.
  • Synthesis of evidence on molecular mechanisms.
  • Analysis of preclinical models.

Main Results:

  • CCH is a universal consequence of CBF dysregulation in VCID.
  • Key molecular mechanisms include Aβ accumulation, inflammation, oxidative stress, blood-brain barrier (BBB) disruption, trophic uncoupling, and white matter lesions (WMLs).
  • These mechanisms interact closely.

Conclusions:

  • CCH is a critical factor in VCID pathogenesis.
  • Understanding CCH-induced molecular mechanisms is vital for developing preventative strategies.
  • Further research into the interactions of these mechanisms is needed.

Keywords:
blood-brain barriercerebral blood flow regulationchronic cerebral hypoperfusionneuroinflammationoxidative stresstrophic uncouplingvascular cognitive impairment and dementiawhite matter lesionsβ-amyloid

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