CBF regulation in hypertension and Alzheimer's disease

Noushin Yazdani1, Mark S Kindy2,3, Saeid Taheri2,4

  • 1College of Public Health, University of South Florida , Tampa, FL, USA.

Insights

Chronic high mean arterial blood pressure (MAP) impairs cerebral blood flow (CBF) autoregulation, potentially causing chronic cerebral diseases like Alzheimer's. Pathology in sensory elements links hypertension and AD impacts on cerebral perfusion.

Area of Science:

  • Neurology
  • Cardiovascular Science
  • Cerebrovascular Research

Background:

  • Chronic high mean arterial blood pressure (MAP) is a significant risk factor for cerebrovascular diseases.
  • Cerebral blood flow (CBF) autoregulation is crucial for maintaining stable brain perfusion.
  • Impairment of CBF autoregulation is increasingly linked to the development and progression of chronic cerebral conditions.

Purpose of the Study:

  • To review recent developments on the effects of chronic high MAP on CBF autoregulation.
  • To explore the connection between impaired CBF autoregulation and chronic cerebral diseases.
  • To support the notion that CBF autoregulation impairment may be a cause of chronic cerebral diseases.

Main Methods:

  • A narrative review methodology was employed.
  • All relevant literature known to the authors was systematically reviewed.
  • Focus was placed on recent advancements in the field.

Main Results:

  • Understanding of the interplay between cerebral perfusion, chronic high MAP, and cerebral disease is evolving.
  • Cerebral perfusion impairment is shifting from being viewed as a result to a potential cause of cerebral diseases.
  • The intertwined impact of hypertension and Alzheimer's disease (AD) on cerebrovascular sensory elements is better understood, identifying vulnerable elements.

Conclusions:

  • Pathology in sensory elements plays a critical role in the intertwined mechanisms of chronic high MAP and AD.
  • These mechanisms significantly impact cerebral perfusion.
  • Further research into sensory element pathology may offer new therapeutic targets for hypertension and AD.
Abstract

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