Altered Amyloid-β42 and BACE-1 Proteins in Plasma Astrocyte-Derived Exosomes in Hypertensive Patients With Cerebral

Xiaoxiao Liu1, Yuanyuan Liu1, Ran Yao1

  • 1Department of Neurology, Weihai Municipal Hospital, Cheeloo College of Medicine, Shandong University, Weihai, China.

PubMed
Abstract

Insights

Hypertension-related cerebral microbleeds (CMBs) are linked to reduced plasma astrocyte-derived exosome levels of amyloid-beta 42 (Aβ42). This suggests a connection between hypertension, CMBs, and Alzheimer

Area of Science:

  • Neuroscience
  • Cardiovascular Research
  • Biochemistry

Background:

  • Cerebral microbleeds (CMBs) are implicated in Alzheimer's disease (AD) progression.
  • Hypertension (HTN) is a key factor in CMBs and an AD risk factor.
  • The link between HTN-related CMBs and AD pathology is not fully understood.

Purpose of the Study:

  • To investigate the relationship between HTN-related CMBs and levels of amyloid-beta 42 (Aβ42) and BACE-1 in plasma astrocyte-derived exosomes (ADEs).

Main Methods:

  • Analysis of 88 hypertensive participants, categorized by CMB presence and location (deep/infratentorial or mixed).
  • Assessment of CMBs using susceptibility-weighted imaging.
  • Quantification of plasma ADE levels of Aβ42 and BACE-1 via ELISA kits.

Main Results:

  • Plasma ADE levels of Aβ42 were lower in hypertensive patients with deep/infratentorial or mixed CMBs compared to those without CMBs.
  • Plasma ADE Aβ42 levels showed a significant association with CMBs in hypertensive patients.
  • No significant differences in plasma ADE BACE-1 levels were observed across the groups.

Conclusions:

  • Reduced plasma ADE Aβ42 levels are significantly associated with CMBs in hypertensive patients.
  • This suggests a potential link between HTN-related CMBs and AD-related amyloid-beta pathology.
  • Findings offer insights into how HTN-related CMBs may accelerate AD progression.