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Vascular ApoE4 Impairs Behavior by Modulating Gliovascular Function.

Yu Yamazaki1, Chia-Chen Liu1, Akari Yamazaki1

  • 1Department of Neuroscience, Mayo Clinic, Jacksonville, FL 32224, USA.

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|December 15, 2020
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Summary
This summary is machine-generated.

The apolipoprotein E4 (APOE4) gene variant impairs brain function and blood flow when specifically expressed in vascular cells. This suggests vascular APOE plays a key role in Alzheimer's disease pathogenesis.

Keywords:
APOEAlzheimer’s diseasegliovascular functionsingle-cell RNA sequencingvascular mural cells

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Area of Science:

  • Neuroscience
  • Genetics
  • Cardiovascular Biology

Background:

  • The apolipoprotein E gene (APOE) has multiple isoforms, with APOE4 being a significant risk factor for Alzheimer's disease (AD) and vascular conditions.
  • ApoE is expressed in various brain cells, including astrocytes, microglia, and vascular mural cells (VMCs).

Purpose of the Study:

  • To investigate the specific role of vascular mural cell (VMC)-expressed apolipoprotein E (ApoE) isoforms (ApoE3 and ApoE4) in brain function and cerebrovascular health.
  • To determine if vascular ApoE isoform expression influences AD pathogenesis.

Main Methods:

  • Utilized genetically modified mice with VMC-specific expression of human ApoE3 or ApoE4.
  • Assessed behavioral phenotypes, cerebrovascular function (arteriole blood flow), and systemic metabolic markers (cholesterolemia, atherosclerosis).
  • Performed single-cell RNA sequencing on vascular and glial cells to analyze cellular responses.

Main Results:

  • Vascular expression of ApoE4, but not ApoE3, in mice led to impaired behavior, reduced arteriole blood flow, and increased anxiety.
  • ApoE3 and ApoE4 expression in VMCs corrected hypercholesterolemia and atherosclerosis in Apoe knockout mice.
  • Single-cell RNA sequencing revealed ApoE4 induced astrocyte activation, while ApoE3 promoted an angiogenic signature in pericytes.

Conclusions:

  • Vascular ApoE exerts cell-autonomous effects on brain homeostasis in an isoform-dependent manner.
  • Vascular ApoE4 contributes significantly to AD pathogenesis through detrimental effects on cerebrovascular function and behavior.
  • Targeting vascular ApoE isoforms may offer new therapeutic strategies for Alzheimer's disease.