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Apolipoprotein E isoforms differentially regulate matrix metallopeptidase 9 function in Alzheimer's disease.

Charis Ringland1, Jonas Elias Schweig2, Daniel Paris2

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Neurobiology of Aging
|August 8, 2020
PubMed
Summary

Apolipoprotein E4 (APOE4) impairs amyloid-beta clearance by increasing active matrix metallopeptidase 9 (MMP-9). This suggests APOE4 exacerbates Alzheimer's disease pathology by affecting MMP-9 levels in the brain.

Keywords:
Alzheimer’s diseaseApolipoprotein EBinding affinityCerebrovasculatureEnzyme regulationMatrix metallopeptidase 9

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Genetics

Background:

  • Apolipoprotein E (APOE) isoforms differentially affect amyloid-beta (Aβ) clearance across the blood-brain barrier.
  • Previous research indicated reduced Aβ transit with APOE4 due to increased lipoprotein receptor shedding.
  • Matrix metallopeptidase 9 (MMP-9) was identified as a key enzyme in APOE-dependent lipoprotein receptor proteolysis impacting Aβ elimination.

Purpose of the Study:

  • To investigate the relationship between APOE and MMP-9 in brain endothelial cells.
  • To determine how APOE isoforms influence MMP-9 secretion and activity.
  • To examine the association between APOE genotype, MMP-9 expression, and Alzheimer's disease (AD) pathology.

Main Methods:

  • Assessed proMMP-9 cellular secretion from brain endothelial cells expressing different APOE isoforms.
  • Utilized cell-free assays to evaluate APOE's dose-dependent effect on MMP-9 activity.
  • Analyzed MMP-9 expression and activity in human and animal AD brain specimens with varying APOE genotypes.

Main Results:

  • APOE influenced proMMP-9 secretion, with APOE2 < APOE3 = APOE4.
  • APOE dose-dependently inhibited MMP-9 activity in vitro, with APOE4 being significantly less effective than APOE2 or APOE3.
  • Elevated MMP-9 expression and activity were observed in the cerebrovasculature of AD brains carrying the APOE4 genotype.

Conclusions:

  • APOE plays a role in regulating MMP-9 levels and activity.
  • The APOE4 isoform exhibits a diminished capacity to inhibit MMP-9 compared to other isoforms.
  • These findings provide a potential mechanism linking APOE4 to increased Aβ pathology in Alzheimer's disease.