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Basic Science and Pathogenesis.

Olivia J Marola1, Jonathan Nyandu Kanyinda1, Eliana C Liporace1,2

  • 1The Jackson Laboratory, Bar Harbor, ME, USA.

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Summary
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Genetic mapping identified loci that influence cerebral amyloid angiopathy (CAA) in Alzheimer's disease (AD) models. Elevating TIE2 activation did not prevent CAA, but candidate genes for CAA susceptibility are being investigated.

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Area of Science:

  • Neuroscience
  • Genetics
  • Pathology

Background:

  • Cerebral amyloid angiopathy (CAA) is common in Alzheimer's disease (AD) and linked to neurodegeneration.
  • Blood-brain barrier (BBB) compromise may worsen CAA by impairing amyloid clearance.
  • TIE2 signaling, regulated by ANGPT2, influences BBB integrity and is a potential target for CAA intervention.

Purpose of the Study:

  • To map genetic loci associated with CAA susceptibility using distinct mouse models.
  • To investigate the therapeutic potential of elevating TIE2 activation (pTIE2) in preventing AD-related CAA.
  • To identify genetic factors contributing to CAA pathogenesis for future therapeutic strategies.

Main Methods:

  • Crossed WSB.APP/PS1 and B6.APP/PS1 mice to generate F1 (BXW.APP/PS1) and F2 offspring for CAA susceptibility mapping.
  • Assessed CAA severity via immunohistochemistry for amyloid deposits and neuronal loss (NEUN+ cells).
  • Investigated the effect of Angpt2 heterozygosity (to increase pTIE2) on AD and CAA progression in BXW.Angpt2-/+APP/PS1 mice.

Main Results:

  • BXW.APP/PS1 mice showed significantly increased CAA compared to founder strains.
  • F2 progeny exhibited variable CAA severity, suggesting mappable susceptibility loci.
  • Angpt2 heterozygosity did not significantly alter plasma amyloid levels, CAA severity, or neuronal cell counts.

Conclusions:

  • Heterozygous genetic loci in BXW.APP/PS1 mice significantly promote CAA.
  • CAA susceptibility loci are likely mappable in F2 progeny, with ongoing SNP analysis.
  • While pTIE2 elevation was ineffective, identified candidate alleles will be tested for CAA attenuation via genetic and pharmacological means.