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Basic Science and Pathogenesis.

Aya Arrar1,2,3, Madison R Longmuir1,2,3, Kate M Onuska2,3,4

  • 1Schulich School of Medicine & Dentistry, London, ON, Canada.

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Summary
This summary is machine-generated.

The Apolipoprotein E4 (ApoE4) genotype accelerates Alzheimer's disease (AD) pathology, including amyloid-beta and tau accumulation, neurodegeneration, and cognitive deficits in novel humanized mouse models. This study highlights ApoE4's significant role in AD pathogenesis.

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Area of Science:

  • Neuroscience
  • Genetics
  • Pathology

Background:

  • Apolipoprotein E (ApoE) isoforms differentially influence Alzheimer's disease (AD) pathology.
  • Preclinical models often fail to capture the combined effects of Aβ, tau, and ApoE on AD progression and cognition.

Purpose of the Study:

  • To develop and evaluate novel humanized mouse models that integrate humanized ApoE variants (ApoE3, ApoE4), amyloid precursor protein (hApp), and tau (hMAPT).
  • To investigate the interactions between ApoE genotype, Aβ, and tau, and their impact on cognitive function, brain structure, and pathological load in AD.

Main Methods:

  • Development of humanized mouse models with specific ApoE, App, and Mapt genotypes.
  • Assessment of cognitive function using the Continuous Performance Task (CPT).
  • Analysis of brain pathology and structure via single nuclei RNA sequencing (snRNA-seq), MRI, immunofluorescence, ELISAs, and Western Blotting.

Main Results:

  • AppNL-F/ApoE4 mice showed accelerated Aβ42 accumulation, increased plaque burden and size, and elevated tau levels compared to AppNL-F/ApoE3 mice.
  • MRI revealed reduced grey matter volume in fronto-cortical regions in AppNL-F/ApoE4 mice.
  • snRNA-seq indicated a decrease in cortical excitatory neurons and increased gliosis in AppNL-F/ApoE4 mice, accompanied by early attentional deficits.

Conclusions:

  • Humanized AppNL-F/MAPT/ApoE4 mice exhibit a human-like AD phenotype, including pathology, neurodegeneration, and cognitive dysfunction.
  • ApoE4 significantly exacerbates AD pathology and cognitive impairments in the presence of Aβ and tau.
  • These models are valuable for studying AD pathophysiology and evaluating therapeutic strategies.