Amyloid pathology and cognitive impairment in hAβ-KI and APPSAA-KI mouse models of Alzheimer's disease

Neurobiol Aging. 2025 Jan:145:13-23. doi: 10.1016/j.neurobiolaging.2024.10.005. Epub 2024 Oct 19.

Abstract

The hAβ-KI and APPSAA-KI are two amyloid models that harbor mutations in the endogenous mouse App gene. Both hAβ-KI and APPSAA-KI mice contain a humanized Aβ sequence, and APPSAA-KI mice carry three additional familial AD mutations. We herein report that the Aβ levels and Aβ42/Aβ40 ratio in APPSAA-KI homozygotes are dramatically higher than those in hAβ-KI homozygotes at 14 months of age. In addition, APPSAA-KI mice display a widespread distribution of amyloid plaques in the brain, whereas the plaques are undetectable in hAβ-KI mice. Moreover, there are no sex differences in amyloid pathology in APPSAA-KI mice. Both APPSAA-KI and hAβ-KI mice exhibit cognitive impairments, wherein no significant differences are found between these two models, although APPSAA KI mice show a trend towards worse cognitive function. Notably, female hAβ-KI and APPSAA-KI mice have a more pronounced cognitive impairments compared to their respective males. Our findings suggest that Aβ humanization contributes to cognitive deficits in APPSAA-KI mice, and that amyloid deposition might not be closely associated with cognitive impairments in APPSAA-KI mice.

Keywords: APP(SAA)-KI mice; Amyloid β (Aβ); Cognitive impairment; HAβ-KI mice; Sex-dependent effects.

MeSH terms

  • Alzheimer Disease* / genetics
  • Alzheimer Disease* / metabolism
  • Alzheimer Disease* / pathology
  • Alzheimer Disease* / psychology
  • Amyloid beta-Peptides* / metabolism
  • Amyloid beta-Protein Precursor* / genetics
  • Amyloid beta-Protein Precursor* / metabolism
  • Animals
  • Brain / metabolism
  • Brain / pathology
  • Cognition Disorders / etiology
  • Cognition Disorders / genetics
  • Cognition Disorders / metabolism
  • Disease Models, Animal*
  • Female
  • Homozygote
  • Humans
  • Male
  • Mice
  • Mice, Transgenic*
  • Mutation
  • Plaque, Amyloid / metabolism
  • Plaque, Amyloid / pathology

Substances

  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor