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Basic Science and Pathogenesis.

Jamie L Fournier1,2,3, Aya Arrar1,2,3, Madison R Longmuir1,2,3

  • 1University of Western Ontario, London, ON, Canada.

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|December 23, 2025
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Alzheimer's Disease research shows amyloid and APOE4 worsen tau pathology. New mouse models reveal aging, amyloid precursor protein (App), and APOE4 increase tau phosphorylation and insoluble tau, especially in APOE4 carriers.

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Area of Science:

  • Neuroscience
  • Genetics
  • Biochemistry

Background:

  • Tau protein dysfunction is central to Alzheimer's Disease (AD).
  • Amyloid-beta (Aβ) and Apolipoprotein E4 (APOE4) individually exacerbate tau pathology.
  • The combined effects of Aβ and APOE4 on human tau levels in vivo remain unclear.

Purpose of the Study:

  • To investigate the synergistic effects of Aβ and APOE4 on human tau pathology.
  • To utilize novel mouse models expressing humanized variants of tau (hMAPT), amyloid precursor protein (AppNL/NL-F), and APOE3/APOE4.

Main Methods:

  • Biochemical assays (Western Blot) and immunofluorescence microscopy were used to quantify phosphorylated tau (AT8) and total tau.
  • Visuospatial learning and memory were assessed using the Paired Associates Learning (PAL) task.

Main Results:

  • Tau phosphorylation (AT8) increased with age, AppNL-F expression, and APOE4 genotype.
  • Insoluble total tau was elevated in aged mice and exacerbated by APOE4.
  • No significant genotype-dependent differences in learning and memory were observed in the PAL task at 12 months.

Conclusions:

  • Aging, APOE4, and Aβ accumulation correlate with increased tau pathology markers.
  • Amyloid and APOE4 can enhance tau markers in models without tau overexpression.
  • Early-stage cognitive deficits may exist despite normal performance on the PAL task.