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Basic Science and Pathogenesis.

Angela Gomez-Arboledas1, Enikö Kramár1, Shimako Kawauchi1

  • 1University of California, Irvine, Irvine, CA, USA.

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Summary
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Human amyloid-beta (hAb) induces long-term potentiation (LTP) deficits, but the human APOE4 (hAPOE4) variant rescues these deficits and prevents synaptic loss. This study highlights hAPOE4

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Area of Science:

  • Neuroscience
  • Genetics
  • Alzheimer's Disease Research

Background:

  • Genome-Wide Association Studies (GWAS) identify Apolipoprotein E4 (ApoE4) as the primary genetic risk factor for late-onset Alzheimer's Disease (LOAD).
  • Development of advanced mouse models is crucial for understanding LOAD pathogenesis and evaluating therapeutic strategies.
  • A novel triple homozygous mouse model (MAD1) was created, integrating humanized amyloid-beta (hAb-KIloxP), humanized ApoE4 (hAPOE4), and humanized MAPT (hMAPT).

Purpose of the Study:

  • To investigate the impact of humanized amyloid-beta (hAb) and humanized Apolipoprotein E4 (hAPOE4) on synaptic function and integrity in a novel LOAD mouse model.
  • To evaluate the protective effects of hAPOE4 against hAb-induced synaptic deficits and microglial synaptic pruning.
  • To assess the interactions between aging, hAPOE4, hMAPT, and hAb in the context of LOAD pathogenesis.

Main Methods:

  • Mice (hAb-KIloxP HO;hApoE4 HO and MAD1 cohorts) were aged to 4, 12, 18, and 24 months.
  • Long-term potentiation (LTP) was recorded from hippocampal slices.
  • Synaptic density and microglial synaptic engulfment were assessed using super-resolution microscopy.

Main Results:

  • hAb-KIloxP mice exhibited significant LTP deficits compared to wild-type (WT) mice, indicating impaired synaptic plasticity.
  • The presence of hAPOE4 rescued the LTP deficits in hAb-KIloxP mice starting at 4 months of age.
  • hAPOE4 prevented hAb-induced pre-synaptic loss and reduced excessive microglial synaptic pruning observed in hAb-KIloxP mice.

Conclusions:

  • Human amyloid-beta (hAb) induces substantial LTP deficits, which are effectively prevented by the human APOE4 (hAPOE4) variant from an early age.
  • The protective effect of hAPOE4 extends to preventing excessive synaptic loss and microglial pruning associated with hAb.
  • Further research is warranted to elucidate the specific mechanisms by which human APOE4 modulates synaptic integrity and function in LOAD.