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Basic Science and Pathogenesis.

Arash Salahinejad1,2,3, Amr Eed1,2,3, Mohammad H Alipour1

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

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Early lecanemab treatment reduced Alzheimer's pathology in APOE4 mice but did not prevent cognitive deficits and may increase microbleeds. This study highlights risks for APOE4 carriers receiving amyloid-targeting therapies.

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Area of Science:

  • Neuroscience
  • Genetics
  • Pharmacology

Background:

  • Alzheimer's disease (AD) is a leading cause of dementia, disproportionately affecting APOE4 carriers.
  • APOE4 carriers exhibit accelerated amyloid-beta (Aβ) accumulation and increased risk of amyloid-related imaging abnormalities (ARIA) with monoclonal antibody (mAb) treatments.
  • Lecanemab, a mAb targeting Aβ protofibrils, reduces amyloid plaques but carries an enhanced risk for APOE4 carriers.

Purpose of the Study:

  • To investigate if early lecanemab (mAb158) treatment can mitigate microbleeds and cognitive decline in APOE4 humanized Alzheimer's disease mouse models.
  • To evaluate the impact of mAb158 on amyloid pathology and brain atrophy in the context of APOE4-associated genetic risk.
  • To establish a preclinical platform for assessing the safety and efficacy of mAb therapies in AD.

Main Methods:

  • Utilized advanced Alzheimer's disease mouse models with humanized APP, Tau, and APOE3/APOE4 genes.
  • Administered murine lecanemab (mAb158) or vehicle weekly for 26 weeks to hAppNL-F-hMAPT-APOE4 and hAppNL-F-hMAPT-APOE3 mice starting at 3 months of age.
  • Assessed cognitive performance using a Continuous Performance Test (CPT) and analyzed brain tissues for amyloid pathology, microbleeds, and Aβ levels via microscopy and biochemical assays.

Main Results:

  • Significant amyloid accumulation was observed in hAppNL-F-hMAPT-APOE4 mice compared to hAppNL-F-hMAPT-APOE3 mice.
  • mAb158 treatment significantly reduced insoluble Aβ accumulation in hAppNL-F-hMAPT-APOE4 mice by 15 months of age.
  • APOE4 mice exhibited cognitive deficits (CPT) starting at 6 months, irrespective of mAb158 treatment, and preliminary data suggest mAb158 may cause microhemorrhages.

Conclusions:

  • Early mAb158 treatment effectively reduces Alzheimer's disease pathology in APOE4 humanized mice but does not prevent attention deficits.
  • The treatment may increase the risk of microbleeds in the vulnerable APOE4 genotype.
  • This study demonstrates a valuable preclinical platform for predicting the safety and efficacy of monoclonal antibody treatments for Alzheimer's disease.