Pharmaron research highlights age-related cognitive decline and molecular differences in APP/PS1 vs. 5xFAD Alzheimer’s mouse model for drug development.

Poster Authors:

Yinjie Li, Ce Zhong, Yufang Yan, Hong Liu, Zhanshan Chen, Jing Ma, Tong Wang, Ruixiu Wang, Yarou Pu, Jingqi Huang

Pharmaron, Beijing, China

Selecting the Optimal Aβ-Driven Alzheimer’s Mouse Model for CNS Drug Discovery

This poster was presented at the SFN Neuroscience conference 2025.

Selecting the most suitable transgenic Alzheimer’s mouse model is a critical step for ensuring the translatability of preclinical findings.

In this poster we compare two widely used Aβ-driven models, APP/PS1 and 5xFAD, to help our clients make strategic decisions for their drug discovery program. Our study characterizes the age-related pathological progression in the animals through behavioral testing, histopathology, and molecular analyses, offering guidance for model selection.

Highlights of Our Alzheimer’s Disease CRO Services

  • Model-Specific Expertise: The APP/PS1 Alzheimer’s mouse model is ideal for studying gradual pathological progression, and the 5xFAD model is well suited for rapid screening of Aβ-targeting compounds.
  • Comprehensive Analytical Capabilities: We offer a full suite of tests, including Morris Water Maze (MWM) for cognitive deficits, immunohistochemistry (IHC) for Aβ plaque quantification, immunoassays for Aβ42 levels, and transcriptomic profiling for gene expression analysis.
  • Diverse Experimental Platforms: In addition to APP/PS1 and 5xFAD mice, Pharmaron’s Alzheimer’s CRO services comprise testing on other transgenic mice (3xTG, Tau P301S, Tau P301L) and utilize pharmacological approaches like scopolamine-induced amnesia, and surgical methods such as bilateral intrahippocampal Aβ1-42 injection. tTo prepare for successful in vivo studies we employ a range of in vitro models for compound testing such as brain slices, iPSC-derived neurons and organoids.

Download our scientific poster for a detailed comparison of the kinetic patterns of cognitive decline, Aβ plaque accumulation, and molecular changes in APP/PS1 and 5xFAD Alzheimer’s mouse models.