APOE4-specific changes in Aβ accumulation in a new transgenic mouse model of Alzheimer disease.

@article{Youmans2012APOE4specificCI,
  title={APOE4-specific changes in Aβ accumulation in a new transgenic mouse model of Alzheimer disease.},
  author={Katherine Lynn Youmans and Leon M. Tai and Evelyn Nwabuisi-Heath and Lisa M. Jungbauer and Takahisa Kanekiyo and Ming Gan and Jungsu Kim and William A. Eimer and Steven Estus and George William Rebeck and Edwin J. Weeber and Guojun Bu and Chunjiang Yu and Mary Jo Ladu},
  journal={The Journal of biological chemistry},
  year={2012},
  volume={287 50},
  pages={41774-86}
}
APOE4 is the greatest risk factor for Alzheimer disease (AD) and synergistic effects with amyloid-β peptide (Aβ) suggest interactions among apoE isoforms and different forms of Aβ accumulation. However, it remains unclear how the APOE genotype affects plaque morphology, intraneuronal Aβ, soluble Aβ42, and oligomeric Aβ (oAβ), particularly in vivo. As the introduction of human APOE significantly delays amyloid deposition in transgenic mice expressing familial AD (FAD) mutations (FAD-Tg), 5xFAD… CONTINUE READING
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