Animal models of human diseases that accurately recapitulate clinical pathology are indispensable for understanding molecular mechanisms and advancing preclinical studies. The Alzheimer's disease (AD) research community has historically used first‐generation transgenic (Tg) mouse models that overexpress proteins linked to familial AD (FAD), mutant amyloid precursor protein (APP), or APP and presenilin (PS). These mice exhibit AD pathology, but the overexpression paradigm may cause additional phenotypes unrelated to AD. Second‐generation mouse models contain humanized sequences and clinical mutations in the endogenous mouse App gene. These mice show Aβ accumulation without phenotypes related to overexpression but are not yet a clinical recapitulation of human AD. In this review, we evaluate different APP mouse models of AD, and review recent studies using the second‐generation mice. We advise AD researchers to consider the comparative strengths and limitations of each model against the scientific and therapeutic goal of a prospective preclinical study.
APP mouse models for Alzheimer's disease preclinical studies
Hiroki Sasaguri,P. Nilsson,Shoko Hashimoto,K. Nagata,T. Saito,B. de Strooper,J. Hardy,R. Vassar,B. Winblad,T. Saido
Published 2017 in EMBO Journal
ABSTRACT
PUBLICATION RECORD
- Publication year
2017
- Venue
EMBO Journal
- Publication date
2017-08-02
- Fields of study
Biology, Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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