APP mouse models for Alzheimer's disease preclinical studies
By Hiroki Sasaguri, P. Nilsson, Shoko Hashimoto, K. Nagata, T. Saito, B. de Strooper, John Hardy, R. Vassar, Bengt Winblad, T. Saido. EMBO Journal, 2017
674 citations recorded by the source corpus.
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.
Subfields: Biological Psychiatry, Neurology, Physiology
View Paper: https://www.semanticscholar.org/paper/7a9a103ad2bf6ffa0455517ae76aeec33e058858
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Citations in the corpus
- The Amyloid-β Oligomer Hypothesis: Beginning of the Third Decade (2018, neutral): “goal of a prospective preclinical study [369].”
- The role of adult hippocampal neurogenesis in brain health and disease (2018, background): “Modeling in animals by overexpressing proteins linked to familial AD such as mutant amyloid precursor proteins (APP) and presenilin partially recapitulates AD pathology, but the animals also have unrelated phenotypes due to the overexpression of transgenes, and therefore interpretations based on stu”