期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 57, 期 4, 页码 1171-1183出版社
IOS PRESS
DOI: 10.3233/JAD-170045
关键词
Alzheimer's disease; amyloid-beta; animal models; apoE; APP; ob mutation; PS1
资金
- Instituto de Salud Carlos III [FIS-PI113-01330]
- Generalitat de Catalunya [SGR-GRC-2014-00885]
- Generalitat de Catalunya/FEDER [2014-PROD00032]
- PIF-UAB student grants
Alzheimer's disease (AD) is a neurodegenerative disorder that nowadays affects more than 40 million people worldwide and it is predicted to exponentially increase in the coming decades. Because no curative treatment exists, research on the pathophysiology of the disease, as well as the testing of new drugs, are mandatory. For these purposes, animal models constitute a valuable, although perfectible tool. This review takes a tour through several aspects of mouse models of AD, such as the generation of transgenic models, the relevance of the promoter driving the expression of the transgenes, and the concrete transgenes used to simulate AD pathophysiology. Then, transgenic mouse lines harboring mutated human genes at several loci such as APP, PSEN1, APOE epsilon 4, and ob (leptin) are reviewed. Therefore, not only the accumulation of the A beta peptide is emulated but also cholesterol and insulin metabolism. Further novel information about the disease will allow for the development of more accurate animal models, which in turn will undoubtedly be helpful for bringing preclinical research closer to clinical trials in humans.
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