中国神经再生研究(英文版) ›› 2020, Vol. 15 ›› Issue (3): 401-406.doi: 10.4103/1673-5374.266046

• 综述:退行性病与再生 • 上一篇    下一篇

小鼠模型可以模仿散发性阿尔茨海默病吗?

  

  • 出版日期:2020-03-15 发布日期:2020-05-25

Can mouse models mimic sporadic Alzheimer’s disease?

Bettina M. Foidl, Christian Humpel   

  1. Laboratory of Psychiatry and Experimental Alzheimer’s Research, Medical University of Innsbruck, Innsbruck, Austria
  • Online:2020-03-15 Published:2020-05-25
  • Contact: Christian Humpel, PhD,christian.humpel@i-med.ac.at.
  • Supported by:
    This work was supported by the Austrian Science Funds (P24734-B24).

摘要: orcid: 0000-0001-7641-4240 (Christian Humpel)

Abstract: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the most common form of dementia worldwide. As age is the main risk factor, > 97% of all AD cases are of sporadic origin, potentiated by various risk factors associated with life style and starting at an age > 60 years. Only < 3% of AD cases are of genetic origin caused by mutations in the amyloid precursor protein or Presenilins 1 or 2, and symptoms already start at an age < 30 years. In order to study progression of AD, as well as therapeutic strategies, mouse models are state-of-the-art. So far many transgenic mouse models have been developed and used, with mutations in the APP or presenilin or combinations (3×Tg, 5×Tg). However, such transgenic mouse models more likely mimic the genetic form of AD and no information can be given how sporadic forms develop. Several risk genes, such as Apolipoprotein E4 and TREM-2 enhance the risk of sporadic AD, but also many risk factors associated with life style (e.g., diabetes, hypercholesterolemia, stress) may play a role. In this review we discuss the current situation regarding AD mouse models, and the problems to develop a sporadic mouse model of AD.

Key words: Alzheimer’s disease, beta-amyloid, cerebral amyloid angiopathy, cognitive impairment, sporadic and genetic mouse models, tau, vascular risk factors