CrossRef Open Access 2018

PO-054 Research on Animal models of Alzheimer’s Disease

Ruilian Liu Honglin Qu

Abstrak

Objective This paper analysis amount of literature about domestic and abroad with establishing the animal model of AD as the basics point of the research, and explore the construction of animal models of AD and the theoretical basis of the study. The purpose of the paper was to better probe AD Pathogenesis and etiology, and how to take appropriate intervention methods to lay the foundation.
 Methods 
 Results Following the analysis, we found that the animal models of AD were mainly modeled by transgenic animal model, modeled by AD histopathological features, cholinergic nerve injury, aging, multifactorial complex, and ischemia and hypoxia. Each modeling method was based on the corresponding theoretical research carried out on the basis of the current research, however, the exact pathogenesis of AD was not clear, so the scholars in a variety of hypotheses on the premise Under the experimental animal model, naturally with a certain degree of one-sidedness. Transgenic animal model is expensive, disease resistance was poor, it was difficult to carry out a large amount of experimental study; cholinergic neuron damage in AD experimental animals for cholinergic function impairment and cognitive function of the ideal study.
 Conclusions The modeling method of AD had many advantages and disadvantages, and the compound animal model of AD was more complex than single factor modeling. Thus, no matter which way AD animal model, it was difficult to replicate all the typical pathological changes in AD, suggesting that the pathogenesis of AD and its pathological changes in the complexity and multi-factor.

Penulis (2)

R

Ruilian Liu

H

Honglin Qu

Format Sitasi

Liu, R., Qu, H. (2018). PO-054 Research on Animal models of Alzheimer’s Disease. https://doi.org/10.14428/ebr.v1i3.10743

Akses Cepat

Lihat di Sumber doi.org/10.14428/ebr.v1i3.10743
Informasi Jurnal
Tahun Terbit
2018
Bahasa
en
Sumber Database
CrossRef
DOI
10.14428/ebr.v1i3.10743
Akses
Open Access ✓