Mouse Models of Alzheimer's Disease

被引:68
|
作者
Yokoyama, Miyabishara [1 ]
Kobayashi, Honoka [1 ]
Tatsumi, Lisa [1 ]
Tomita, Taisuke [1 ]
机构
[1] Univ Tokyo, Grad Sch Pharmaceut Sci, Lab Neuropathol & Neurosci, Tokyo, Japan
来源
基金
日本学术振兴会; 日本科学技术振兴机构;
关键词
Alzheimer's disease; beta-amyloid; tau; therapeutics; mouse model; AMYLOID-BETA-PROTEIN; GAMMA-SECRETASE INHIBITORS; PAIRED HELICAL FILAMENTS; CENTRAL-NERVOUS-SYSTEM; A-BETA; TRANSGENIC MICE; CEREBROSPINAL-FLUID; NEUROFIBRILLARY TANGLES; SENILE PLAQUES; COGNITIVE DEFICITS;
D O I
10.3389/fnmol.2022.912995
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by memory loss and personality changes, eventually leading to dementia. The pathological hallmarks of AD are senile plaques and neurofibrillary tangles, which comprise abnormally aggregated beta-amyloid peptide (A beta) and hyperphosphorylated tau protein. To develop preventive, diagnostic, and therapeutic strategies for AD, it is essential to establish animal models that recapitulate the pathophysiological process of AD. In this review, we will summarize the advantages and limitations of various mouse models of AD, including transgenic, knock-in, and injection models based on A beta and tau. We will also discuss other mouse models based on neuroinflammation because recent genetic studies have suggested that microglia are crucial in the pathogenesis of AD. Although each mouse model has its advantages and disadvantages, further research on AD pathobiology will lead to the establishment of more accurate mouse models, and accelerate the development of innovative therapeutics.
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页数:14
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