Genetic Dissection of Alzheimer's Disease Using Drosophila Models

被引:29
|
作者
Jeon, Youngjae [1 ]
Lee, Jae Ha [1 ]
Choi, Byoungyun [1 ]
Won, So-Yoon [2 ]
Cho, Kyoung Sang [1 ]
机构
[1] Konkuk Univ, Dept Biol Sci, Seoul 05029, South Korea
[2] Chungbuk Natl Univ, Coll Med, Dept Biochem, Cheongju 28644, South Korea
关键词
AD model; Alzheimer's disease; amyloid beta; Drosophila; functional genomics; AMYLOID PRECURSOR PROTEIN; A-BETA OLIGOMERS; GLYCOGEN-SYNTHASE KINASE-3-BETA; GLIAL-CELL PROLIFERATION; INDUCED ER STRESS; OXIDATIVE STRESS; TRANSGENIC MICE; SYNAPTIC PLASTICITY; MOUSE MODEL; MEDIATED NEURODEGENERATION;
D O I
10.3390/ijms21030884
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Alzheimer's disease (AD), a main cause of dementia, is the most common neurodegenerative disease that is related to abnormal accumulation of the amyloid (3 (A(3) protein. Despite decades of intensive research, the mechanisms underlying AD remain elusive, and the only available treatment remains symptomatic. Molecular understanding of the pathogenesis and progression of AD is necessary to develop disease-modifying treatment. Drosophila, as the most advanced genetic model, has been used to explore the molecular mechanisms of AD in the last few decades. Here, we introduce Drosophila AD models based on human AP and summarize the results of their genetic dissection. We also discuss the utility of functional genomics using the Drosophila system in the search for AD-associated molecular mechanisms in the post-genomic era.
引用
收藏
页数:27
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