Using Optogenetics to Model Cellular Effects of Alzheimer's Disease

被引:3
|
作者
Tiwari, Prabhat [1 ]
Tolwinski, Nicholas S. [2 ,3 ]
机构
[1] Kansas State Univ, Dept Biochem & Mol Biophys, Manhattan, KS 66506 USA
[2] Yale NUS Coll, Div Sci, Singapore 138527, Singapore
[3] Duke NUS Med Sch, Program Canc & Stem Cell Biol, Singapore 169857, Singapore
关键词
Alzheimer's disease; amyloid; acetylcholinesterase; optogenetics; AMYLOID-BETA; TOXICITY; TAU; ACTIVATION; OLIGOMERS; PEPTIDE; PATHWAY; INSULIN;
D O I
10.3390/ijms24054300
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
Across the world a dementia case is diagnosed every three seconds. Alzheimer's disease (AD) causes 50-60% of these cases. The most prominent theory for AD correlates the deposition of amyloid beta (A beta) with the onset of dementia. Whether A beta is causative remains unclear due to findings such as the recently approved drug Aducanumab showing effective clearance of A beta, but not improving cognition. New approaches for understanding A beta function, are therefore necessary. Here we discuss the application of optogenetic techniques to gain insight into AD. Optogenetics, or genetically encoded, light-dependent on/off switches, provides precise spatiotemporal control to regulate cellular dynamics. This precise control over protein expression and oligomerization or aggregation could provide a better understanding of the etiology of AD.
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页数:11
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