Restored glial glutamate transporter EAAT2 function as a potential therapeutic approach for Alzheimer’s disease
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Author
Takahashi, Kou
Kong, Qiongman
Lin, Yuchen
Stouffer, Nathan
Schulte, Delanie A.
Lai, Liching
Liu, Qibing
Chang, Ling-Chu
Dominguez, Sky
Xing, Xuechao
Cuny, Gregory D.
Lin, Chien-Liang Glenn
Note: Order does not necessarily reflect citation order of authors.
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https://doi.org/10.1084/jem.20140413Metadata
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Takahashi, K., Q. Kong, Y. Lin, N. Stouffer, D. A. Schulte, L. Lai, Q. Liu, et al. 2015. “Restored glial glutamate transporter EAAT2 function as a potential therapeutic approach for Alzheimer’s disease.” The Journal of Experimental Medicine 212 (3): 319-332. doi:10.1084/jem.20140413. http://dx.doi.org/10.1084/jem.20140413.Abstract
Glutamatergic systems play a critical role in cognitive functions and are known to be defective in Alzheimer’s disease (AD) patients. Previous literature has indicated that glial glutamate transporter EAAT2 plays an essential role in cognitive functions and that loss of EAAT2 protein is a common phenomenon observed in AD patients and animal models. In the current study, we investigated whether restored EAAT2 protein and function could benefit cognitive functions and pathology in APPSw,Ind mice, an animal model of AD. A transgenic mouse approach via crossing EAAT2 transgenic mice with APPSw,Ind. mice and a pharmacological approach using a novel EAAT2 translational activator, LDN/OSU-0212320, were conducted. Findings from both approaches demonstrated that restored EAAT2 protein function significantly improved cognitive functions, restored synaptic integrity, and reduced amyloid plaques. Importantly, the observed benefits were sustained one month after compound treatment cessation, suggesting that EAAT2 is a potential disease modifier with therapeutic potential for AD.Other Sources
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4354363/pdf/Terms of Use
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