Synaptic Protein α1-Takusan Mitigates Amyloid-β-Induced Synaptic Loss via Interaction with Tau and Postsynaptic Density-95 at Postsynaptic Sites

The synaptic toxicity of soluble amyloid-β (Aβ) oligomers plays a critical role in the pathophysiology of Alzheimer's disease (AD). Here we report that overexpressed α1-takusan, which we previously identified as a protein that enhances synaptic activity via interaction with PSD-95, mitigates ol...

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Autors principals: Nakanishi, Nobuki, Ryan, Scott D., Zhang, Xiaofei, Khan, Adnan, Holland, Timothy, Cho, Eun-Gyung, Huang, Xiayu, Liao, Francesca-Fang, Xu, Huaxi, Lipton, Stuart A., Tu, Shichun
Format: Artigo
Idioma:Inglês
Publicat: Society for Neuroscience 2013
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Articles
Accés en línia:https://ncbi.nlm.nih.gov/pmc/articles/PMC3756761/
https://ncbi.nlm.nih.gov/pubmed/23986251
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1523/JNEUROSCI.4646-10.2013
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