Reversing EphB2 depletion rescues cognitive functions in Alzheimer model

Amyloid-β oligomers may cause cognitive deficits in Alzheimer's disease by impairing neuronal NMDA-type glutamate receptors, whose function is regulated by the receptor tyrosine kinase EphB2. Here we show that amyloid-β oligomers bind to the fibronectin repeats domain of EphB2 and trigger EphB2...

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Detaylı Bibliyografya
Asıl Yazarlar: Cissé, Moustapha, Halabisky, Brian, Harris, Julie, Devidze, Nino, Dubal, Dena B., Sun, Binggui, Orr, Anna, Lotz, Gregor, Kim, Daniel H., Hamto, Patricia, Ho, Kaitlyn, Yu, Gui-Qiu, Mucke, Lennart
Materyal Türü: Artigo
Dil:Inglês
Baskı/Yayın Bilgisi: 2010
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Article
Online Erişim:https://ncbi.nlm.nih.gov/pmc/articles/PMC3030448/
https://ncbi.nlm.nih.gov/pubmed/21113149
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1038/nature09635
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