Protein kinase C mediates amyloid β-protein fragment 31–35-induced suppression of hippocampal late-phase long-term potentiation in vivo

2009 ◽  
Vol 91 (3) ◽  
pp. 226-234 ◽  
Author(s):  
Jun-Fang Zhang ◽  
Jin-Shun Qi ◽  
Jian-Tian Qiao
Nature ◽  
2002 ◽  
Vol 416 (6880) ◽  
pp. 535-539 ◽  
Author(s):  
Dominic M. Walsh ◽  
Igor Klyubin ◽  
Julia V. Fadeeva ◽  
William K. Cullen ◽  
Roger Anwyl ◽  
...  

Synapse ◽  
2010 ◽  
Vol 64 (1) ◽  
pp. 83-91 ◽  
Author(s):  
Fen Guo ◽  
Wei Jing ◽  
Cun-Gen Ma ◽  
Mei-Na Wu ◽  
Jun-Fang Zhang ◽  
...  

2002 ◽  
Vol 30 (4) ◽  
pp. 552-557 ◽  
Author(s):  
D. M. Walsh ◽  
I. Klyubin ◽  
J. V. Fadeeva ◽  
M. J. Rowan ◽  
D. J. Selkoe

Despite extensive genetic and animal modelling data that support a central role for the amyloid β-protein (Aβ) in the genesis of Alzheimer's disease, the specific form(s) of Aβ which causes injury to neurons in vivo has not been identified. In the present study, we examine the importance of soluble, pre-fibrillar assemblies of Aβ as mediators of neurotoxicity. Specifically, we review the role of cell-derived SDS-stable oligomers, their blocking of hippocampal long-term potentiation in vivo and the finding that this blocking can be prevented by prior treatment of oligomer-producing cells withγ-secretase inhibitors.


2008 ◽  
Vol 283 (24) ◽  
pp. 16790-16800 ◽  
Author(s):  
Dean M. Hartley ◽  
Chaohui Zhao ◽  
Austin C. Speier ◽  
Gavitt A. Woodard ◽  
Shaomin Li ◽  
...  

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