| First Author | Jo J | Year | 2011 |
| Journal | Nat Neurosci | Volume | 14 |
| Issue | 5 | Pages | 545-7 |
| PubMed ID | 21441921 | Mgi Jnum | J:172292 |
| Mgi Id | MGI:5006884 | Doi | 10.1038/nn.2785 |
| Citation | Jo J, et al. (2011) Abeta(1-42) inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3beta. Nat Neurosci 14(5):545-7 |
| abstractText | Amyloid-beta(1-42) (Abeta) is thought to be a major mediator of the cognitive deficits in Alzheimer's disease. The ability of Abeta to inhibit hippocampal long-term potentiation provides a cellular correlate of this action, but the underlying molecular mechanism is only partially understood. We found that a signaling pathway involving caspase-3, Akt1 and glycogen synthase kinase-3beta is an important mediator of this effect in rats and mice. |
