Aβ inhibition of LTP is prevented by manipulation of a signalling pathway involving caspase-3, Akt and GSK-3β
Amyloid-β1-42 (Aβ) is thought to be a major mediator of the cognitive deficits in Alzheimer's disease (AD). The ability of Aβ to inhibit hippocampal long-term potentiation (LTP) provides a cellular correlate of this action but the underlying molecular mechanism is only partially understood. We...
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| Veröffentlicht in: | Nature neuroscience 2011-03 |
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| container_title | Nature neuroscience |
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| creator | Cho, Kwangwook Jo, Jihoon Whitcomb, Daniel Olsen, Kimberly Moore Kerrigan, Talitha Lynn Lo, Joyce Shin-Ching Bru-Merci, Gilles Dickinson, Bryony Scullion, Sarah Sheng, Morgan Collingridge, Graham L |
| description | Amyloid-β1-42 (Aβ) is thought to be a major mediator of the cognitive deficits in Alzheimer's disease (AD). The ability of Aβ to inhibit hippocampal long-term potentiation (LTP) provides a cellular correlate of this action but the underlying molecular mechanism is only partially understood. We report a prominent role for a signaling pathway involving caspase-3, Akt1 and glycogen synthase kinase-3β in this effect in rats and mice. |
| doi_str_mv | 10.1038/nn.2785 |
| format | Article |
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| source | SpringerLink Journals; Nature Journals Online |
| title | Aβ inhibition of LTP is prevented by manipulation of a signalling pathway involving caspase-3, Akt and GSK-3β |
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