Aβ(1-42) inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β

Jihoon Jo; Daniel J Whitcomb; Kimberly Moore Olsen; Talitha L Kerrigan; Shih-Ching Lo; Gilles Bru-Mercier; Bryony Dickinson; Sarah Scullion; Morgan Sheng; Graham Collingridge; Kei Cho

doi:10.1038/nn.2785

Aβ(1-42) inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β

Jihoon Jo, Daniel J Whitcomb, Kimberly Moore Olsen, Talitha L Kerrigan, Shih-Ching Lo, Gilles Bru-Mercier, Bryony Dickinson, Sarah Scullion, Morgan Sheng, Graham Collingridge, Kei Cho

Research output: Contribution to journal › Article (Academic Journal) › peer-review

273 Citations (Scopus)

Abstract

Amyloid-β(1-42) (Aβ) is thought to be a major mediator of the cognitive deficits in Alzheimer's disease. The ability of Aβ 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-3β is an important mediator of this effect in rats and mice.

Translated title of the contribution	Aβ(1-42) inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β
Original language	English
Pages (from-to)	545 - 547
Number of pages	3
Journal	Nature Neuroscience
Volume	14
Issue number	5
Early online date	27 Mar 2011
DOIs	https://doi.org/10.1038/nn.2785
Publication status	Published - May 2011

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http://www.nature.com/neuro/journal/v14/n5/full/nn.2785.html

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title = "Aβ(1-42) inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β",

abstract = "Amyloid-β(1-42) (Aβ) is thought to be a major mediator of the cognitive deficits in Alzheimer's disease. The ability of Aβ 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-3β is an important mediator of this effect in rats and mice.",

author = "Jihoon Jo and Whitcomb, {Daniel J} and Olsen, {Kimberly Moore} and Kerrigan, {Talitha L} and Shih-Ching Lo and Gilles Bru-Mercier and Bryony Dickinson and Sarah Scullion and Morgan Sheng and Graham Collingridge and Kei Cho",

year = "2011",

month = may,

doi = "10.1038/nn.2785",

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T1 - Aβ(1-42) inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β

AU - Jo, Jihoon

AU - Whitcomb, Daniel J

AU - Olsen, Kimberly Moore

AU - Kerrigan, Talitha L

AU - Lo, Shih-Ching

AU - Bru-Mercier, Gilles

AU - Dickinson, Bryony

AU - Scullion, Sarah

AU - Sheng, Morgan

AU - Collingridge, Graham

AU - Cho, Kei

PY - 2011/5

Y1 - 2011/5

N2 - Amyloid-β(1-42) (Aβ) is thought to be a major mediator of the cognitive deficits in Alzheimer's disease. The ability of Aβ 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-3β is an important mediator of this effect in rats and mice.

AB - Amyloid-β(1-42) (Aβ) is thought to be a major mediator of the cognitive deficits in Alzheimer's disease. The ability of Aβ 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-3β is an important mediator of this effect in rats and mice.

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U2 - 10.1038/nn.2785

DO - 10.1038/nn.2785

M3 - Article (Academic Journal)

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SP - 545

EP - 547

JO - Nature Neuroscience

JF - Nature Neuroscience

IS - 5

ER -

Aβ(1-42) inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β

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THE EFFECTS OF ACUTE STRESS ON GLUTAMATE RECEPTOR TRAFFICKING AND SYNAPTIC PLASTICITY IN THE HIPPOCAMPUS

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Aβ(1-42) inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β

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THE EFFECTS OF ACUTE STRESS ON GLUTAMATE RECEPTOR TRAFFICKING AND SYNAPTIC PLASTICITY IN THE HIPPOCAMPUS

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