Cited by 305Alzheimer's disease research and treatmentsNeuroscience and Neuropharmacology ResearchMemory and Neural Mechanisms

Aβ1-42 inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β

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Jo, Jihoon, Whitcomb, Daniel J, Olsen, Kimberly Moore, Kerrigan, Talitha L, Lo, Shih-Ching, Bru-Mercier, Gilles, Dickinson, Bryony, Scullion, Sarah +3 more·2011·Nature Neuroscience

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.

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Crossref · 10.1038/nn.2785

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16 of 16 references verified0 citation errors · 0 not checkable

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Authors
Jo, J., Whitcomb, D. J., Olsen, K. M., Kerrigan, T. L., Lo, S.-C., Bru-Mercier, G., Dickinson, B., Scullion, S., Sheng, M., Collingridge, G., & Cho, K.
Affiliations
  • University of Bristol (GB)
  • Genentech (US)
Corresponding author
Cho, Kwangwook
Venue
Nature Neuroscience
Published
2011-03-27
Volume
14
Issue
5
Pages
545-547
ISSN
  • 1097-6256 (ISSN-L)
  • 1546-1726
OpenAlex
W1893185987
Cited by
305
References
16
Citations by year
2026: 8 · 2025: 10 · 2024: 13 · 2023: 15 · 2022: 13 · 2021: 12 · 2020: 19 · 2019: 18 · 2018: 16 · 2017: 28 · 2016: 25 · 2015: 23 · 2014: 32 · 2013: 30 · 2012: 31
FWCI
22.82
Type
journal article
Language
en
Open access
Locations
  • Nature Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion, other-oa)
  • Bristol Research (University of Bristol) (submittedVersion)
  • Trinity's Access to Research Output (TARA) (Trinity College Dublin) (submittedVersion)
Funders
  • Wellcome Trust (089703)
  • Medical Research Council (MC_G1000734)
  • Biotechnology and Biological Sciences Research Council (BB/G003963/1)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords
amyloid-beta 42, long-term potentiation, caspase-3, AKT1, glycogen synthase kinase-3β, hippocampus, Alzheimer's disease, synaptic plasticity, signaling pathways, cognitive impairment
MeSH terms
Glycogen Synthase Kinase 3 beta, Animals, Animals, Newborn, Biophysics, Electric Stimulation, Enzyme Inhibitors, Hippocampus, Neurons, Organ Culture Techniques, Peptide Fragments, Pyridines, Pyrimidines, Transfection, Signal Transduction, Amyloid beta-Peptides, Rats, Wistar, Long-Term Potentiation, Mice, Knockout, Patch-Clamp Techniques, Glycogen Synthase Kinase 3, Green Fluorescent Proteins, Proto-Oncogene Proteins c-akt, Mice, Rats, X-Linked Inhibitor of Apoptosis Protein, Caspase 3

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