Aβ1-42 inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β
Open accessAbstract
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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- 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
- green
- hal.science
- Licence
- other-oa
- www.springer.com/tdm (tdm)
- 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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