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Exposure of rat hippocampal neurons to amyloid β peptide (25–35) induces the inactivation of phosphatidyl inositol-3 kinase and the activation of tau protein kinase I/glycogen synthase kinase-3β
Abstract
Exposure of rat hippocampal neurons to the peptide amyloid beta (A beta) (25-35) as well as A beta (1-40) peptides enhances phosphorylation of tau to a paired helical filament (PHF)-state through activation of tau protein kinase I (TPK I)/glycogen synthase kinase-3 beta (GSK-3 beta) [Busciglio, J., Lorenzo, A., Yeh, J. and Yankner, B.A., Neuron, 14 (1995) 879-888; Takashima, A., Ishiguro, K., Noguchi, K., Michel, G., Hoshi, M., Sato, K., Takahashi, M., Hoshino, T., Uchida, T. and Imahori, K., Neurosci. Meeting Abstr., 671 (1995) 17]. In order to examine the effects of A beta treatment on intracellular signaling mechanism, we have investigated the role of phosphatidyl inositol-3 (PI-3) kinase in the phosphorylation of tau. A beta (25-35) exposure induced an inactivation of PI-3 kinase and an activation of TPK I/GSK-3 beta in rat hippocampal culture. Wortmannin, an inhibitor of PI-3 kinase, also activated TPK I/GSK-3 beta, leading to an enhancement of tau phosphorylation and neuronal death in hippocampal culture. These results suggest that A beta (25-35) inhibition of PI-3 kinase results in the activation of TPK I/GSK-3 beta, the phosphorylation of tau, and resultant neuronal death in rat hippocampal neurons.
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“The GSK3β can orchestrate pathological tau-phosphorylation at over two-dozen disease-associated sites [181–184].”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [183]
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Neurotrophic and Neurotoxic Effects of Amyloid β Protein: Reversal by Tachykinin Neuropeptides
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Neurodegeneration induced by beta-amyloid peptides in vitro: the role of peptide assembly state
Pike, C., Burdick, D., Walencewicz, A., Glabe, C., & Cotman, C. (1993) · The Journal of Neuroscience · doi:10.1523/jneurosci.13-04-01676.1993 · Cited by 1,417
Requirement for Phosphatidylinositol-3 Kinase in the Prevention of Apoptosis by Nerve Growth Factor
Yao, R., & Cooper, G. M. (1995) · Science · doi:10.1126/science.7701324 · Cited by 1,393
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β-Amyloid fibrils induce tau phosphorylation and loss of microtubule binding
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Tau protein kinase I is essential for amyloid beta-protein-induced neurotoxicity.
Takashima, A., Noguchi, K., Sato, K., Hoshino, T., & Imahori, K. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.16.7789 · Cited by 385
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Datta, S. R., Brunet, A., & Greenberg, M. E. (1999) · Genes & Development · doi:10.1101/gad.13.22.2905 · Cited by 4,216
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Grimes, C. A., & Jope, R. S. (2001) · Progress in Neurobiology · doi:10.1016/s0301-0082(01)00011-9 · Cited by 1,440
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Lucas, J. J., Hernández, F., Gómez‐Ramos, P., Morán, M. A., Hen, R., & Avila, J. (2001) · The EMBO Journal · doi:10.1093/emboj/20.1.27 · Cited by 913
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Metadata
- Authors
- Takashima, A., Noguchi, K., Michel, G., Mercken, M., Hoshi, M., Ishiguro, K., & Imahori, K.
- Corresponding author
- Takashima, Akihiko
- Venue
- Neuroscience Letters
- Publisher
- Elsevier BV
- Published
- 1996-01
- Volume
- 203
- Issue
- 1
- Pages
- 33-36
- ISSN
- 0304-3940 (ISSN-L)
- OpenAlex
- W1986537744
- Cited by
- 260
- References
- 18
- Citations by year
- 2026: 5 · 2025: 9 · 2024: 5 · 2023: 9 · 2022: 4 · 2021: 9 · 2020: 5 · 2019: 11 · 2018: 12 · 2017: 3 · 2016: 3 · 2015: 7 · 2014: 15 · 2013: 13 · 2012: 13
- FWCI
- 3.21
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience Letters (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- amyloid beta 25-35, Aβ40, phosphatidylinositol 3-kinase, glycogen synthase kinase-3β, tau phosphorylation, paired helical filaments, hippocampal neurons, neuronal cell death, wortmannin, Alzheimer's disease
- MeSH terms
- Wortmannin, Alzheimer Disease, Androstadienes, Animals, Cells, Cultured, Dose-Response Relationship, Drug, Enzyme Inhibitors, Glycogen Synthase, Hippocampus, Phosphotransferases, Amyloid beta-Protein Precursor, tau Proteins, Rats
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