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A survey of Cdk5 activator p35 and p25 levels in Alzheimer's disease brains
Open accessAbstract
P25, a calpain cleavage product of the cyclin‐dependent kinase 5 (Cdk5) activator p35, causes prolonged activation of Cdk5. Although p25 has been shown to accumulate in brains of patients with Alzheimer's disease (AD), it is not known whether p25 accumulation in AD is brain region‐specific. We analyzed the amounts of p25 and p35 in human autopsy samples from multiple brain regions including frontal cortex, inferior parietal cortex and hippocampus using immunoblotting assays. Our results show that the p25–p35 indices are higher in AD than in the control groups in all three brain regions. The most significant difference in p25–p35 indices between AD and control groups is in the frontal cortex. No significant difference in calpain activity between AD and control groups is observed, indicating that postmortem calpain activation cannot account for the elevation of p25/p35 ratios in AD brains. Our results support the notion that p25 accumulation deregulates Cdk5 activity in AD brains, and the deregulated Cdk5 activity may contribute to the pathogenesis of AD.
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“In support of this, increased GSK3β expression and CDK5 activity, decreased expression of PP1 and PP2A, and decreased PP2A activity has been observed in specific brain regions in AD patients [148–152].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [149]
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Ischemic Cell Death in Brain Neurons
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Conversion of p35 to p25 deregulates Cdk5 activity and promotes neurodegeneration
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Self-citationNeurotoxicity induces cleavage of p35 to p25 by calpain
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Self-citationProline-directed and non-proline-directed phosphorylation of PHF-tau
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Self-citationCalpain-dependent Proteolytic Cleavage of the p35 Cyclin-dependent Kinase 5 Activator to p25
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An Isoform of the Neuronal Cyclin-dependent Kinase 5 (Cdk5) Activator
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Inhibition of tau phosphorylating protein kinase cdk5 prevents β‐amyloid‐induced neuronal death
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Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease
Guo, T., Zhang, D., Zeng, Y., Huang, T. Y., Xu, H., & Zhao, Y. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00391-7 · Cited by 994
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Cruz, J. C., Tseng, H.-C., Goldman, J. A., Shih, H., & Tsai, L.-H. (2003) · Neuron · doi:10.1016/s0896-6273(03)00627-5 · Cited by 609
Self-citationCdk5 Is a Key Factor in Tau Aggregation and Tangle Formation In Vivo
Noble, W. J., Olm, V., Takata, K., Casey, E., Mary, O., Meyerson, J. L., Gaynor, K., LaFrancois, J. J., Wang, L., Kondo, T., et al. (2003) · Neuron · doi:10.1016/s0896-6273(03)00259-9 · Cited by 511
The role of tau in neurodegeneration
Gendron, T. F., & Petrucelli, L. (2009) · Molecular Neurodegeneration · doi:10.1186/1750-1326-4-13 · Cited by 478
Metadata
- Authors
- Tseng, H.-C., Zhou, Y., Shen, Y., & Tsai, L.-H.
- Affiliations
- Howard Hughes Medical Institute (US)
- Banner Sun Health Research Institute (US)
- Corresponding author
- Tsai, Li-Huei
- Venue
- FEBS Letters
- Publisher
- Wiley
- Published
- 2002-06-18
- Volume
- 523
- Issue
- 1-3
- Pages
- 58-62
- ISSN
- 0014-5793 (ISSN-L)
- 1873-3468
- OpenAlex
- W2092765133
- Cited by
- 198
- References
- 20
- Citations by year
- 2026: 4 · 2025: 12 · 2024: 7 · 2023: 2 · 2022: 3 · 2021: 6 · 2020: 7 · 2019: 5 · 2018: 4 · 2017: 9 · 2016: 6 · 2015: 6 · 2014: 4 · 2013: 4 · 2012: 19
- FWCI
- 7.79
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- FEBS Letters (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Alzheimer's Association
- National Institutes of Health
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Calpain Protease Function and Regulation
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, cyclin-dependent kinase 5, p35, p25, calpain cleavage, brain region-specific expression, frontal cortex, hippocampus, inferior parietal cortex, postmortem brain
- MeSH terms
- Alzheimer Disease, Brain, Calpain, Frontal Lobe, Hippocampus, Humans, Nerve Tissue Proteins, Parietal Lobe, Postmortem Changes
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