Degradation of Caytaxin Causes Learning and Memory Deficits via Activation of DAPK1 in Aging
Abstract
Loss of memory is an inevitable clinic sign in aging, but its underlying mechanisms remain unclear. Here we show that death-associated protein kinase (DAPK1) is involved in the decays of learning and memory in aging via degradation of Caytaxin, a brain-specific member of BNIP-2. DAPK1 becomes activated in the hippocampus of mice during aging. Activation of DAPK1 is closely associated with degradation of Caytaxin protein. Silencing Caytaxin by the expression of small interfering RNA (siRNA) that targets specifically to Caytaxin in the hippocampus of adult mice impairs the learning and memory. Genetic inactivation of DAPK1 by deletion of DAPK1 kinase domain prevents the degradation of Caytaxin and protects against learning and memory declines. Thus, activation of DAPK1 impairs learning and memory by degrading Caytaxin during aging.
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DAPK1 is a calcium-dependent serine/threonine kinase highly expressed in the cortex in Alzheimer's disease, after ischemic damage, and in physiological ageing where it may play a role in the decay of learning and memory.
“DAPK1 (FC = 1.08, p = 0.05) is a calcium-dependent serine/threonine kinase that is highly expressed in the cortex in AD [167], after ischemic damage [154], and in physiological ageing where it has been suggested to play a role in the decay of learning and memory with age [51].”
From Early onset senescence and cognitive impairment in a murine model of repeated mTBI (2021) · cites this paper as [51]
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References 42 · Cited by 19
- Authors
- Guo, Y., Li, H., Ke, X., Deng, M., Wu, Z., Cai, Y., Afewerky, H. K., Zhang, X., Pei, L., & Lu, Y.
- Affiliations
- Huazhong University of Science and Technology (CN)
- Corresponding author
- Pei, Lei
- Lu, Youming
- ORCID
- Venue
- Molecular Neurobiology
- Published
- 2018-08-17
- Volume
- 56
- Issue
- 5
- Pages
- 3368-3379
- ISSN
- 0893-7648 (ISSN-L)
- 1559-1182
- OpenAlex
- W2887375527
- Cited by
- 19
- References
- 42
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 4 · 2023: 2 · 2022: 3 · 2021: 3
- FWCI
- 0.45
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Molecular Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (31721002, 91632306, 51627807, 81571078)
- the Medjaden Academy & Research Foundation for Young Scientists (MARFYS) (MJR20160057)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Antioxidants, Aging, Portulaca oleracea
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- DAPK1, DAPK, protein degradation, learning and memory impairment, aging, hippocampus, siRNA knockdown, age-related memory decline
- MeSH terms
- Aging, Animals, Enzyme Activation, Male, Memory, Memory Disorders, Mice, Inbred C57BL, Nerve Tissue Proteins, Neurons, Gene Silencing, Caspase 3, Proteolysis, Death-Associated Protein Kinases
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