The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.
Therapeutic effects of PKC activators in Alzheimer's disease transgenic mice
Open accessAbstract
Alzheimer's disease (AD) characteristically presents with early memory loss. Regulation of K+channels, calcium homeostasis, and protein kinase C (PKC) activation are molecular events that have been implicated during associative memory which are also altered or defective in AD. PKC is also involved in the processing of the amyloid precursor protein (APP), a central element in AD pathophysiology. In previous studies, we demonstrated that benzolactam (BL), a novel PKC activator, reversed K+channels defects and enhanced secretion of APPα in AD cells. In this study we present data showing that another PKC activator, bryostatin 1, at subnanomolar concentrations dramatically enhances the secretion of the α-secretase product sAPPα in fibroblasts from AD patients. We also show that BL significantly increased the amount of sAPPα and reduced Aβ40 in the brains of APP[V717I] transgenic mice. In a more recently developed AD double-transgenic mouse, bryostatin was effective in reducing both brain Aβ40 and Aβ42. In addition, bryostatin ameliorated the rate of premature death and improved behavioral outcomes. Collectively, these data corroborate PKC and its activation as a potentially important means of ameliorating AD pathophysiology and perhaps cognitive impairment, thus offering a promising target for drug development. Because bryostatin 1 is devoid of tumor-promoting activity and is undergoing numerous clinical studies for cancer treatment in humans, it might be readily tested in patients as a potential therapeutic agent for Alzheimer's disease.
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Cites
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Self-citationIsolation and structure of bryostatin 1
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Alzheimer’s disease: Clinical trials and drug development
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Aβ40 Inhibits Amyloid Deposition In Vivo
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“Reduction in A levels by increased -secretase activity or by enhanced proteolysis of A has been linked to prevention of high mortality in APP transgenic mice and Drosophila (Leissring et al., 2003; Etcheberrigaray et al., 2004; Finelli et al., 2004).”
BackgroundAndrade, S., Ramalho, M. J., Loureiro, J. A., & Pereira, M. D. C. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20092313 · Cited by 240
Metadata
- Authors
- Etcheberrigaray, R., Tan, M., Dewachter, I., Kuipéri, C., Van der Auwera, I., Wera, S., Qiao, L., Bank, B., Nelson, T. J., Kozikowski, A. P., Van Leuven, F., & Alkon, D. L.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2004-07-19
- Volume
- 101
- Issue
- 30
- Pages
- 11141-11146
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2063661531
- Cited by
- 342
- References
- 51
- FWCI
- 11.02
- Type
- journal article
- Language
- en
- Open access
- green
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