Abstract
Phosphodiesterase-4 (PDE-4) regulates the intracellular level of cyclic adenosine monophosphate. Recent studies demonstrated that PDE-4 inhibitors can counteract deficits in long-term memory caused by aging or increased expression of mutant forms of human amyloid precursor proteins, and can influence the process of memory function and cognitive enhancement. Therapeutics, such as ketamine, a drug used in clinical anesthesia, can also cause memory deficits as adverse effects. Targeting PDE-4 with selective inhibitors may offer a novel therapeutic strategy to prevent, slow the progress, and, eventually, treat memory deficits.
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Abbreviations
- PDE-4:
-
Phosphodiesterase-4
- cAMP:
-
Cyclic adenosine monophosphate
- UCR:
-
Upstream conserved regions
- LTP:
-
Long-term potentiation
- PKA:
-
Protein kinase A
- CREB:
-
cAMP response element binding protein
- CBP:
-
CREB-binding protein
- ERK:
-
Extracellular regulated protein
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Acknowledgments
This work was supported by the National Natural Science Foundation of China (Grant No. 81000469) and the Scientific Foundation from Health Office of Jiangsu province (Grant No. H201070).
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Peng, S., Sun, H., Zhang, X. et al. Effects of Selective Phosphodiesterases-4 Inhibitors on Learning and Memory: A Review of Recent Research. Cell Biochem Biophys 70, 83–85 (2014). https://doi.org/10.1007/s12013-014-9930-7
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DOI: https://doi.org/10.1007/s12013-014-9930-7