Sci. Aging Knowl. Environ., 8 February 2006
Vol. 2006, Issue 5, p. pe5
[DOI: 10.1126/sageke.2006.5.pe5]


When Good Cdk5 Turns Bad

Qing Guo

The author is in the Department of Physiology at The University of Oklahoma Health Sciences Center, College of Medicine, Oklahoma City, OK 73104. E-mail: qing-guo{at}

Key Words: Alzheimer's disease • cyclin-dependent kinase 5 • p25 • amyloid beta peptide • tau

Abstract: The cyclin-dependent kinase-5 (Cdk5) is critical to normal mammalian development and has been implicated in synaptic plasticity, learning, and memory in the adult brain. But Cdk-5 activity has also been linked to neurodegenerative diseases. Could a single protein have opposing effects? A new study shows that production of a neuronal protein capable of regulating Cdk-5 activity can turn Cdk-5 from "good" to "bad." The findings may have implications for the development and treatment of conditions like Alzheimer's disease.

Citation: Q. Guo, When Good Cdk5 Turns Bad. Sci. Aging Knowl. Environ. 2006 (5), pe5 (2006).

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