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JCI online early table of contents: Jan. 2, 2008
Date:1/2/2008

rized by astrogliosis, a brain pathology evidenced by a complex series of changes in the morphology and function of brain cells known as astrocytes. Little is known about how astrogliosis relates to the dysfunction of brain cells known as neurons in individuals with epilepsy, but filling in the blanks in our knowledge could lead to new possibilities for therapeutic intervention. A study using mice by Detlev Boison and colleagues at Legacy Clinical Research, Portland, has now identified the protein ADK in astrocytes as a molecular link between astrogliosis and neuronal dysfunction in epilepsy.

The authors observed in a mouse model of epilepsy that ADK upregulation and spontaneous seizures occurred in the region of the brain affected by astrogliosis. In addition, overexpression of ADK in a specific region of the brain triggered seizures in the absence of astrogliosis. Conversely, mice engineered to express less ADK in specific regions of the brain were protected from chemical-induced epilepsy. Furthermore, as ADK-deficient ES cellderived implants protected normal mice from chemical-induced astrogliosis, ADK upregulation, and seizures, it was suggested that ADK-based treatment strategies might provide a new approach for the treatment of individuals with epilepsy.

TITLE: Adenosine kinase is a target for the prediction and prevention of epileptogenesis in mice

AUTHOR CONTACT:
Detlev Boison
Legacy Clinical Research, Portland, Oregon, USA.
Phone: (503) 413-1754; Fax: (503) 413-5465; E-mail: dboison@downeurobiology.org.

View the PDF of this article at: https://www.the-jci.org/article.php?id=33737


ONCOLOGY

AHRR: Aim Here to taRget canceR

Various genes regulate the development of cancer, including those that enhance and those that suppress tumor formation, oncogenes
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Journal of Clinical Investigation
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