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Overactivation of proteins known as calpains, which are involved in memory formation, has been linked to Alzheimer disease. Ottavio Arancio and colleagues, at Columbia University, New York, have now shown that two different drugs that inhibit calpains can improve memory in a mouse model of Alzheimer disease (APP/PS1 mice), leading them to suggest drugs that target calpains might stop or slow down the memory loss that occurs as Alzheimer disease progresses.

It is thought that dysfunctional signaling between nerve cells contributes to the impaired cognition experienced by individuals with Alzheimer disease. In the study, analysis of cells and tissue slices from APP/PS1 mice, specifically cells from the part of the brain known as the hippocampus and hippocampal slices, indicated that exposure to calpain inhibitors restored signaling between nerve cells to normal. The authors therefore suggest that calpain inhibitors improve memory in APP/PS1 mice because they reestablish normal signaling between nerve cells.

TITLE: Inhibition of calpains improves memory and synaptic transmission in a mouse model of Alzheimer disease

AUTHOR CONTACT:
Ottavio Arancio
Columbia University, New York, New York, USA.
Phone: (212) 851-4617; Fax: (212) 851-4602; E-mail: oa1@columbia.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=34254

Phenylketonuria (PKU) is an inherited disease characterized by progressive mental retardation and seizures because the individual is deficient in the protein PAH. Most of the genetic mutations that cause PKU do so because the PAH protein that is generated by the mut
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