Link between aging and Huntington's disease provides candidate therapeutic target

Aging is a major risk factor for the progression of neurodegenerative diseases, including Huntington disease (HD). Morris White and colleagues, at Harvard Medical School, Boston, have now determined that modulating levels of the signaling protein Irs2 changes disease progression in a mouse model of HD. Specifically, increasing Irs2 levels in the brain increased nerve cell damage and reduced lifespan. Conversely, decreasing Irs2 levels reduced nerve cell damage, attenuated symptoms of disease, and increased lifespan. It has been previously shown that reducing Irs2 signaling increases the life span of mice; the data generated by White and colleagues suggests something more specific, that reducing IRS2 signaling could help slow the progression of HD.

TITLE: IRS2 increases mitochondrial dysfunction and oxidative stress in a mouse model of Huntington disease

AUTHOR CONTACT:
Morris F. White
Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts, USA.
Phone: 617.919.2846; Fax: 617.730.0244; E-mail: morris.white@childrens.harvard.edu.

View this article at: http://www.jci.org/articles/view/46305?key=ee2dfb41e6329f0f6012