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Controlling the triggers of age-related inflammation could extend 'healthspan'
Date:10/21/2013

mprove the healthspan and may also lower healthcare costs as the aging population increases in the U.S."

Dixit and his colleagues investigated the normal aging process of mice that were free of diseases, and fed a normal diet. The research team found that immune sensor Nlrp3 inflammasome is activated in response to aging. They then tested mice to determine if reducing the activity of Nlrp3 inflammasome lowers inflammation, and aging-associated decline in function. Results showed that animals with lower Nlrp3 activation were protected from many age-related disorders such as dementia, bone loss, glucose intolerance, cataracts, and thymus degeneration. Functionally, the mice also performed better, were less frail, and ran for longer durations. The researchers also tested another immune sensor called caspase11, which is activated in response to certain infections, and found that it was not linked to the age-related inflammation process.

"Now that we've identified this mechanism in the Nlrp3 sensor, we might be able to manipulate this immune sensor to delay, or reduce inflammation," Dixit said. "This could lead to the possibility of prolonging healthspan, potentially leading to an old age relatively free of disease or disability."

Dixit said additional studies are needed to explore whether the Nlrp3 mechanism can be safely manipulated without impairing the immune system. He points out that although there are several anti-inflammatory drugs available, none seem to be effective in expanding the healthspan. "One of our long-term goals is to develop therapies or specific diets that could dampen the excessive inflammation process as a means to prevent chronic diseases," he said.


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Contact: Karen Peart
karen.peart@yale.edu
203-432-1326
Yale University
Source:Eurekalert  

Page: 1 2

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