Experimental drug increase life span in mice

Last Updated: Friday, May 2, 2014 - 11:54
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Washington: Researchers have newly identified a protein's key role in cell and physiological aging and have developed an experimental drug that inhibits the protein's effect and prolonged the lifespan in a mouse model of accelerated aging.

 

The rapidly aging mice fed the experimental drug lived more than four times longer than a control group, and their lungs and vascular system were protected from accelerated aging, the new study reports.

The experimental drug could potentially be used to treat human diseases that cause accelerated aging such as chronic kidney disease, diabetes and HIV infection as well as the effects of cigarette smoking.

While the experimental drug is in the early stages of testing, Douglas Vaughan, M.D., senior author of the study, said, "It makes sense that this might be one component of a cocktail of drugs or supplements that a person might take in the future to extend their healthy life."

The experimental drug, TM5441, is one of only several chosen each year by the National Institute on Aging to be tested in its Interventions Testing Program, which investigates treatments with the potential to extend lifespan and delay disease in mice.

For the study, he and colleagues used mice bred to be deficient in a gene (Klotho) that suppresses aging. These mice exhibit accelerated aging in the form of arteriosclerosis, neurodegeneration, osteoporosis and emphysema and have much shorter life spans than regular mice. Vaughan determined that these rapidly aging mice produce increased levels of PAI-1 in their blood and tissue.

Then scientists fed the rapidly aging mice TM5441 - the experimental drug - in their food every day. The result was a decrease in PAI-1 activity (the aging protein Vaughan's team had identified), which quadrupled the mice's life span and kept their organs healthy and functioning.

The study has been published in Proceedings of the National Academy of Sciences. 

 

ANI

First Published: Friday, May 2, 2014 - 11:54

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