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Rapamycin Inhibits The Effects Of Senescent Cells

November 22nd, 2017

Rapamycin is one of the most well-known longevity drugs under study. It was initially discovered as an antifungal metabolite produced by Streptomyces hygroscopicus from a soil sample of Easter Island1.

Prior research has revealed it could impact on something called the senescence – associated secretory phenotype or SASP.  The increase in cellular senescence associated with aging, and the inflammation also associated, can help set the stage for a variety of degenerative diseases, such as dementia and Alzheimer’s. In laboratory animals, once senescent cells are cleared out, they are known to live longer and contract fewer diseases. Rapamycin can have similar effects.

New research has shown that Rapamycin acts through an additional mechanism and is able to directly act on the SASP itself through another pathway. This reveals that Rapamycin works via a two-pronged approach and effectively inhibiting the SASP produced by the senescent cells.

Other studies have shown that astrocyte cells that aid to protect neuron function and health can be damaged by SASP. This may be one of the causes of neurologic diseases, including Alzheimer’s.

Further Reading

 

  • Rong Wang, Zhen Yu, Bharath Sunchu, James Shoaf, Ivana Dang, Stephanie Zhao, Kelsey Caples, Lynda Bradley, Laura M. Beaver, Emily Ho, Christiane V. Löhr, Viviana I. Perez.Rapamycin inhibits the secretory phenotype of senescent cells by a Nrf2-independent mechanism.Aging Cell, 2017; DOI: 1111/acel.12587

 

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