Rapamycin and short telomeres increase age-related disease in mice

Rapamycin can be harmful when telomeres short

Researchers have discovered in recent decades that biochemical processes can influence the rate of aging, and that these processes, at least for animal models, are controllable in the lab. Telomeres shortening is a process that can be controlled in the laboratory. Another is the cells’ ability to detect nutrients through the mTOR proteins. Scientists have been able prolong the life of many species through either one. What if they manipulate them both?

The results were unexpected. A team at the Spanish National Cancer Research Centre CNIO studied the phenomenon for the first. The treatment of healthy mice with rapamycin (an mTOR inhibitor) delays aging, but it causes premature aging and diseases in mice that have short telomeres. This discovery has significant implications for treating diseases associated with short or short-telomeric telomeres as well as age-related diseases. Iole Ferrara Romeo is the first author of the study by the Telomeres and Telomerase Group at the CNIO headed by Maria Blasco.

Telomeres are regions of repeated nucleotide patterns at the ends of chromosomes that preserve genetic information. As they age, they become shorter and eventually no longer serve their purpose: the cells stop dividing while tissues age because they can’t regenerate.


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