A new study redefines age-accelerating 'zombie cells'

Researchers have discovered a new pathway by which 'zombie cells' that promote aging accumulat.

"Zombie cells are still alive, but they can't divide, so they can't help replenish tissue," said senior author Patricia Opresko, P.

When a healthy human cell divides into two identical cells, a bit of DNA is clipped off the tip of each chromosome, causing telomeres to shorten with each divisio.

This hypothesis could not be tested before because the techniques used to damage DNA are non-specific, causing damage throughout the chromosom.

"Our new tool acts like a molecular sniper," explained first author Ryan Barnes, PhD, a postdoc in Opresko's la.

In human cells grown in petri dishes, the researchers found that damage to the telomeres turned the cells into a zombie state after just 4 days -- a repeat of the cells needed to induce senescence by shortening telomeres in the lab Splitting weeks or months is much faste.

"We discovered a new mechanism for inducing cellular senescence that is entirely telomere-dependent," explains Opresk.

Sunlight, alcohol, smoking, poor diet and other factors produce reactive oxygen species molecules that damage DN.

"Now that we understand the mechanism, we can start testing interventions to prevent aging," Barnes sai.

The discovery also informs the development of new drugs called senolytics that target zombie cells and kill the.

"By reducing the accumulation of zombie cells that contribute to degenerative diseases, we may be able to increase 'healthspan' - the length of time a person is healthy," he adde.

Reference: Telomeric 8-oxo-guanine drives rapid premature senescence in the absence of telomere shortening