Scientists are now looking at roundworms to get a better grasp of humanity's long quest for longevity and understand the process of aging.
Researchers from the University of Michigan Life Sciences Institute used Caenorhabditis elegans or roundworms as a genetic model organism for studying aging. Interestingly, they found the cause of the decline in physiological function in tiny aging worms and figured out how to delay the process.
The new study was published in the journal Science Advances on Jan. 2.
Cause Of Physiological Functional Decline
Humans and animals get older over time, resulting in a progressive deterioration of their motor functions. Roundworms or nematodes, which are about a millimeter long, show almost exact aging patterns to other animals.
"We previously observed that as worms age, they gradually lose physiological functions," said Shawn Xu, the senior author of the study. "Sometime around the middle of their adulthood, their motor function begins to decline."
But what actually caused the decline? In their study, the researchers discovered a molecule known as SLO-1, which stands for "slowpoke potassium channel family member 1." This molecule is mainly responsible for inhibiting the neurons' activity that causes a declining motor function.
According to their findings, a genetic knockdown or pharmacological inhibition of SLO-1 in an old worm can hamper the molecule's function, thereby promoting better healthspan and lifespan.
Genetic Knockdown Or Pharmacological Inhibition
The scientists manipulated SLO-1 either by genetic knockdown or pharmacological inhibition. First, they initially utilize genetic tools and second, they use the drug paxilline.
Both cases show significant effects on roundworms. The research team found that the worms were able to keep an improved motor function later in life. The nematodes also indicated a longer lifespan compared to normal roundworms.
A longer lifespan is not essentially ideal in the absence of improvements in health or strength, explained Xu, who is also a professor at LSI. However, he and his colleagues found that these interventions improved both health and strength and the worms became healthier and lived longer.
The findings further demonstrate that the timing of the intervention is significant. Although the manipulation in the activity of SLO-1 resulted in an improved motor function and lifespan in mid-adult worms, it caused a detrimental effect on the motor function in young worms.