Scientists have uncovered a cause of declining motor function and increased frailty in tiny ageing worms - and a way to slow it down. The findings, published in the journal Science Advances, identify a molecule that can be targeted to improve motor function and indicate that similar pathways may be at play in ageing mammals as well. As humans and animals age, our motor functions progressively deteriorate. Millimetre-long roundworms called nematodes exhibit ageing patterns remarkably similar to those of other animals, and they only live about three weeks, making them an ideal model system for studying ageing.
"We previously observed that as worms age, they gradually lose physiological functions," said Shawn Xu, a professor at the University of Michigan in the US.
"Sometime around the middle of their adulthood, their motor function begins to decline. But what causes that decline?" Xu said.
To better understand how the interactions between cells changed as worms aged, Xu and his colleagues investigated the junctions where motor neurons communicate with muscle tissue.
They identified a molecule called SLO-1 (for "slowpoke potassium channel family member 1") that acts as a regulator for these communications.
The molecule dampens neurons' activity, slowing down the signals from neurons to muscle tissue and reducing motor function.
The researchers manipulated SLO-1, first using genetic tools and then using a drug called paxilline.
In both cases, they observed two major effects in the roundworms.
Not only did they maintain better motor function later in life, they also lived longer than normal roundworms.
"It's not necessarily ideal to have a longer lifespan without improvements in health or strength," said Xu.
"But we found that the interventions improved both parameters -- these worms are healthier and they live longer," he said.
The timing of the interventions drastically changed the effects on both motor function and lifespan.
When SLO-1 was manipulated early in the worms' life, it had no effect on lifespan and in fact had a detrimental effect on motor function in young worms.
However, when the activity of SLO-1 was blocked in mid-adulthood, both motor function and lifespan improved.
Since the SLO-1 channel is preserved across many species, Xu hopes these findings will encourage others to examine its role in ageing in other model organisms.
"Studying aging in organisms with longer lifespans is a major investment," he said.
"But now we have identified a molecular target, a potential site and specific timing, which should facilitate further investigation," Xu said.