For a tiny worm called Caenorhabditis elegans, it’s not the brain that goes in old age; it’s the muscles. This millimeter-long nematode, say researchers, may provide insights on why aging people also lose muscle power.
Over the past few decades, C. elegans has earned scientific fame because its transparent body and small total number of cells have enabled scientists to document the worm’s development from a fertilized egg into an adult animal. Three scientists who studied that phase of the nematode’s life just won a Nobel prize (SN: 10/12/02, p. 229: Available to subscribers at Nobel prizes honor innovative approaches).
Now, another group of researchers has taken a close look at the other end of the worm’s life. In the Oct. 24 Nature, Monica Driscoll of Rutgers University in Piscataway, N.J., and her colleagues document how cells and tissues change in aging worms and report that the old worms may have much in common with old people.
With a typical lifespan of just 12 to 18 days, the worms start out moving vigorously, but then slow down. Driscoll and her colleagues hypothesized that a gradual degradation of the nervous system was responsible for this age-related sluggishness.
To better visualize the nematode’s nervous system, they genetically engineered worms so that a fluorescent protein attaches to various proteins used by nerve cells. Using microscopes, the investigators then observed worms at various points in the animals’ lives.
“The nervous system did not change over time at all,” says Driscoll. “We never saw [nerve cell] loss. We were shocked.”
In this respect, worms may mirror people. Neuroscientists had long assumed that the human brain loses nerve cells as it ages, but recent research indicates that healthy peoples’ brains may remain intact, notes Driscoll (SN: 9/7/96, p. 150).
On the other hand, aging people do gradually lose muscle mass and become weaker, a phenomenon called sarcopenia (SN: 8/10/96, p. 90: https://www.sciencenews.org/sn_arch/8_10_96/bob1.htm). As Driscoll continued investigating why old worms move less, her team found that a form of sarcopenia also plagues C. elegans. “When we looked at muscle [in aging worms], we saw this midlife onset of muscle decline,” says Driscoll.
The cellular changes in worm muscles are remarkably similar to those seen in people undergoing sarcopenia, she adds. For example, muscle fibers are normally bundled together neatly but with age become disorganized.
“The finding that neurons age at a different rate from muscles is fascinating,” says Cynthia Kenyon of the University of California, San Francisco, who studies aging in C. elegans.
Other scientists caution that it may not be easy to extrapolate the new work to elderly people. In a commentary accompanying the Nature paper, Thomas B.L. Kirkwood of the University of Newcastle upon Tyne in England and Caleb E. Finch of the University of Southern California in Los Angeles note that adult worms, unlike people, don’t have dividing cells other than in their gonads.
“C. elegans can never be a model for the important contributions to human aging that come from impaired cell proliferation in the many mammalian tissues and organs that maintain themselves by cell renewal,” Kirkwood and Finch say. Human skeletal muscle, for example, is replenished by so-called satellite cells, which worms don’t possess.
Nonetheless, Driscoll and her colleagues argue that further study of C. elegans aging may suggest ways of treating sarcopenia. “We think the worm will have a significant lesson to teach,” she says.
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