-- Mary Elizabeth Dallas
SUNDAY, Feb. 16, 2014 (HealthDay News) -- As millions of aging
Baby Boomers know, muscle tone and strength declines with advancing
age, regardless of gym workouts. Now scientists say they might have
uncovered a clue as to why that happens -- and new cell targets to
help reverse it.
In studies in aging mice, researchers at Stanford University
found that, over time, the stem cells that help repair damaged
muscle cells after injury are less able to do so.
This helps explain why regaining strength and recovering from a
muscle injury gets more difficult with age, the researchers said in
work published online Feb. 16 in the journal
But there was good news too: The study might also point to a way
to make older muscle stem cells function more like younger ones.
But research in mice often doesn't translate to humans, so the
researchers stressed that more study is needed to determine if this
technique could ever be used in people.
"In the past, it's been thought that muscle stem cells themselves don't change with age, and that any loss of function is primarily due to external factors in the cells' environment," study senior author Helen Blau, director of Stanford's Baxter Laboratory for Stem Cell Biology, said in a university news release.
"However, when we isolated stem cells from older mice, we found that they exhibit profound changes with age," said Blau, a professor of microbiology and immunology at the university. "Two-thirds of the cells are dysfunctional when compared to those from younger mice, and the defect persists even when transplanted into young muscles."
The research also revealed, however, that there is a defect
specific to old muscle stem cells that can be corrected, allowing
scientists to rejuvenate the cells.
"Most exciting is that we also discovered a way to overcome the defect," Blau said. "As a result, we have a new therapeutic target that could one day be used to help elderly human patients repair muscle damage."
The muscle stem cells in 2-year-old mice are the equivalent of
those found in 80-years-old humans. In conducting the study, the
researchers found that many muscle stem cells from these mice had
increased activity in a certain biological pathway that interferes
with the production of the stem cells.
A certain drug that blocks this pathway in old stem cells,
however, allowed the aged stem cells to make a larger number of new
cells that could effectively repair muscle damage.
"In mice, we can take cells from an old animal, treat them for seven days -- during which time their numbers expand as much as 60-fold -- and then return them to injured muscles in old animals to facilitate their repair," Blau said.
Once the mice received their rejuvenated muscle stem cells, the
researchers assessed if they regained their muscle strength with
the help of the study's co-author Scott Delp, a professor in the
School of Engineering. Delp developed a way to measure muscle
strength in animals that underwent stem cell therapy for muscle
Study lead author Benjamin Cosgrove, a postdoctoral scholar at
the university, said: "We were able to show that transplantation of
the old, treated muscle stem cell population repaired the damage
and restored strength to injured muscles of old mice. Two months
after transplantation, these muscles exhibited forces equivalent to
young, uninjured muscles. This was the most encouraging finding of
The study's authors said they plan to continue their research to
determine if people could benefit from this technique.
"If we could isolate the stem cells from an elderly person, expose them in culture to the proper conditions to rejuvenate them and transfer them back into a site of muscle injury, we may be able to use the person's own cells to aid recovery from trauma or to prevent localized muscle atrophy and weakness due to broken bones," Blau said.
"This really opens a whole new avenue to enhance the repair of specific muscles in the elderly, especially after an injury," she said. "Our data pave the way for such a stem cell therapy."
The U.S. National Institutes of Health provides more information
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