By: Justine Alford..
Hailed as the long sought-after elixir of youth ever since
scientists demonstrated that it could reverse signs of aging in old mice, there
has been a lot of interest in young blood as a potential rejuvenation factor.
While scientists thought they may have pinpointed the responsible molecule,
describing its impressive effects in several high-profile publications, its
age-defying abilities have this week been called into question by a new study.
But it seems scientists shouldn’t fall at the first hurdle as, interestingly, a
new investigation has come out that showed that young blood can help old broken
bones heal faster.
As described in Nature Communications, circulating the blood
of young mice in older mice with fractures sped up the healing process, an
effect that they could replicate by also giving the elderly mice a bone marrow
transplant from youthful individuals. Furthermore, they were also able to
pinpoint a signaling pathway that is at least partly responsible, although what
causes it to go wrong in the elderly remains unknown.
The signaling molecule in question is a protein called
beta-catenin, which previous work demonstrated is essential for the repair of
bone fractures. During certain stages of healing, levels of this protein must
be tightly regulated. That’s because as the repair process kicks in, too much
beta-catenin can cause immature cells that would be committed to forming new
bone cells to actually become a different type of cell, leading to the
production of tissue that is more like scar than bone, which inhibits repair.
Since we know that fractured or broken bones take longer to
heal in older individuals, scientists from Duke University wanted to find out
more about how the age of cells and the circulation affect the bone
regeneration process. To do this, they used a technique called parabiosis to
hook up the circulatory systems of two mice of varying ages whilst they were
still alive.
They found that fractured bones in older mice healed much
faster when their circulation contained blood from young mice, compared with
mice of a similar age. This, they found, was at least in part due to a
reduction in beta-catenin signaling during the early stages of fracture repair.
Conversely, broken bones in young mice healed slower when their circulations
were joined with old mice. Furthermore, the same rejuvenation effect was seen
when older mice were given bone marrow transplants from young mice.
These intriguing findings challenge the long-held belief
that the reparative ability of bone cells diminishes over time; instead, it
seems that slow bone healing in older people is due to factors in our blood.
“It’s not that bone cells can’t heal as effectively as we
age, but that they actually can heal if they are given the right cues from
their environment,” senior author Benjamin Alman said in a statement. “It’s a
matter of identifying the right pathway to target, and that’s what’s exciting
about this work.”
Although it’s evident that there seems to be a reduction in
the control of beta-catenin levels during the repair process in older
individuals, what is causing this still remains unknown, so there is plenty
more work to be done. But if they can find the responsible agent, it could be
possible to eventually target it with drugs, which could be of huge benefit to
the elderly.
Sources: iflscience | edicalxpress | nature.com | newscientist
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