Breaking research demonstrates that running in brain-damaged mice
triggers the production of a molecule that repairs brain tissue and
extends their lifespan.
The investigators hope that the findings could lead to innovative treatments for certain neurodegenerative disorders.
A study investigating brain-damaged mice finds that running reduces the deficit.
As with most physical activities, running is known to hold a range of health benefits.
However,
breaking research published in Cell Reports found that, in a certain
type of mouse, running has a significant beneficial impact on brain
health.
Although the findings are specific to a single strain of
mouse and cannot yet be scaled up to humans, they open an interesting
new avenue of research.
A team of researchers from the Ottawa Hospital and the University of Ottawa in Canada ran trials on Snf2h-null ataxic mice.
These mice are born with a particularly small cerebellum, a part of the brain important for balance and coordination.
Because
of the deficits in their brains, these mice find it difficult to
balance themselves and have a shorter lifespan – just 25 to 40 days.
The
researchers allowed some of the mice the opportunity to run by
installing a wheel into their cages. Surprisingly, the mice given the
opportunity to run lived more than 12 months (a relatively normal
lifespan for a mouse).
On top of their extended lives, the running
mice also put on more weight and achieved a better sense of balance,
compared with their less active siblings.
Lead author, Dr. Matías Alvarez-Saavedra, said: “We saw that the
existing neurons became better insulated and more stable. This means
that the unhealthy neurons worked better and the previously damaged
circuits in the brain became stronger and more functional.”
However,
these changes were reversed if the opportunity to exercise was taken
away. Once the running wheel was removed, the symptoms returned, and
their lives were once more cut short. When the nervous systems of the
running and resting mice were inspected and compared, the researchers
found clear differences. The neurons in the cerebellum of the exercised
mice showed an increase in myelin.
Myelin is a white, lipid-based
substance that coats the majority of nerve fibers; it acts in a similar
way to electrical insulation on cables. Without it, nerves cannot carry
their messages as quickly or efficiently.
Once the team had
observed the increased myelination, they needed to understand what
molecules were driving this renewed production of insulation.
To this end, the team investigated the differences in gene expression between the two mice.
A
genetic deep-dive produced a prime candidate – a substance called VGF,
which is a nerve growth factor known to influence synaptic plasticity
and metabolism. It is just one of hundreds of molecules that the brain
and muscles release during exercise. VGF appears to have an
antidepressant effect and helps make exercise feel good.
To test
whether VGF could be the molecule that induced the positive effects in
the mice, the team devised another arm to their study. They used a
non-replicating virus to introduce the VGF protein into the bloodstream
of mice without access to a running wheel.
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