NIH-funded Researchers Show Possible Trigger for MS Nerve Damage
Using high-resolution
images from a technique called in-vivo two-photon laser scanning microscopy,
researchers from the Gladstone Institute for Neurological Disease have provided
evidence for how nerves may be damaged during the early stages of multiple
sclerosis (MS).
Previous studies have
suggested that the leakage of fibrinogen, a blood clotting protein, through a
disruption in the blood-brain barrier and into the central nervous system
activated resident macrophages called microglia. This in turn caused the immune cells to
destroy myelin and eventually cause nerve damage. Using a mouse model, the researchers found
that the fibrinogen leakage was followed by the clustering of microglia and
other immune cells around the blood vessels. Furthermore, microglial activation
occurred only days before any damage to the nerves began.
The researches also found
data suggesting that fibrinogen binding to the microglial receptor CD11b/CD18
caused the microglia to release reactive oxygen molecules that caused neuronal
damage. Genetically modifying
fibrinogen’s blood clotting activity, in turn, prevented activation of the
microglia and nerve damage, suggesting a new direction for therapeutic strategies.
We’d previously spoken
about MS in class as one of our SNBAL assignments, but we spoke about the use
of stem cells as a treatment for MS instead.
I found this article interesting because after providing some evidence
for the mechanism of neuronal damage, they provided a new strategy to prevent
the onset of MS. Stopping the disease early
on would prevent any permanent damage.
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