A new mouse
model study has identified a faulty "brake" within immune cells, one
that should control inflammation, and points to a potential target for
developing new therapies to treat multiple sclerosis. The results suggest new
research models of multiple sclerosis symptoms such as movement disorders and
balance control problems.
A mutation
in the gene Nlrp12 was causing a malfunction in T cells. Normally, the protein
the gene produces acts as a brake within T cells to control the inflammatory
response. But a mutation in that gene disrupts the natural process and provokes
severe inflammation. The resulting inflammation produced MS symptoms such as
movement disorders and problems with balance control.
Results of
mouse model studies sometimes do not translate to humans and may be years away
from being a marketable treatment. However, according to researcher John
Lukens, Ph.D., of the University of Virginia School of Medicine, "It's
important to note that MS is a spectrum disorder - some patients present with
paralyzing conditions and some patients don't. Not everybody's symptoms are the
same, so this might give us a glimpse into the etiology or pathogenesis of that
family of MS."
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