Now
be important in the development
of MS.
One mutation is in the gene
that instructs kif1b, a “motor
protein” that helps nerve cells
transport other proteins so they
can function normally. Dr. Talbot’s
team has shown that normal
kif1b is required for myelin to
form properly around nerve fibers
and for the proper development
of nerve fibers themselves. These
findings suggest that disruption
of this protein in MS may reduce
the capacity for myelin formation
and repair in MS (Nature
Genetics 2009;41:854).
Dr. Talbot and his colleagues
are continuing their search
using zebrafish models for the
genes that are crucial to myelin
formation. The discovery of
such genes could lead to a new
understanding of how to stop MS
damage and devise strategies for
restoring function.
PHOTO BY THINKSTOCK
Sea anemones are now the basis of a novel therapeutic strategy for MS.
Dr. Bruce Appel (University
of Colorado, Aurora) also is
using zebrafish in his work. He is
studying the genes that regulate
how myelin-making cells wrap
myelin around nerve fibers. His
team is also evaluating whether
mice, whose myelin closely
matches that of people, have these
same genes. With funding from
the Society, his team found eight
genes that had not been previously
linked with the development
of myelin-making cells
(Developmental Dynamics
2010;239:2041).
Now the Society’s funding of
his work has been leveraged to
making it easy to observe the
formation of myelin (the substance
that surrounds nerves and is a
major target for the immune
attack in MS) and other processes.
