Marjorie Hamill, 41, watches
her eight-year-old niece Megan spin around on the lawn,
collapsing finally from dizziness. It's a sensation that
Marjorie can empathize with -- she suffers from multiple
sclerosis (MS) and often has dizzy spells. Unlike Megan
though she doesn't know what exactly is behind her vertigo.
In fact, on the molecular level, how nerves of MS patients
are irreversibly damaged remains a mystery. Results of
an investigation into the problem, published in the May
25 issue of the Proceedings of the National Academy
of Sciences, "provide, for the first time, important
clues about the molecular basis for permanent and irreversible
damage in [muscular sclerosis]," according to Dr
Stephen Waxman of Yale University in New Haven, Connecticut,
and the lead investigator of the study.
The structural breakup of
nerve fibres that occur in secondary MS cripples millions
of people around the world. To figure out why this degeneration
occurs, Dr Waxman and his colleagues examined spinal
cord tissue from recently deceased people with MS, comparing
the molecular makeup of the nerve tissue to that from
people without MS.
Researchers spotted differences in two molecules called
Nav1.6 and NCX. The first of the suspect pair forms
a channel through the nerve cell membrane that allows
sodium to move into the cell. This inward moving river
of sodium triggers the NCX protein to move a lethal
load of calcium inside the soon-to-be-dead nerve cell.
In control samples, Nav1.6 was confined to the nodes
of Ranvier -- gaps in the myelin sheath. On the other
hand, in the degenerated nerves of MS patients, Nav1.6
was found more generally along the length of the nerve,
especially in areas where myelin breakdown had occurred.
The researchers also showed that Nav1.6 and NCX were
grouped together along with another molecule called
beta-amyloid protein -- a sure sign of axon injury.
In other words, these proteins are likely to show up
at the sites of nerve damage.
Putting two and two together, researchers propose that
Nav1.6 and NCX are playing a role, maybe the
role, in nerve damage. Although no confirmation has
been put forth yet, this proposition is definitely a
smoking gun.
The researchers hope that this latest study will pave
the way to deactivate the protein culprits. In particular,
blocking the movement of sodium into nerve cells would
keep the cells alive and, hopefully, functioning normally.
This strategy has worked in an animal model.
"But going from an animal to a human is a big leap,"
says Dr Waxman, who cautions physicians that there "are
miles to go" from the lab to the real MS world.
For now, he says, those with MS can take heart in the
"small army of energetic researchers at work around
the globe" working to find a cure.
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