Anti-anxiety Drug Reduces Severity of MS Model in Mice

Working with models of MS in
mice, UC Davis scientists have detected a novel molecular target for the design
of drugs that they say could be safer and more effective than current
FDA-approved medications against MS.


The findings of the research
study, published online in the journal EMBO
Molecular Medicine, could have therapeutic applications for MS
as well as all disorders associated with loss of white matter, which is the
brain tissue that carries information between nerve cells in the brain and the
spinal cord.


The target, a protein
referred to as mitochondrial translocator protein (TSPO), had been previously
identified but not linked to MS. The mitrochronical TSPO is located on the
outer surface of mitochondria, cellular structures that supply energy to the
cells. Damage to the fatty coating, or myelin, slows the transmission of the
nerve signals that enable body movement as well as sensory and cognitive
functioning.


The scientists identified
mitochondrial TSPO as a potential therapeutic target when mice that had
symptoms of MS improved after being treated with the anti-anxiety drug
etifoxine, which interacts with mitochondrial TSPO. When etifoxine, a drug
clinically available in Europe, was administered to the MS mice before they had
clinical signs of disease, the severity of the disease was reduced when
compared to the untreated lab animals. When treated at the peak of disease
severity, the animals’ MS symptoms improved.


“Etifoxine has a novel
protective effect against the loss of the sheath that insulates the nerve
fibers that transmit the signals from brain cells,” said Wenbin Deng,
principal investigator of the study and associate professor of biochemistry and
molecular medicine at UC Davis.


“Our discovery of
etifoxine’s effects on an MS animal model suggests that mitochondrial TSPO
represents a potential therapeutic target for MS drug development,” said
Deng.

“Drugs designed to more
precisely bind to mitochondrial TSPO may help repair the myelin sheath of MS
patients and thereby even help restore the transmission of signals in the
central nervous system that enable normal motor, sensory and cognitive
functions,” he said.

Current FDA-approved
therapies do not repair the damage of immune attacks on the myelin sheath.

Source: MSFYi News
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