Published May 17, 2013 by Science Daily
Summary
New
research done by scientists at UC Davis have found a new possible
approach in improving drugs to treat multiple sclerosis (MS) and other demyelinating
diseases. MS is a disease in which the myelin sheath of neurons is
damaged, slowing the transmission of nerve signals. The scientists
identified a protein that could be targeted in designing drugs to treat
the disease. The protein is known as mitochondrial translocator protein
(TSPO) and is located on the outer surface of mitochondria. It was
previously known but not linked to MS. Scientists identified the protein
as a possible therapeutic target when mice with symptoms of MS were
treated with the anti-anxiety drug etifoxine, which interacts with TSPO.
The results of their study showed that mice given the drug before
clinical signs of the disease then had less severe disease symptoms than
those that were not treated. At the peak of the severity of MS, mice
who were given the drug improved. The discovery of etifoxine’s
beneficial effects in treating MS suggests that drugs that
bind to TSPO may be able to help repair the myelin sheath, which is important
because current FDA-approved treatments do not do so.
Connection
This
connects to our study of the nervous system, since the disease affects
the myelin sheaths of neurons in the central nervous system. It also
relates to our study of homeostasis and the relationship between
structure and function; in MS, when the myelin sheath is damaged,
function is consequently disrupted because the transmission of nerve
signals is impaired.
What is TSPO's function in the body and how might it react with etifoxine?
ReplyDeleteTSPO is used to transport cholesterol across the mitochondrial membrane where is used in steroid synthesis, among other functions such as being involved with apoptosis, the programmed cell death that is important for human development.
DeleteAccording to this article (http://jnm.snmjournals.org/content/early/2011/04/15/jnumed.110.086629.full.pdf), research suggests that there are multiple TSPO binding sites and they are not very well understood so I am not entirely sure but maybe the drug somehow interacts with these binding sites.