Treatment with a small molecule could delay the damage that
Multiple sclerosis (MS) is a disabling disease that destroys the myelin sheath that protects nerve fibers, causing loss of signaling and nerve cell damage in the central nervous system (CNS).
Now, a recent study from the University of Chicago in Illinois has revealed how a small molecule that bears the name Sephin1 can delay myelin damage in a mouse model of MS.
The journal Brain has recently published an account of the findings.
The study reveals that Sephin1 works by prolonging an inbuilt, integrated stress response (ISR) that reduces the harm that inflammation causes to myelin-producing cells, or oligodendrocytes.
First study author Yanan Chen, a postdoctoral scholar in the Department of Neurology, says that Sephin1 appears to offer “therapeutic potential with no measurable adverse effects.”
However, what triggers the immune system to behave in this way is a mystery. Some studies have suggested that genes are involved, although none has proved that people can inherit MS. Others have shown that environmental factors, such as smoking and low levels of vitamin D, might also raise the risk for MS.
Current treatments for MS aim to reduce the inflammation attacks on myelin and oligodendrocytes. However, because these dampen the immune system, they are not without risk. They can, for example, make the brain vulnerable to “opportunistic infections.”
So, the researchers behind the recent study decided to explore another option: instead of dampening the immune system, why not help the cells that MS affects to resist the damage that inflammation inflicts?
The team decided to investigate the ISR because it is an innate process that protects tissue cells from inflammation attacks by the immune system.
Tests have revealed that the high blood pressure drug guanabenz can enhance ISR in oligodendrocytes. However, the drug also leads to side effects, which include headache, weakness, dry mouth, and sleepiness. It can also bring on coma.