Researchers at the Ann & Robert H. Lurie Children's Hospital of Chicago, along with colleagues, have made a new discovery in the area of hypomyelination that could help direct future research in multiple sclerosis (MS).
In MS, inflammation causes damage to the fatty sheaths (myelin) on your neurons. This leads to a state called hypomyelination, where there isn’t enough fat left on your neurons for signals to accurately pass from one to the next. This causes many of the symptoms of MS.
Researchers were originally trying to replicate conditions that lead to certain brain cancers by producing too much of a growth factor receptor, called PDGFRA. Instead of getting tumors, the researchers created hypomyelination in the mice. The mice had tails that trembled and they lost their balance. These are symptoms that researchers have also seen in mice that were intentionally hypomethylated.
PGDFRA is a receptor for a growth factor called PDGF-A. These proteins affect the development of cells that create the cells that make myelin. When too much PGDFRA was created, like the researchers wanted, myelin production decreased.
In previous studies, though, researchers had found that when no PDGF-A was produced, hypomyelination also occurred. This means that there’s a delicate "goldilocks" zone for this growth factor-receptor system where myelination is normal. If too much PDGF-A is detected, you’ll have hypomyelination, and if too little is produced, you also get hypomyelination.
In the future, researchers may be able to figure out the right technique and timing for blocking PDGFRA. Their aim is to strike the right balance in this growth factor receptor system in order to optimize myelin production. Eventually, this could help treat the symptoms of MS.
We need more studies, first to research this process in humans and then to turn the knowledge into a treatment. Every step helps increase our understanding of multiple sclerosis and its underlying causes.
