Multiple sclerosis may be initiated by brain cell death, which triggers an autoimmune response against myelin.
Multiple sclerosis (MS) may be triggered by the death of myelin-producing brain cells (oligodendrocytes), which causes an autoimmune response against myelin. The findings come from researchers at the University of Chicago and Northwestern Medicine who developed novel mouse models to conduct their study. The researchers found that the death of oligodendrocytes initiates an autoimmune response against myelin, triggering multiple sclerosis-like symptoms in mice.
On the other hand, the researchers found that the reaction can be prevented using the specially developed nanoparticles even after the loss of brain cells. These nanoparticles are now being developed in clinical trials with prospects for future treatments in humans
Co-senior author Brian Popko said, “Although this was a study in mice, we’ve shown for the first time one possible mechanism that can trigger MS — the death of the cells responsible for generating myelin can lead to the activation of an autoimmune response against. Protecting these cells in susceptible individuals might help delay or prevent MS.”
In their genetically engineered mouse model, the researchers targeted the myelin-producing cells. After oligodendrocytes were killed, the mice experienced multiple sclerosis-like symptoms that impaired their walking ability. But after this event, the nervous system started regenerating the oligodendrocytes once again, which allowed the mice to resume walking. After six months, however, the mice experienced difficulty walking again, the researchers noted.
Coauthor Maria Traka added, “To our knowledge, this is the first evidence that oligodendrocyte death can trigger myelin autoimmunity, initiating inflammation and tissue damage in the central nervous system during MS.”
Death of oligodendrocytes could be caused by developmental abnormalities, viruses, bacterial toxins, or environmental pollutants. The researchers speculate that multiple sclerosis can occur in humans after a single brain trauma, which can lead to death of oligodendrocytes.