Brain Cell Death May Trigger Multiple Sclerosis
Nanoparticles found to stop disease progression in a model of chronic MS.
One trigger for multiple sclerosis (MS) might the death of brain cells that make myelin, according to a study published in the journal Nature Neuroscience.
Researchers from the University of Chicago and Northwestern Medicine developed genetically engineered mice models in order to investigate whether cell death could cause this autoimmune response.
The researchers used the mice to target the brain cells that make myelin, called oligodendrocytes. Then, the investigators killed the oligodendrocytes and observed the changes in the way the mice walked.
After the initial cell death, the central nervous system in the mice regenerated and the animals’ gait returned to normal. However, after 6 months, the MS like symptoms, including impaired walk, came back in the mice models.
“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 myelin,” study co-senior author Brian Popko, PhD said in a press release. “Protecting these cells in susceptible individuals might help delay or prevent MS.”
The researchers believe that oligodendrocyte death can be caused by a variety of factors, including developmental abnormalities, viruses, bacterial toxins, or environmental pollutants. For human patients, it may not be until years after an initial injury that the brain triggers oligodendrocyte death, the study authors hypothesize.
The study also allowed the researchers to test new drugs that work against progressive MS in the mice models. The researchers administered nanoparticles, which created tolerance to the myelin antigen in order to prevent progressive MS from continuing. The drugs that were tested are in the development stages for use in human patients.
“We’re encouraged that the nanoparticles could stop disease progression in a model of chronic MS as efficiently as it can in progressive remitting models of MS,” study collaborator Stephen Miller, PhD, added.
The results of this study offer the idea that MS might begin from the patients’ brains, regardless of their susceptibility to genetic predispositions, the authors continued in the statement. They explained that the damaged or dead oligodendrocytes might cause an outright immune response, causing demyelination and the continuation of the MS progression cycle.
The researchers concluded by saying that the exact nature of this process in humans will be exciting to unravel as will the search for effective therapies.