Failure of Brain Development in Early MS Suggests Need for Neuroprotection
Researchers from Canada and the U.S. have found that brains of young people with multiple sclerosis fail to develop fully. The article appeared November 5, 2014 in the journal Neurology entitled, “Onset of multiple sclerosis before adulthood leads to failure of age-expected brain growth.”
Multiple sclerosis is caused by an immune system attack on a fatty substance called myelin, which insulates the axons that branch off of brain cells, and speeds the flow of information in the brain and spinal cord. Myelin appears white, leading to the term “white matter,” as opposed to “grey matter,” which refers to cell bodies that are not wrapped with myelin. MS has been mostly viewed as a white matter disorder, however, new evidence may point toward degeneration of the grey matter as well.
Led by Dr. Bérengère Aubert-Broche of the Montreal Neurological Institute at McGill University, the scientists used magnetic resonance imaging (MRI) in thirty-six patients who had been diagnosed with relapsing-remitting MS before they were 18. Relapsing-remitting is the most common MS type. Images were taken at the beginning of the study and two years later. They also looked at the MRI scans of 364 healthy people without MS who were in the same age range, taken over two years, to see what typical brain growth looks like.
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The images showed an unfortunate finding. Brain growth was not as great in the people with MS, especially in a region called the thalamus. The thalamus is the “central station” of the brain, where information from lower and higher brain regions comes together. In young people with MS, having a smaller thalamus also corresponds with a smaller region of the spinal cord, known as thoracic region 2, which is found in the upper back.
The authors of this study concluded “Our data provide compelling evidence that neurodegeneration is an early aspect of MS pathology, rather than a late effect of chronic disease, even in children and adolescents. Such information has import not only to the study of MS pathobiology, but also to considerations for neuroprotection and neurorepair.”
The study could help direct new treatments, which in the past only focused on inhibiting the immune attack on myelin. Future therapies may also focus on inhibiting general death of cells in the brain, known as “neuroprotective strategies.” Neuroprotective strategies have been explored in degenerative diseases such as Alzheimer’s and Parkinson’s disease. The present study suggests that neuroprotection, particularly at early stages, could be helpful for treating MS.
