Low Levels of Sugar Metabolite Drives Worsening of Multiple Sclerosis

Low levels of the sugar metabolite are found to be associated with progressive disability and neurodegeneration in multiple sclerosis (MS).

Low serum levels of the sugar N-acetylglucosamine (GlcNAc), is associated with progressive disability and neurodegeneration in multiple sclerosis (MS), as per an Irvine-led study titled, "Association of a Marker of N-Acetylglucosamine With Progressive Multiple Sclerosis and Neurodegeneration," at the University of California, published in JAMA Neurology.

Multiple Sclerosis (MS) is an autoimmune neurological disease, characterized by recurrent episodes of neurologic dysfunction resulting from acute inflammatory demyelination. Progressive MS is distinguished by continuous inflammation, failure to remyelinate, and progressive neurodegeneration, causing accrual of irreversible neurologic disability.

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‘Low levels of the sugar metabolite, N-acetylglucosamine (GlcNAc), are found to be associated with progressive disability and neurodegeneration in multiple sclerosis (MS). This creates new potential avenues to identify patients at risk of disease progression and neurodegeneration for further development of therapies.’

Neurodegeneration is the major contributor to progressive neurological disability in MS patients, yet mechanisms are poorly understood and there are no current treatments for neurodegeneration.

Sugar metabolite in Multiple Sclerosis

GlcNAc regulates protein glycosylation, a fundamental process that decorates the surface of all cells with complex sugars. Previous preclinical, human genetic and ex vivo human mechanistic studies revealed that GlcNAc reduces pro-inflammatory immune responses, promotes myelin repair, and decreases neurodegeneration.

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The present study suggests that GlcNAc, which has been previously shown to promote re-myelination and suppress neurodegeneration in animal models of MS, is reduced in serum of progressive MS patients and those with worse clinical disability and neurodegeneration.

"We found the serum levels of a marker of GlcNAc was markedly reduced in progressive MS patients compared to healthy controls and patients with relapsing-remitting multiple sclerosis" says Michael Demetriou, MD, Ph.D., FRCP(C), professor of neurology, microbiology and molecular genetics at UCI School of Medicine, and senior author on the paper.

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The lower GlcNAc serum marker levels correlated with multiple measures of neurodegeneration in MS, namely worse expanded disability status scale scores, lower thalamic volume, and thinner retinal nerve fiber layer. The low baseline serum levels also correlated with a greater percentage of brain volume loss at 18 months.

The data thereby suggests that GlcNAc deficiency may promote progressive disease and neurodegeneration in patients with MS. However, additional human clinical studies are required to confirm this hypothesis.

"Our findings open new potential avenues to identify patients at risk of disease progression and neurodegeneration, so clinicians can develop and adjust therapies accordingly," says Michael Sy, MD, Ph.D., assistant professor in residence in the Department of Neurology at UCI and a co-author of the study.

Source-Medindia