Is Vitamin B12 Important in Multiple Sclerosis?

Research Summary: FTY720 requires vitamin B12-TCN2-CD320 signaling in astrocytes to reduce disease in an animal model of multiple sclerosis

The treatment of multiple sclerosis has improved greatly over the past decade.  Today, we are going to summarise a recent publication that has identified a factor that may help improve the effectiveness of an existing therapy.

What?

Using an animal model of multiple sclerosis (MS), this article looks at the role Vitamin B12 may play in disease severity and how it could impact the effectiveness of an existing therapy.

Who?

This research was conducted by a team at the Sanford Burnham Prebys Medical Discovery Institute in California, USA.

Where?

The article was published in Cell Reports.  The full-text is currently freely available and can be viewed here.

When?

The study was published online in December, 2023.

BACKGROUND #1: It is known that Vitamin B12 deficiency causes symptoms that are similar to those experienced in MS, such as cognitive issues and muscle weakness.

BACKGROUND #2:  Fingolimod is an approved oral therapy for the treatment of relapsing-remitting multiple sclerosis.  While it is known to work by generally altering the action of immune cells, some of the specifics of this mechanism are still unclear.

FINDING #1:  A genetic analysis was performed on cells (astrocytes) known to be important in MS.  This analysis showed that vitamin binding pathways were impacted during disease.

FINDING #2:  The expression of a specific gene, which codes for a protein called CD320, was significantly decreased during disease in an animal model of MS (EAE).  The expression of this same gene was also found to be lower when MS brain tissue was analysed.  CD320 is a protein that is important for transporting Vitamin B12 into the central nervous system.

FINDING #3: It was found that removing the gene for CD320 led to worse disease outcomes in mice with EAE.  Similarly, there was increased disease severity in mice that had a diet deficient in Vitamin B12.

FINDING #4: When mice with EAE were treated with fingolimod, they recovered from their disease.  This recovery was associated with an increase in the expression of CD320.  The effectiveness of fingolimod was reduced in mice that either had the gene for CD320 removed or were deficient in Vitamin B12.  This indicates that part of the mechanism of action for fingolimod involves this Vitamin B12 pathway.

There is always a lot of interest when research discusses factors that may be related to diet or supplementation, but it is important to keep studies such as this in context.  Importantly, this is a research summary and should not be seen as any sort of clinical recommendation.

THOUGHT #1:  The findings are very interesting in terms of what they might tell us about the mechanisms behind disease progression, but also about how fingolimod works.  There is an interesting suggestion from this data that Vitamin B12 deficiency could be associated with worse disease outcomes, at least in an animal model.  As well as this, the understanding of how this may be involved in increasing the effectiveness of an existing therapy is very interesting, but needs further studies to confirm it.

THOUGHT #2: The results from this study are very preliminary and are based on an animal model of multiple sclerosis.  Considering this, we need to make sure that we don’t jump to conclusions about how they may translate to people living with multiple sclerosis.  Currently, there is no suggestion that people living with MS should use these results to supplement with vitamin B12, and any change to medication and/or supplements should be discussed with your healthcare professional.

If you have questions on this study, please don’t hesitate to post them under this article or on any of our social media channels.

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