Scientists have discovered a molecular link between vitamin B12 deficiency and multiple sclerosis (MS), shedding light on potential ways to improve MS treatment through central nervous system (CNS)-B12 supplementation.
The study, published in Cell Reports, was led by Dr. Jerold Chun and Dr. Yasuyuki Kihara from Sanford Burnham Prebys, collaborating with other institutions.
Vitamin B12 deficiency and MS share neurological symptoms such as numbness, vision loss, mobility issues, and cognitive dysfunction. Researchers investigated the molecular functioning of fingolimod (Gilenya), an FDA-approved MS drug that suppresses immune cells attacking the CNS.
In animal models and post-mortem human brains, the study found that fingolimod suppresses neuroinflammation by regulating B12 communication pathways.
Precisely, it elevates CD320, a B12 receptor required for B12 uptake when bound to transcobalamin 2 (TCN2), which distributes B12, including to the CNS. This interaction occurs within astrocytes—a type of glial cell in the brain.
Impact of CD320 and B12 Restriction
The research revealed that lower CD320 levels or dietary B12 restrictions worsened the disease in animal models and reduced fingolimod’s efficacy.
Fingolimod binds to the TCN2-B12 complex, facilitating its delivery to astrocytes via interactions with CD320. Disruptions in this process exacerbated the disease.
The study supports B12 supplementation, especially for delivering vitamin B12 to astrocytes within the brain.
It also suggests that other S1P receptor modulators, such as Mayzent, Zeposia, and Ponvory, may access parts of this CNS mechanism, potentially improving their efficacy.
Future Directions
The research opens new avenues for understanding how the B12-TCN2-CD320 pathway is regulated by sphingolipids, like fingolimod, with implications for treating neuroinflammatory and neurodegenerative conditions.
These findings may result from brain-targeted B12 formulations and novel treatments for various neurological disorders.
The study highlights the importance of considering vitamin B12 and astrocyte-related mechanisms in MS treatment, offering hope for more effective therapies and improved patient outcomes.
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The research findings can be found in Cell Reports.
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