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A new study published in Cell Reports revealed a molecular link between vitamin B12 deficiency and multiple sclerosis (MS). A vitamin B12 deficiency produces similar neurological symptoms as multiple sclerosis. Effects like numbness and tingling, vision loss, difficulty walking or speaking, and memory issues are common. Because of this similarity, scientists have been exploring that connection for decades.
The Research
Researchers identified a connection that occurs in astrocytes, non-neuronal glial cells in the brain. The study suggests potential ways to enhance MS treatment through central nervous system (CNS) - vitamin B12 supplementation. The hope is that it will reduce neuroinflammantion and neurodegeneration.
The research focused on the molecular functioning of the FDA-approved MS drug fingolimod. Fingolimod, a sphingosine 1-phosphate (S1P) receptor modulator, suppresses the activity of immune cells attacking the brains of MS patients. The study found that fingolimod regulates B12 communication pathways, specifically elevating a B12 receptor called CD320, which is crucial for the uptake and utilization of B12 when bound to transcobalamin 2 (TCN2). TCN2 distributes B12 throughout the body, including the central nervous system. The interaction between fingolimod and astrocytes was observed in both an animal model of MS and human MS brains.
Lower levels of CD320 or dietary B12 restriction worsened the disease in the animal model and reduced the efficacy of fingolimod. The study suggests that B12 supplementation, especially targeted to astrocytes in the brain, may improve MS treatment. Additionally, the research proposes that other S1P receptor modulators on the market may also impact this central nervous system mechanism.
Implications
The findings support the development of brain-targeted B12 formulations. The researchers believe this knowledge could contribute to improving future therapies. Hopefully, it won't be limited to only MS, but can expand to other neuroinflammatory and neurodegenerative conditions.
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