There is a link between sclerosis and vitamin B12 deficiency
Vitamin B12 is important for the development and function of our central nervous system. In the past decades, science has also found similarities between sclerosis and the neurological symptoms that occur in people who lack vitamin B12. In a new study that is published in Cell Reports, scientists have found the molecular relation between vitamin B12 and the function of supportive brain cells.
Sclerosis is an autoimmune disorder of the central nervous system (CNS) that is characterized by chronic inflammation and where the immune system attacks the protective myelin sheath that surrounds nerve cells. This results in neurodegeneration and a variety of symptoms that get worse as time goes by. Many of the neurological symptoms such as fatigue, poor memory and other cognitive impairments, sensory disturbances in the hands and feet, impaired vision, and problems with walking and talking may also occur in people who lack vitamin B12.
In their new study, researchers from Sanford Burnham Prebys, California, in collaboration with other scientists found the molecular link between vitamin B12 and sclerosis, which happens in something called glial cells (supportive cells) in the central nervous system. These glial cells are called astrocytes and represent 20-50 percent of the volume in different parts of the brain.
Astrocytes are involved in the energy turnover of the central nervous system, the development of the central nervous system, and the removal of signal substances and neuroactive toxins. In sclerosis, astrocytes have a destructive role because they activate the T cells of the immune defense by producing proinflammatory cytokines.
Vitamin B12, astrocytes, and the interaction with sclerosis medication
Vitamin B12, also called cobalamin, is important for blood formation, energy levels, DNA synthesis, and the nervous system. After being absorbed in the blood, vitamin B12 binds to a carrier protein called transcobalamin (TCN). According to the new study, the molecular effect of transcobalamin resembles the effect of a type of a sclerosis drug called fingolimod (FTY720)
The scientists say that vitamin B12 combined with fingolimod or similar molecules may improve current and future therapies for treating sclerosis.
In their study, they also describe how fingolimod reduces the distribution of T cells and other cell types that attack the brain in sclerosis patients. That way, fingolimod reduces neuroinflammation, demyelination, and degeneration of nerve tissue.
By studying mice with sclerosis and brains from deceased sclerosis patients the scientists have found how fingolimod suppresses inflammation in the nervous system through it ability to regulate the signaling pathways of vitamin B12. This also happens by increasing the vitamin B12 receptors (CD320) in cells throughout the entire body that need to absorb and utilize vitamin B12. This includes cells in the central nervous system.
Science recently discovered that fingolimod’s ability to regulate the signaling pathways of vitamin B12 also takes place in astrocytes and, very importantly, in the brains of those with sclerosis. Studies of animal models have shown that low levels of the vitamin B12 receptor CD320 or lack of dietary vitamin B12 can accelerate the development of sclerosis and impair the therapeutic effect of fingolimod.
The new discoveries support the use of vitamin B12 supplementation in sclerosis – namely with regard to the vitamin’s function in the astrocytes. Moreover, fingolimod can improve the disrupted astrocyte-vitamin B12-signaling pathway in sclerosis patients, which means vitamin B12 can improve the effect of the drug.
The authors claim that vitamin B12 supplements targeted at the brain may lead to new therapies for treating other diseases that are characterized by inflammation and brain degeneration. Vitamin B12 also plays a role in the prevention of sclerosis in combination with vitamin D and omega-3 fatty acids that have an anti-inflammatory effect.
Vitamin B12’s absorption and signaling pathways
- Vitamin B12 is also known as cobalamin
- The uptake of vitamin B12 requires sufficient stomach acid and a carrier protein called intrinsic factor that transports vitamin B12 from the small intestine to the blood
- Vitamin B12 in the blood is bound to transcobalamin, which is a transport protein
- Vitamin B12 receptors (CD320) on the cells are required for cellular uptake of the nutrient
- Vitamin B12 supplements in the form of lozenges give better absorption because the nutrient is taken up by the oral mucosa.
- Vitamin B12 injections are used to treat severe vitamin B12 deficiency
FTY720 requires vitamin B12-TCN2-CD320 signaling in astrocytes to reduce disease in an animal model of multiple sclerosis. Cell Reports, December 2023
Sanford-Burnham Prebys. Similarity between vitamin B12 loss and multiple sclerosis revealed. ScienceDaily 2023
Michaela Tanja Haindl et al. Vitamin D – An Effective Antioxidant I
in an Animal Model of Progressive Sclerosis. Nutrients 2023
Anni Lennon. Multiple sclerosis (MS): High doses of omega-3 reduce symptoms in animal study. Medical News Today.
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