Multiple sclerosis (MS) is an autoimmune disease in which the body’s immune cells mistakenly attack the central nervous system.
As of this writing, there is no cure for MS. If treatment is started early enough in the progress of the disease, the effects can be minimized and progress slowed.
Unfortunately, research shows autoimmune conditions are 50 percent higher in older adults than they were 25 years ago.
But groundbreaking research has found that MS drugs and vitamin B12 have something in common — and that this similarity may provide hope for better and quicker MS treatment.
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How MS attacks the body
People deficient in vitamin B12 can experience symptoms such as muscle weakness, trouble walking, fatigue and increased heart rate. This isn’t new information.
But a B12 deficiency can also produce neurological symptoms that are startlingly similar to those of MS, including tingling/numbness in the hands and feet, vision loss, depression and cognitive problems.
For years, the reasons for this crossover in symptoms have remained unclear.
But recently, researchers have discovered that a novel molecular link exists between vitamin B12 and MS that takes place in astrocytes, which are important non-neuronal glial cells in the brain.
This overlap produces a chain reaction involving both B12 and the MS drug fingolimod.
It’s kind of like a game where you pass a ball down a line of people, from person to person.
Here’s how it works:
Fingolimod enters the B12 pathway, where it binds to S1P1 receptors, which elevate another type of receptor known as CD320.
CD320 grabs vitamin B12 from TCN2, a carrier protein that delivers B12 to different parts of the body, including the central nervous system.
“The shared molecular binding of the brain’s vitamin B12 carrier protein, known as transcobalamin 2 or TCN2, with the FDA-approved MS drug fingolimod, provides a mechanistic link between B12 signaling and MS, towards reducing neuroinflammation and possibly neurodegeneration,” said Dr. Jerold Chun, the study’s lead author.
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Vitamin B12 and the future of MS therapies
Dr. Chung says “Augmenting brain B12 with fingolimod or potentially related molecules could enhance both current and future MS therapies.”
He and his colleagues witnessed how fingolimod “hitchhikes” by binding to the TCN2 protein as it delivers B12. They also found that restricting B12 made MS symptoms worse, and more quickly.
These new findings further support the use of B12 supplementation — especially in terms of delivering the vitamin to astrocytes within the brain — while revealing that fingolimod can correct the impaired astrocyte-B12 pathway in people with MS.
And, there’s hope that this same B12 formula could help with neurodegenerative diseases like Parkinson’s or Alzheimer’s.
In the meantime, there’s no harm in making sure you’re getting all the B12 you need every day — from foods like liver, beef, tuna and clams, fortified cereals or soy milk.
Previous research from Johns Hopkins found that a nutritious diet and lifestyle can cut MS symptoms by 50 percent. More proof of that is research by Harvard that found low levels of vitamin D increase the risk of developing MS.
All this suffices to stress the importance of nutrients that are coming to the forefront of disease prevention and treatment.
Sources:
Similarity between vitamin B12 loss and multiple sclerosis revealed — Science Daily
FTY720 requires vitamin B12-TCN2-CD320 signaling in astrocytes to reduce disease in an animal model of multiple sclerosis — Cell Reports
B12 Deficiency and Multiple Sclerosis Share Intriguing Similarities — Neuroscience News and Research
Why It Pays to Start Multiple Sclerosis (MS) Treatment Early — Healthline
Similarity between vitamin B12 loss and multiple sclerosis revealed — Sanford Burnham Prebys