Vitamin B-3 may help to stop the death of nerve cells that occurs in Parkinson’s disease, according to a recent German-led study that may lead to new treatments for the brain-wasting disease.
The researchers’ paper is now published in the journal Cell Reports. In it, they report how a form of vitamin B-3 called nicotinamide riboside helped to preserve nerve cells by boosting their mitochondria, or energy-producing centers.
“This substance,” explains senior study author Dr. Michela Deleidi, who leads brain research projects at the University of Tubingen and the Helmholtz Association – both in Germany – “stimulates the faulty energy metabolism in the affected nerve cells and protests them from dying off.” In the case of Parkinson’s disease, studies have shown that the dopamine cells that die off have damaged mitochondria.
Dr. Deleidi and her colleagues wondered whether faulty mitochondria are a cause or whether they are “merely a side effect” of the disease. First, they took skin cells from individuals with Parkinson’s disease who carried versions of the GBA gene that are known to increase risk for the disease.
They got the skin cells to regress into immature stem cells, and they then coaxed the stem cells to become nerve cells. These nerve cells show similar mitochondrial dysfunction as that found in the brain cells in Parkinson’s disease.
The team then fed the cells with a form of vitamin B-3 called nicotinamide riboside, which is a precursor of the coenzyme. This caused NAD levels to rise in the cells and resulted in new mitochondria and increased energy production.
The next stage was to test a living organism. The scientists chose flies with defective GBA genes that also develop symptoms of Parkinson’s disease as they age and their dopamine cells diminish. The researchers used two groups of flies with defective GBA. They added vitamin B-3 to the food for one group, but not the other. The team observed significantly fewer dead nerve cells and longer retention of mobility in the files that received the vitamin, compared with those that did not.
Dr. Deleidi suggests that the results show that “loss of mitochondria does indeed play a significant role” in the development of Parkinson’s disease. She and her colleagues are now going to test the effects of the vitamin on patients with Parkinson’s disease.
I previously wrote a blog about vitamin B-3 and Parkinson’s disease posted on February 26, 2018. Please review this blog by going to my blog site (drlongstreth.com) and typing in “NAD” in the search box in the upper left hand corner. I review the various forms and uses of vitamin B-3 in that blog.
Of note in this research is the ability of the researchers to take skin cells, regress them into stem cells, then get the stem cells to become nerve cells. Using these techniques, science soon will be able to do this with healthy cells creating heart cells for heart repair, connective tissue cells for knee repair, etc.
I believe the technology already exists but is being held back because the negative effects of health care economics. Imagine the economic loss to the health care industry if open heart surgery, knee and hip replacement became obsolete. It would bankrupt every major hospital in the U.S.
The Bottom Line:
Ongoing research on vitamin B-3 is quite interesting. However, advances in stem cell therapy holds more promise if recent advances are incorporated into current health care.
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