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 Tübingen and the Helmholtz Association — both in Germany — “stimulates the faulty energy metabolism in the affected nerve cells and protects them from dying off.”
Parkinson’s disease and mitochondria
Parkinson’s disease is a condition that worsens over time and arises due to death of neurons, or nerve cells, in a part of the brain that is responsible for movement.
The cells produce a chemical called dopamine that is important for controlling movement. As the disease progresses, walking, coordination, and balance all become increasingly difficult.
Other symptoms such as sleep disruption, memory problems, fatigue, and depression may also develop.
There are around 1 million people living with Parkinson’s disease in the United States, where 60,000 new cases are diagnosed every year.
The prevailing view among scientists is that the disease results from genetic and environmental factors working together.
Each of our cells contains hundreds of tiny compartments called mitochondria that, among other things, convert food into energy for the cell.
Because they are hungrier for energy than other cells, nerve cells are “particularly dependent on mitochondria.”
Problems with mitochondrial function are a common feature of diseases that are accompanied by death of brain tissue, such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and Huntington’s disease.
In the case of Parkinson’s disease, studies have shown that the dopamine cells that die off have damaged mitochondria.
Cause or side effect of disease?
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.
To test whether it might be possible to trigger the growth of new mitochondria in the cells, the team increased their levels of the coenzyme nicotinamide adenine dinucleotide (NAD).
The team did this by “feeding” the cells with a form of vitamin B-3 called nicotinamide riboside, which is a precursor of the coenzyme.
Precursors of NAD “have been proposed to ameliorate age-related metabolic decline and disease,” the authors note in their study paper.
This caused NAD levels to rise in the cells and resulted in new mitochondria and increased energy production.
Vitamin B-3 led to fewer dead nerve cells
Thus far, the experiments had been confined to effects on cells grown in the laboratory. So, the next stage was to test them in a living organism.
The scientists chose flies with defective GBA genes because they 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 flies 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. Evidence from other studies already shows that the vitamin does not produce side effects in healthy individuals.
“Administering nicotinamide riboside may be a new starting point for treatment.”
Dr. Michela Deleidi
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