Parkinson's disease: vitamin B3 could stop brain cell death

How does the intake of vitamin B3 could affect the diagnosis of the Parkinson's disease?

The researchers' work has now been published in the journal Cell Reports. In it, it is reported how a form of vitamin B-3 called nicotinamide riboside helped preserve nerve cells by increasing their mitochondria, or energy production centers.

La Dr. Michela Deleidi, senior author of the study, who leads brain research projects at the University of Tübingen and the Helmholtz Association-both in Germany, explains:

“This substance stimulates defective energy metabolism in affected nerve cells and protects them from death.“.

Parkinson's disease and mitochondria

La Parkinson's disease is a condition that worsens over time and occurs as a result of the death of neurons or nerve cells in a part of the brain responsible for movement.

The cells produce a chemical called dopamine that is important for controlling movement. As the disease progresses, walking, coordination and balance become increasingly difficult.

Other symptoms such as sleep disturbances, memory problems, fatigue, and depression may also occur.

The most common view among scientists is that the disease results from both genetic and environmental factors. 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 energy-hungry compared to other cells, nerve cells are “particularly dependent on mitochondria”.

Problems with mitochondrial function are a common feature of diseases that are accompanied by the 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 dopamine cells that die have damaged mitochondria.

Cause or side effect of the disease?

The Dr. Deleidi and his colleagues questioned whether the defective mitochondria are the cause of the disease or if they are “just a side effect.”.

First, they took skin cells from individuals with Parkinson's disease who had degenerations of the GBA gene, known to increase the risk of the disease.

They caused skin cells to regress into immature stem cells, which were then induced in turn to become nerve cells. These nerve cells show similar mitochondrial dysfunction as that found in brain cells in Parkinson's disease.

To test whether it is possible to trigger the growth of new mitochondria in cells, the team increased 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 coenzyme precursor.

Vitamin B-3 resulted in fewer dead nerve cells

So far, experiments had only been done regarding the effects on cells grown in the laboratory. So, the next stage was to test them in a living organism.

The scientists chose flies with damaged GBA genes because they also develop Parkinson's disease symptoms as they age and their dopamine cells decline.

The researchers used two groups of flies with damaged GBA. They added the vitamin B-3 to food for one group, but not the other.

The team observed that flies that had taken vitamin b3 along with their food had far fewer nerve cells dead and had greater retention of mobility, compared with those that had not taken the vitamin.

Dr. Deleidi suggests that the results show that. “loss of mitochondria does indeed play a significant role.” In the development of Parkinson's disease.

Now the doctor together with colleagues will test the effects of the vitamin on patients with Parkinson's disease. Already other studies have shown that the vitamin produces no side effects in healthy individuals.