A form of vitamin B3 can prevent degeneration and death of nerve cells linked to Parkinson’s and other neurodegenerative diseases.
The study with that finding, “The NAD+ precursor, nicotinamide riboside, rescues mitochondrial defects and neuronal loss in iPSC and fly models of Parkinson’s disease,” was published in Cell Reports.
It was shown recently that defective mitochondria are responsible for the death of dopaminergic neurons in the substantia nigra, a brain region particularly affected in Parkinson’s disease.
Mitochondria — tiny structures located inside cells that function as their powerhouse — produce the energy necessary for cell survival and function. However, their role in Parkinson’s is still controversial as alternative lines of research have suggested that mitochondrial defects may actually protect the brain by preventing the formation of protein aggregates.
“In our study we aimed to investigate whether damaged mitochondria were merely a side effect or whether they cause Parkinson’s disease,” Michela Deleidi, MD, said in a press release. Deleidi is a researcher at the German Center for Neurodegenerative Diseases and the University of Tübingen, and senior author of the study.
The team collected skin cell samples from Parkinson’s patients. They then converted skin cells into stem cells — which can give rise to almost any type of cell in the body — and then into nerve cells.
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These cells had a defect in the GBA gene — the most frequent gene risk for Parkinson’s — and their mitochondria. Consequently, their energy production was impaired. Importantly, these cells produced higher levels of damaging oxygen molecules, also known as ROS.
This type of mitochondrial dysfunction and overall damaging response has been associated previously with aging and the decline of an important metabolic compound called NAD+.
No significant changes were observed concerning NAD+ levels in GBA-defective neurons compared to healthy study participants.
However, when researchers analyzed the brains of a fish model of Parkinson’s disease, which also had a mutation in the GBA gene, they found the animals had less nicotinamide mononucleotide, which is the molecule that gives rise to NAD+ compounds.
By feeding GBA-defective neurons with a form of vitamin B3 (called nicotinamide riboside), the levels of available NAD+ were increased and consequently cells’ energy balance improved.
“The nerve cells’ energy budget improved considerably. New mitochondria formed and energy production rose,” Deleidi said.
Treatment with nicotinamide riboside also prevented the loss of motor function in a fly model of Parkinson’s disease. “The substance had a positive effect here as well. In the flies which were treated, far fewer nerve cells died off,” Deleidi added.
Researchers believe that impaired mitochondria play an important role in the development of Parkinson’s and that nicotinamide riboside may represent a potential treatment to overcome this process.
The team is planning to further test the effects of nicotinamide riboside and assess if the vitamin can be of real help for patients with Parkinson’s, as studies have shown this form of vitamin B3 is well-tolerated by healthy subjects and also boosts their energy metabolism.
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