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  • Writer's pictureShelly Albaum

Nicotinamide Riboside May Protect Against Parkinson's Disease

UPDATE January 2019:

Parkinsons News Today says: “Vitamin B3 Compound May Prevent Motor Decline in Parkinson’s Disease, Study Says -- Our most widely read article of 2018 reported that a form of vitamin B3 — nicotinamide riboside — prevented the loss of motor function and lessened nerve cell death in a fly model of Parkinson’s. It also increased the levels of a metabolic compound called NAD+ and improved energy balance in fish neurons with a defective GBA gene — the most frequent gene risk for Parkinson’s — and defects in mitochondria, the cell’s powerhouse. The researchers suggested that this form of vitamin B3 may help treat impaired mitochondria function, which has been linked to Parkinson’s development."

UPDATE August 2018:, which knows way more about this than I do, agrees that there may be something important with NR supplementation and Parkinson's.

UPDATE June 2018:

New Research published in Cell describes "remarkable" results from nicotinamide riboside in models of Parkinson's Disease: "Our findings suggest NR as a viable clinical avenue for neuroprotection in Parkinson's and other neurodegenerative diseases." The study found that mitochondrial dysfunction is a cause, not a symptom, of Parkinson's, and "NR administration caused a significant increase of NAD+," which in turn prevented neuron death and rescued declining motor ability.

The research studies quoted below suggest the following mechanism by which Niagen (Nicotinamide Riboside) supplementation might prevent the mitochondrial dysfunction and resulting neuron death that causes Parkinson's Disease. Of course we await human studies, but this is where some of the research is pointing: 1. Alpha-synuclein (a-syn) is a protein that helps neurons communicate. Excess a-syn is normally cleared by lysosomes.

2. However, when lysosomes are unable to clear excess a-syn, the accumulation of a-syn causes NAD+ depletion in the cells, which starves the cells of energy, eventually killing them.

3. Parkinson's Disease is a neurogenerative disorder caused by cell death resulting from a-syn accumulation.

4. Although it is not known what causes a-syn accumulation in nerve cells, or how to prevent the accumulation, it is possible to protect the nerve cells by preventing NAD+ depletion. Dietary NAD+ supplementation completely rescued mitochondrial function and was neuroprotective.

5. Nicotinamide Riboside -- a form of Vitamin B3 sold as "Niagen" -- is the simplest and most effective method of NAD+ supplementation. NR is transformed by the body into NAD+, and thus there is potential that it could delay the neuronal death associated with mitochondrial dysfunction seen in models of Parkinson's Disease.


Quotes From Supporting Research

"Parkinson’s disease (PD) is a multicentred neurodegenerative disorder characterised by the accumulation and aggregation of alpha-synuclein (α-syn) in several parts of the central nervous system...Impaired proteosomal/lysosomal degradation can promote the uptake and accumulation of α-syn in enteric neurons. Enteric neurons exposed to α-syn can also lead to impaired mitochondrial complex I activity, reduced mitochondrial function, and NAD+depletion culminating in cell death via energy restriction." (Neurotoxicity Research, February 2014)

"NAD( + )supplementation may be beneficial for MeHg-induced toxicities and preventing cellular damage involved in Parkinson's disease." (Toxicological Sciences, May, 2016)

"Our results indicate time-dependent aSyn fibril propagation from the gut to the central nervous system via the vagus nerve following gut PFF inoculation that triggers early GI dysfunction and subsequent motor deficits. ("Over the course of months, clumps of a protein implicated in Parkinson’s disease can travel from the gut into the brains of mice, scientists have found.") (Neuroscience, November 2016)

"Dietary supplementation with the NAD(+) precursor nicotinamide rescues mitochondrial function and is neuroprotective...and could be used to delay neuronal death associated with mitochondrial dysfunction" seen in models of Parkinson's Disease. (Cell Death & Disease, March 2016)

"We show that...neuronal demise (in neurodegenerative disease such as Parkinson's) is due to severe, neuron-specific, nicotinamide adenine dinucleotide (NAD+) depletion..and are completely rescued by treatment with NAD+ or its precursor nicotinamide because of restoration of physiological NAD+ levels...toxic prion protein-induced degeneration of hippocampal neurons is prevented dose-dependently by intracerebral injection of NAD+...We propose the development of NAD+ replenishment strategies for neuroprotection in prion diseases and possibly other protein misfolding neurodegenerative diseases. (Brain, April 2015)

"Lysosomes' inability to clear a-syn causes a-syn accumulation which results in neuron-death: (Journal of Neuroscience, March 2012)

"Macroautophagy, but not the proteasome, also contributes to alpha-synuclein degradation. Therefore, two separate lysosomal pathways, CMA and macroautophagy, degrade wild type alpha-synuclein in neuronal cells. It is hypothesized that impairment of either of these two pathways, or of more general lysosomal function, may be an initiating factor in alpha-synuclein accumulation and sporadic PD pathogenesis.' (Autophagy, August 2008)

"Nicotinamide Riboside robustly increases the NAD metabolome, especially NAD+ in a manner kinetically different than any other NAD+ precursor. I provide the first evidence of effective NAD+ supplementation from NR in a healthy, 52-year-old human male, suggesting the metabolic promoting qualities of NR uncovered in rodent studies are translatable to humans...NR is superior to other B3 vitamins effecting the NAD metabolome and increasing NAD+." (Dissertation of Samuel Trammell, Spring 2016)

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