• Oral NR increases brain NAD levels in individuals with Parkinson’s disease
• NR intake alters cerebral metabolism in Parkinson’s disease
• Cerebral NAD increase is associated with clinical improvement in Parkinson’s disease
• NR induces transcription of mitochondrial, lysosomal, and proteasomal pathways
Summary
We conducted a double-blinded phase I clinical trial to establish whether nicotinamide adenine dinucleotide (NAD) replenishment therapy, via oral intake of nicotinamide riboside (NR), is safe, augments cerebral NAD levels, and impacts cerebral metabolism in Parkinson’s disease (PD). Thirty newly diagnosed, treatment-naive patients received 1,000 mg NR or placebo for 30 days. NR treatment was well tolerated and led to a significant, but variable, increase in cerebral NAD levels—measured by 31phosphorous magnetic resonance spectroscopy—and related metabolites in the cerebrospinal fluid. NR recipients showing increased brain NAD levels exhibited altered cerebral metabolism, measured by 18fluoro-deoxyglucose positron emission tomography, and this was associated with mild clinical improvement. NR augmented the NAD metabolome and induced transcriptional upregulation of processes related to mitochondrial, lysosomal, and proteasomal function in blood cells and/or skeletal muscle. Furthermore, NR decreased the levels of inflammatory cytokines in serum and cerebrospinal fluid. Our findings nominate NR as a potential neuroprotective therapy for PD, warranting further investigation in larger trials.
Just phase 1 that primarily addresses safety concerns. Still a long way to go - has to show EFFICACY - both statistically and clinically. Have been giving my mother Tru Niagen since almost a year - not sure if it is helping.
Very interesting. Thanks for sharing. That cell.com article is chock full of info. You can even download their spreadsheets! cell.com/cell-metabolism/fu...
niacinamide (NAM) - does not cause flushing, found in fish and many multivitamins
nicotinic acid (NA) - causes flushing, found in mushrooms, used for cholesterol reduction, interacts with GPR109a
nicotinamide riboside (NR) & nicotinamide mononucleotide (NMN) are B3 derivatives that are touted as being better at boosting NAD+ than the 2 forms above, but there was a human study showing NA boosted NAD+, and there is some evidence that the liver converts both NR and NMN to niacinamide. There's lots of back and forth on whether NR or NMN is better; there are financial interests at stake.
At high doses NA and NAM can be hard on the liver, don't know about NR or NMN.
Great explanation Rhyothemis. I vote for nicotinic acid (NA) as it interacts with GPR109a and reduces inflammation. And it was the one used in the Auburn trial. And it is cheap!
The subject of vitamin B3 is very hot and misunderstood by propaganda journalists of youth supplements since its inception.
However it must be taken seriously by PD sufferers to resolve various deficiencies typical of PWPs as well described here in Science of Parkinson's by Simon:
This protocol describes the NOPARK Open Label Extension Study. The NOPARK Open Label Extension study is an optional extension of the clinical phase II NOPARK study. Participants who have been included in the NOPARK study will upon completing their participation in the NOPARK study (i.e., after 52 weeks) be offered to receive the study drug Nicotinamide Riboside (NR) 12000 mg P.O. per day, until the NOPARK trial is completed, and the data analyzed with a conclusion of the primary outcome. Individuals enrolled into the NOPARK Open Label Extension Study will be followed with yearly visits. The goal of the NOPARK Open Label Extension Study is to monitor long term safety and study long term neuroprotective and other biological effects of NR use.
Detailed Description:
The primary objective of the NOPARK open label extension study is to monitor NR use for long term safety. The secondary objective of the NOPARK open label study is to monitor long term NR use among PD patients and observe the clinical progression of PD. The NOPARK open label extension study is an open label study, where subjects enrolled in the NOPARK study (ClinicalTrials.gov: NCT03816020), upon completion of the study, will be offered the NR study drug for continuous use, until the NOPARK study is completed and the primary end-point assessed (31/12/2025). The dose of NR is 12000mg NR daily, divided into 5600mg twice daily. The reason for the slightly higher dose compared to NOPARK (i.e., 200mg higher) is the fact that the active compound is now available in capsules of 300mg which cannot be divided. From a clinical and scientific perspective, given current knowledge of safety and efficacy of NR in PD, a dose of 1200 mg is both safe and of a higher potential benefit to patients. The study is multi-site, identical to NOPARK. The primary endpoint of the study, which is safety, will be analyzed using descriptive statistics. The secondary endpoint, which is if long-term NR use delays PD progression will be analyzed using the clinical MDS-UPDRS score. Exploratory objectives will assess PD progression relative to the general PD-population and whether long-term NR use affects methylation metabolism. Stratification of analyses is dependent on the duration of administered NR, sex and age. Exploratory stratification will be done based on results from biological data analysis based on data from NOPARK or blood samples collected in the NOPARK open label extension study.
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Ambroxol in Parkinson's: Results of Phase ll Trial Published
NAD+, NMN, SARM1 and neuroprotection.
Could the NAD+ precursor, Niagen, be the best supplement ever? 
