It is exaggerated percentage wise compared to wild type. But additional NAD+ are consumed by PARp1. So NR generated more NAD+ than the percentage indicates.
No matter what I don’t see anywhere that indicate NMN is better than NR. Not a single evidence.
As you know, there are no head to head studies, so it definitely depends on how you want to interpret the data.
I have pointed out the two studies on Friedrichs Ataxia, where NMN restored heart function, while NR failed in nearly the same situation.
I don’t know if my assessment was accurate. The 2-3 times I posted this looking for expert interpretation, no-one responded either way.
Nicotinamide mononucleotide requires SIRT3 to improve cardiac function and bioenergetics in a Friedreich’s ataxia cardiomyopathy model
“Remarkably, NMN administered to FXN-KO mice restores cardiac function to near-normal levels. “
NAD+ replacement therapy with nicotinamide riboside does not improve cardiac function in a model of mitochondrial heart disease
“In conclusion, NAD+ supplementation with NR in the FRDA model of mitochondrial heart disease does not alter SIRT3 activity or improve cardiac function.”
Also, last week, I pointed out 2 studies on Alzheimers, where both NMN and NR showed positive results, but NMN decreased β-amyloid buildup, while NR did not.
https://www.medicaln...cles/320879.php
"NR lessened pTau pathology in both 3xTgAD and 3xTgAD/Polβ+/− mice but had no impact on amyloid β peptide (Aβ) accumulation"
The results of the NMN study:
"NMN decreased β-amyloid production, amyloid plaque burden, synaptic loss, and inflammatory responses in AD-Tg mice"
Again, I don’t know how significant that is, but when I posted the question, noone responded.
Edited by able, 20 February 2018 - 01:15 AM.