NMN, a precursor to NAD+, has been shown to improve various parameters of health in mice, such as:
- Physical endurance and muscle strength
- Neurological function
- Heart health
- Insulin sensitivity
- Body weight
- Gene expression
NMN REPAIRS DNA IN MICE
A study in mice, found that NAD+ has a key role as a regulator in protein-to-protein interactions that control DNA repair.
Specifically, it has been found that NMN, a NAD+ precursor, improved mice cells ability to repair DNA damage.
“The cells of the old mice were indistinguishable from the young mice, after just one week of treatment,” said Dr David Sinclair.
NMN ANTI-AGING POTENTIAL IN MICE
A study in mice showed that supplementing healthy mice with NMN can compensate for the loss of energy production, reducing signs of aging, such as weight gain, loss of insulin sensitivity and declines in physical activity.
This study showed that when NMN is dissolved in drinking water and given to mice, it appears in the bloodstream in less than three minutes.
It was also found that NMN in the blood is quickly converted to NAD+ in multiple tissues.
Researchers found a verity of beneficial effects of NMN supplementation in older mice including in:
- Skeletal muscle
- Liver function
- Bone density
- Eye function
- Insulin sensitivity
- Immune function
- Body weight and physical activity levels.
NMN INHIBITS JNK ACTIVATION TO REVERSE ALZHEIMER'S DISEASE
A study in mice, showed that NAD+ is related to the decline of amyloid-β (Aβ) oligomers, which have been accepted as major neurotoxic agents in the therapy of Alzheimer's disease (AD).
NMN, a precursor of NAD+, is produced during the reaction of nicotinamide phosphoribosyl transferase (Nampt).
What this study aims to demonstrate is the potential therapeutic effect of NMN in behavioral measures of cognitive impairments compared to control AD-Tg mice.
What has been found is that NMN effectively controlled JNK activation, potently progressed nonamyloidogenic amyloid precursor protein (APP) and suppressed amyloidogenic APP by mediating the expression of APP cleavage secretase in AD-Tg mice.
The findings of this study suggest that NMN substantially decreases multiple AD-associated pathological characteristically at least partially by the inhibition of JNK activation.
CARDIOPROTECTION BY NMN
In this study in mice, researchers hypothesized that NMN may confer cardiovascular protection in part via direct stimulation of cardiac glycolysis.
What was found is that NMN was cardioprotective when delivered acutely at reperfusion (recovery 39±8%).
This effect of NMN was not additive with acidosis, suggesting overlapping mechanisms.
In conclusion, acute cardioprotective benefits of NMN are mediated in part via glycolytic stimulation, with the downstream protective mechanism involving enhanced ATP synthesis during ischemia and/or enhanced acidosis during reperfusion.