NAD: Longevity Molecules
A short video on NAD as part of the longevity molecule series:
– What is NAD?
– What does NAD do?
– How is NAD linked to ageing?
– How is NAD created?
– Some studies related to Alzeheimer Disease treatment
Nicotinamide adenine dinucleotide (NAD+) Longevity molecules series
Nicotinamide adenine dinucleotide (NAD+) is a coenzyme found in every living cell in the human body.
It serves two primary functions: acting as a coenzyme, transporting high-energy molecules from the food we eat to the cells and enzymes that need them for vital chemical reactions.
It also acts as a cosubstrate for other enzymes such as the sirtuins and Poly (ADP-ribose) polymerases (PARPs) which are essential for longevity.
It is generally accepted that Intracellular NAD+ levels decline with age which, in turn, has a negative impact on both health and life span.
Declining or low NAD+ levels have been associated with (but not limited to) the following symptoms of ageing (1):
– Skin Damage
– Weight Gain and Insulin Resistance
– Cardiovascular Disease
– Immune System Function
– Systemic Inflammation
– Impaired Neurological Function (something we’ll be discussing shortly).
First, a quick run-through on how NAD+ is synthesised…
Three metabolic pathways create Nicotinamide Adenine Dinucleotide endogenously (inside the body).
The first is the de novo (Kynurenine) pathway, which utilises amino acids (Tryptophan in animals) to synthesise NAD+.
Due to the sheer amount of NAD+ required by the human body, there are two other pathways the body utilises to create NAD+.
The Salvage Pathway recycles nicotinamide (a form of Vitamin B3) and the Preiss-Handler pathway, which uses Niacin (B3) and various enzymes to create NAD+.
In a future post, we will go into the exact mechanisms of each; however, for the moment, we’d like to bring your attention back to the following studies and the potential promise NAD+ precursors hold for the treatment of neurological disorders, specifically Alzheimer’s Disease.
In a 2018 study (2), scientists at the Johns Hopkins School of Medicine collaborated with researchers from the National Insititute on Aging to understand the foundational mechanisms behind Alzheimer’s Disease (AD) development.
Their findings indicated that supplementation with Nicotinamide Riboside (NR) improved overall cognition in a mouse model resembling AD.
These conclusions were drawn up when the investigators noted improved scores in multiple behavioural tests indicating an, at least partial, restoration in synaptic plasticity.
In a second 2022 study (3), Hu and colleagues from the Shanghai Geriatric Institute of Chinese Medicine demonstrated that increasing NAD+ levels reverses Alzheimer’s Diseases (AD) defects in a mouse model for AD.
The mice were given either NMN, an NAD+ precursor that drives NAD+ or cyclic ADP ribose hydrolase (CD38, an NAD+ degrading enzyme).
The results showed that NMN or the CD38 inhibitor improved the learning and memory of the mice.
There was also a net reduction in inflammation, a well-studied hallmark of ageing.
Additionally, they found there was a drop in total Amyloid beta (Aβ), in later life, can become a corrupted form which can destroy nerve cells.
These studies indicate the potential therapeutic value of NAD+ supplementation in an anti-ageing protocol.
1 – https://health.selfdecode.com/blog/nad-important-increase/#:~:text=NAD%2B%20is%20sometimes%20called%20the,disease%2C%20and%20other%20harmful%20conditions.
2 – https://pubmed.ncbi.nlm.nih.gov/29432159/
3 – https://link.springer.com/article/10.1186/s40659-022-00379-1