Mayo Clinic Study Shows Spinal Cord Nerves Depend on NAD+

·         Diets high in fat adversely impact the survival and function of myelin-producing cells called oligodendrocytes by reducing NAD+ levels in mice.
·         Inactivating CD38 — an NAD+ consuming enzyme — by genetic or drug-based manipulation enhances oligodendrocyte survival.
·         Restoring NAD+ levels with the NAD+ precursor NMN prevents oligodendrocyte loss and promotes myelin repair.    

For conscious and subconscious tasks, from giving a hug to breathing, our nervous system needs to send electric signals at lightning speed. To achieve biological fiber-optic-like transmission, our nerve cells called neurons are insulated in myelin — a conductive cover for speedy nerve communication. But when myelin is disrupted, which happens with age, certain genetic conditions like multiple sclerosis, and poor metabolism, we become susceptible to permanent spinal cord and brain damage. So, all that fast food and inactivity isn’t just bad for your metabolism; it can deteriorate myelin coating to severely weaken nerve signals essential for everyday life. 

Research from the Mayo Clinic published in The Journal of Neuroscience shows that the white matter, where myelin-wrapped nerve projections run through the brain and spinal cord, can be impaired by high-fat consumption. This occurs by disrupting levels of a vital metabolic coenzyme called nicotinamide adenine dinucleotide (NAD+), leading to the loss of nervous system cells called oligodendrocytes — cells that add myelin to neurons. But increasing NAD+ levels, either by blocking the consumption of NAD+ or supplementing with the precursor nicotinamide mononucleotide (NMN), attenuated oligodendrocyte loss and promoted myelin regeneration.