A new study indicates age-related inflammation can stimulate CD38 positive immune cell consumption of NAD+.
Researchers show that an enzyme called CD38 on immune cells exhausts levels of an essential molecule for life called NAD+ and its precursor NMN during aging.
Nicotinamide mononucleotide (NMN) intervention protects neurons and memory from diabetes-induced brain degeneration in rats.
UPenn researchers identify an elusive mechanism for the entry of NAD+ into the power plant of the cell.
Scientists elaborate how NAD+ depletion compromises the ability of mitochondria to counteract free radical and reactive oxygen species buildup.
Excessive alcohol consumption and binge drinking reduce levels of free nicotinamide adenine dinucleotide (NAD+) critical to cellular health and energy production, resulting in liver and organ damage.
Miscommunication between mitochondria and the nucleus accelerates aging, but NAD+ supplementation helps restore the conversation and reverses signs of aging.