NAD+ Depletion Primes Cells for Inflammatory Behavior

Today's open access paper provides an interesting view on the age-related reduction in cellular NAD+ levels, a topic of interest in the longevity community these past years. Nicotinamide adenine dinucleotide (NAD) is an important piece of molecular machinery in the function of the electron transport chain in mitochondria. The primary role of mitochondria is to generate the chemical energy store molecule adenosine triphosphate (ATP), used to power the cell. NAD cycles between NAD+ and NADH during this process, and lower levels of NAD imply a growing dysfunction in cellular energy metabolism. Separately, researchers here show that lowered levels of NAD act to prime a cell for inflammatory activity. Mitochondrial dysfunction with age may affect levels of chronic inflammation in tissues via this mechanism. As we all know by now, chronic inflammation sustained over years provides a sizable contribution to degenerative aging, disrupting the normal processes of tissue maintenance, changing cell behavior for the worse, and accelerating many of the common age-related conditions. Given this, it is interesting that fairly direct, compensatory restoration of NAD levels via the various approaches based on supplementation of vitamin B3 derivatives (niacin, nicotinamide riboside, nicotinamide mononucleotide, and so forth) perform so indifferently in clinical trials. They do not address deeper causes of this age-related decline, but do compensate in the production of more NAD. ...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs