Dysregulated nicotinamide adenine dinucleotide metabolome in patients hospitalized with COVID-19.

Nicotinamide adenine dinucleotide (NAD) depletion has been postulated as a contributor to the severity of COVID-19; however, no study has prospectively characterized NAD and its metabolites in relation to disease severity in patients with COVID-19. We measured NAD and its metabolites in 56 hospitalized patients with COVID-19 and in two control groups without COVID-19: (1) 31 age- and sex-matched adults with comorbidities, and (2) 30 adults without comorbidities. Blood NAD concentrations in COVID-19 group were only slightly lower than in the control groups (p < 0.

NAD+ precursors prolong survival and improve cardiac phenotypes in a mouse model of Friedreich's Ataxia.

Friedreich's ataxia (FRDA) is a progressive disorder caused by insufficient expression of frataxin, which plays a critical role in assembly of iron-sulfur centers in mitochondria. Individuals are cognitively normal but display a loss of motor coordination and cardiac abnormalities. Many ultimately develop heart failure.