Researchers at Case Western Reserve University and their collaborators described the use of P7C3-A20, a compound that restores nicotinamide adenine dinucleotide (NAD+) homeostasis, as a potential strategy to reverse Alzheimer’s disease (AD) pathology in advanced Aβ- and tau-driven AD models.

Adult skeletal muscle tolerates a lack of the coenzyme nicotinamide adenine dinucleotide (NAD), according to a study led by scientists at the University of Copenhagen. Their results suggest that adverse effects previously associated with congenital NAD depletion in this tissue may be due to impaired muscle development rather than to a deficiency of this molecule.

A multi-omics analysis led by Chinese scientists at Tsinghua University in Beijing has demonstrated that aberrant metabolism of the co-enzyme nicotinamide adenine dinucleotide (NAD+) was responsible for microcephaly induced by Zika virus infection during pregnancy.