Reprinted with the kind permission of Life Extension.
February 07 2018. Research reported on February 5, 2017 in the Proceedings of the National Academy of Sciences found a benefit for supplementation with nicotinamide riboside, a compound that increases cellular levels of nicotinamide adenine dinucleotide (NAD+), in a mouse model of Alzheimer’s disease.
The study utilized mice bred to show increased features of human Alzheimer’s disease, including age-dependent amyloid beta plaques, intraneuronal Tau tangles, and cognitive deficits. These animals were subsequently modified to have a decreased ability to repair DNA, resulting in greater DNA damage and neuron death in specific brain regions, thereby more closely mimicking features of human Alzheimer’s disease. Researchers Vilhelm A. Bohr of the National Institutes of Health and colleagues observed that the animals had a decreased cerebral ratio of NAD+ to NADH (NADH is the chemically reduced form of NAD).
The team supplemented the drinking water of four groups of mice with nicotinamide riboside or gave them plain water for 6 months. Compared to untreated DNA repair-deficient Alzheimer’s disease mice, supplementation with the with nicotinamide riboside normalized the cerebral NAD+ to NADH ratio, decreased phosphorylated tau pathologies, and lowered DNA damage, neuroinflammation and apoptosis (programmed cell death) in the brain’s hippocampus (which is involved in memory) while increasing the activity of the sirtuin SIRT3, a protein involved in metabolic regulation. The mice also exhibited improvements in cognitive function and hippocampal synaptic plasticity, as did the original Alzheimer’s disease model animals that received nicotinamide riboside.
“This study suggests that nicotinamide riboside/NAD+ can target several aspects of Alzheimer’s disease, including traditional endpoints like Tau pathology and inflammation, maybe via DNA repair enhancement,” conclude authors Yujun Hou and colleagues. “We believe that this work sets the stage for using NAD+ for treating Alzheimer’s disease in humans.”