In a DNA-repair-deficient mouse model of Alzheimer's disease (AD), researchers report that the mice exhibited reduced cerebral nicotinamide adenine dinucleotide (NAD+), a cellular metabolite involved in mitochondrial health and biogenesis; supplementation of NAD+ with nicotinamide riboside treatment normalized NAD+ levels, reduced DNA damage and neuroinflammation, and improved cognitive function in the mice, findings with potential implications for AD treatment.
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Article #17-18819: "NAD+ supplementation normalizes key Alzheimer's features and DNA damage responses in a new AD mouse model with introduced DNA repair deficiency," by Yujun Hou et al.
MEDIA CONTACT: Vilhelm Bohr, National Institute on Aging, National Institutes of Health, Baltimore, MD; tel: 410-558-8162, 443-850-4026; e-mail: vbohr@nih.gov
Journal
Proceedings of the National Academy of Sciences