In 2017, Dr. David Sinclair and his team identified a critical step in the molecular process that facilitates the repair of DNA damage . We experience DNA damage on a daily basis from sunlight and other environmental sources.
DNA damage is thought to contribute to the rising risk of cancer as we age and is implicated in various age-related diseases. Our cells have the innate ability to repair that damage, but, unfortunately, that ability to repair declines as we grow older.
In a 2017 study, the researchers identified that the metabolite NAD+, which occurs naturally in every single cell in our body, has a critical role in DNA repair by regulating the protein-to-protein interactions involved in that process.
They found that treating mice with the NAD+ precursor known as NMN boosted the cells’ ability to repair DNA damage caused by aging or radiation exposure.
“The cells of the old mice were indistinguishable from the young mice after just one week of treatment,” said lead author Professor David Sinclair of UNSW School of Medical Sciences and Harvard Medical School Boston.
As well as boosting DNA repair, it has also been established that NAD+ activates all seven of the sirtuins, which are genes associated with longevity and health.
The next step is to take NMN to human clinical trials, which could potentially lead to the development of the first therapy that directly targets the aging processes to combat age-related diseases and ill health.
 Li, J., Bonkowski, M. S., Moniot, S., Zhang, D., Hubbard, B. P., Ling, A. J., … & Aravind, L. (2017). A conserved NAD+ binding pocket that regulates protein-protein interactions during aging. Science, 355(6331), 1312-1317.