4 Things We Learned at the 2019 NAD+ Metabolism and Signaling Conference
Learn the latest from the NAD+ field, where researchers from all over the world presented their findings.
Leaders in the NAD+ field met at Trinity College in Dublin, Ireland in late June to present and discuss the latest developments in the rapidly growing field of NAD+ research. The NAD+ Metabolism and Signaling Conference, hosted by the Federation of American Societies for Experimental Biology and sponsored by Elysium, has been occurring bi-annualy since 2009.
“The NAD+ conference is a fantastic opportunity to hear about the latest developments in the field of NAD+ research,” says Holly Holmes, PhD, Elysium’s Manager of Scientific Affairs.
“As interest in the role of NAD+ in healthy aging continues to grow, the conference provides a platform for researchers from all over the world to present their findings to the scientific community.”
The conference kicked off with an opening keynote from Eric Verdin, MD, President and CEO of the Buck Institute for Research on Aging in California. Verdin’s opening speech hinted at what the rest of the conference would cover: the modulation of lifespan by calorie restriction, how sirtuins function in the presence of NAD+, the relevance of CD38 in regards to what we know about aging and senescence, and much more.
“There are so many things we need to understand,” he said. Here’s what we learned at the conference.
The NAD+ Pool Varies by Tissue
Melanie McRyenolds, PhD, a postdoctoral research associate at Princeton University’s Rabinowitz Lab, which focuses on cellular metabolism, presented on NAD+ flux during aging. Her presentation, and the research she’s currently conducting, focuses on the tissue-specific location of NAD+ decline. In other words, how does the NAD+ pool vary by tissue?
McRyenolds said she felt empowered during her presentation on the topic and throughout the conference. As a student of the field for nearly a decade, she found herself being congratulated by the very scientists whose research she studied when she first learned of NAD+.
“All of their papers established my foundation so to be here now and collaborating with them is full circle,” Melanie said. “I’m not only being accepted but celebrated.”
NAD+ Consumption by Sirtuins and Other Enzymes Could Increase with Age
Another speaker was Vera Gorbunova, PhD, an Elysium Health Scientific Advisory Board Member, co-director of the Rochester Aging Research Center, and co-director of the Gorbunova and Seluanov Laboratory at the University of Rochester.
Gorbunova gave the keynote lecture on the SIRT6 variant, or sirtuin 6 — one of the proteins that can only function in the presence of NAD+. Gorbunova explained that mice lacking SIRT6 exhibit severe premature aging phenotypes and genomic instability, while mice overexpressing SIRT6 have been reported to live longer.
This is particularly interesting as SIRT6, along with the other human sirtuins (of which there are seven total), are NAD+-consuming enzymes. The largest theme of hypotheses presented by many at the conference was that NAD+ synthesis does not necessarily go down with age but that NAD+ consumption increases with age.
The Decline of NAD+ Is Linked with CD38 and Cellular Senescence
Eduardo Chini, MD, PhD, researcher for Mayo Clinic’s Robert and Arlene Kogod Center on Aging, presented 15 years worth of research on CD38, a main NAD+-consuming enzyme (also known as an NADase) in mammalian tissues. To explain, Chini charted the history of NAD+, dating it back to the early 1900s, when it was first identified during fermentation. Chini went on to discuss the latest CD38 research, which was published in May 2019 in a paper with his wife Claudia Chini, PhD, also a researcher for Mayo Clinic’s Robert and Arlene Kogod Center on Aging. Claudia was the lead study author and found that CD38 expression in cells can be induced by factors associated with cellular senescence (cells that no longer divide and resist death), which gives us a possible link between cellular senescence and the decline of NAD+.
Newer Research Proves Promising for Boosting and Maintaining NAD+
When it came to new research, Shin Ichiro-Imai, MD, PhD, a professor of developmental biology at Washington University in St. Louis, presented his latest findings on NMN, or nicotinamide mononucleotide, and the newly identified transporter that allows NMN into the cell. And Joseph A. Baur, PhD, associate professor of physiology at the University of Pennsylvania Perelman School of Medicine Institute for Diabetes, Obesity and Metabolism, showed that inhibiting NAMPT — an enzyme that catalyzes the conversion of NAM to NR — decreases the amount of NAD+ in the cytoplasm, but with relative preservation of mitochondrial NAD+ levels. These findings suggest that the mitochondria are able to maintain NAD+ levels at all costs.