The scientific community now recognizes aging as a modifiable process that can be slowed or even reversed, heralding a new era of cellular regenerative medicine aimed at both managing visible signs of aging and developing therapies to restore internal well-being. Central to aging is the decline in cellular nicotinamide adenine dinucleotide (NAD+), crucial for metabolism and as a co-substrate for enzymes that influence aging pathways. Enhancing NAD+ levels may decelerate aging, prompting significant interest in NAD+ restoration methods. To effectively translate these scientific advancements into clinical practice, collaboration between basic scientists exploring cellular aging mechanisms and clinicians offering anti-aging treatments is essential. This integration could profoundly impact healthcare, allowing individuals to not only look younger but also feel internally rejuvenated.
Research on cellular aging has highlighted nicotinamide adenine dinucleotide (NAD+) as a crucial metabolic intermediary directly connected to aging hallmarks. NAD+, vital for metabolic and signaling reactions, participates in redox reactions to generate ATP and regulates enzymes affecting protein function through posttranslational modifications. Maintaining NAD+ levels is essential for tissue homeostasis and responding to bioenergetic stress.
An age-related decrease in NAD+ is common across species, contributing to aging through its role as a co-substrate for enzymes like sirtuins (SIRTs) and poly(ADP-ribose) polymerases (PARPs), which are pivotal in cellular repair and longevity. Preclinical studies show that restoring NAD+ in mice leads to improved cardiovascular health, metabolic conditions, muscle function, and mitochondrial efficiency. Additionally, NAD+ boosts regenerative capacities in organs and can reverse neurodegenerative and age-related retinal degeneration symptoms.
In human clinical trials, restoring NAD+ has shown potential benefits such as improved cardiovascular function, reduced inflammatory markers, enhanced mitochondrial function in heart failure patients, and restored fertility in aged mice. This underscores NAD+’s broad protective and regenerative potential and its pivotal role in mitigating aging’s cellular hallmarks.
