In recent years, cell senescence has fallen into the biomedical limelight, with these ‘zombie cells’ serving up a rich source of opportunities for innovative therapeutic development in aging and age-related diseases.

An in-depth look into cell senescence and how these zombie cells contribute to developments in age-related diseases and aging.

This indicator can facilitate research and clinical trials of drugs that target age-related diseases

An indicator to evaluate drugs that target aged cells can help with research for anti-aging and age-related disease purposes.

Study shows that NAD+ supplementation postpones the senescence of bone marrow-derived stem cells

Treating bone marrow stem cells with NAD+ postpones their transition to an aged, non-proliferating (senescent) state where they lose function.

Scientists uncover blood metabolic byproducts as signs of aging that may provide targets for age-related disease prevention through supplementation.

Researchers find blood metabolite markers indicative of aging and age-related diseases which may translate to identifying therapeutic supplement targets.

Basic Research

Back to back research papers show CD38 enzymes on immune cells driving age-related decline of the critical molecule.

Two recent studies published in Nature Metabolism indicate CD38 enzymes on M1 macrophages consume NAD+ and NMN leading to progressive NAD+ level reductions with age.

CD38 Enzymes on Immune Cells Drive NAD+ Decline

Dihydronicotinamide riboside (NRH) promoted cell toxicity in cancerous human cells

NRH reduced cancerous cell line viability but not embryonic cell viability.

NMN’s restoration of youthful kidney protein levels in aged mice may translate therapeutically to humans.

NMN rejuvenates kidney protein levels in aged mice, which may translate therapeutically to humans.

NMN and Anti-Aging in Kidneys

Researchers review evidence supporting the importance of how nicotinamide adenine dinucleotide (NAD+) is distributed to different cell structures in health, disease, and aging.

Researchers review NAD+ distribution between cellular structures in health, disease, and aging. Future discoveries in NAD+ biology will come from scientists with distinct skill sets.

Subdivision of NAD+ is Critical to Mammalian Life | NMN

Nicotinamide mononucleotide represents an effective protective mechanism to maintain healthy endothelial cells

Supplementation with nicotinamide mononucleotide (NMN) represents an effective means to protect blood vessels and maintain healthy endothelial cells.

Scientists repurposed a blood cancer treatment using genetically modified immune cells called CAR T cells to reverse age-associated tissue damage.

A cellular therapy typically used against blood cancer called CAR T therapy improved tissue health by destroying senescent cells in mice.

Others

UC Irvine scientists demonstrate that damaged cells undergo a metabolic shift to survive that arises from NAD+ depletion.


Cell damage initiates a metabolic shift toward reliance on oxidative phosphorylation as opposed to glycolysis, and NMN reverses this metabolic shift restoring viability.

SBI-797812 turns NAMPT into a “super catalyst” that more efficiently generates NMN

A small molecule called SBI-797812 acts as a "super catalyst" generating NMN and significantly increases cellular NAD+ levels.

Scientists from Washington University School of Medicine in St. Louis identify a nicotinamide mononucleotide (NMN)-specific transporter, Slc12a8, in mice.


A research duo from WashU and MIT discusses the progress in determining cell enzyme consumers of NAD+ and their link to the anti-aging therapeutic NMN.

NAD+ consuming enzymes PARPs, sirtuins, and CD38 play key roles in diminished NAD+ levels during aging linked to age-associated diseases.

Studies

NEWS

NMN Induces Metabolic Shift in Damaged Cells to Promote Survival

A Small Molecule That Activates NAMPT Boosts NAD+ Levels

Scientists Identify Slc12a8 Transporter in Mice

The Role of NAD+ Consuming Enzymes in Aging and Disease