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NAD+, NMN & Cancers. What Is The Result

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As life expectancy increases, people experience poor health and age-related illnesses, causing enormous financial and societal consequences. Immune system decline is a major contributor to age-related illnesses. NK cells that kill cancerous and virally contaminated cells lose effectiveness. Currently, there is no cure for aging NK cells. Compounds that activate NK cells may so prevent or delay age-related diseases.

NMN Boosts Cancer-Fighting Immune Cell Activation

The researchers used nicotinamide mononucleotide (NMN) to restore NK cell cytotoxicity – the capacity to kill defective cells.

The age-related reduction in immune function is connected to a chemical called nicotinamide adenine dinucleotide (NAD+) levels. However, increasing NAD+ levels improved immunological function in mice. Increased NAD+ levels have been demonstrated to boost immunity and reduce tumor growth in mice. In elderly mice, the NAD+ precursor NMN assists with insulin insensitivity and metabolic abnormalities such as obesity. Therefore, it may also increase anti-tumor NK cell function. The ability of NMN to restore immunity in NK cells is important to decide if it is the molecule, we need to restore their cytotoxicity.

The researchers administered NMN into mice of various ages to assess NK cell activation and cytotoxicity. The researchers gave 36-week-old mice varied dosages of NMN for four days, then extracted NK cells from the liver and spleen. We next placed these killer cells into a plate containing cancer cells and measured their cytotoxicity by the proportion of cancer cells eliminated. Injecting 313 mg/kg or more of NMN increases the ability of elderly NK cells to eliminate defective cells in mice.

NMN Protects Mice from Chemotherapy-Induced Cognitive Impairment

In a study by Mayo Clinic revealed that chemotherapeutics reduces NAD+ levels in mature mouse brains and human brain cells. However, boosting NAD+ levels with nicotinamide mononucleotide (NMN) reversed cisplatin-induced brain impairments ranging from individual cell and tissue structure to cognitive function. Notably, NMN had no influence on cisplatin’s anti-tumor activity.

To investigate the relationship between NAD+, chemotherapeutics, and brain health, the research pretreated female adult mice with NMN at a daily dosage of 250 mg/kg, followed by cisplatin 4 hours later. Then they employed multiple tests to assess memory in mouse models of brain diseases, including hippocampal dysfunction. They began with the NOR challenge, which utilizes mice’ predisposition to investigate unfamiliar items over familiar ones. In the end, the researchers replaced one of the familiar objects with a novel one and tested their willingness to study the new ones. In cisplatin-treated mice, memory function was reduced compared to untreated animals. This finding supports the concept that NMN boosts cognition in both untreated and cisplatin-treated mice.

The neuroprotective effects of NMN on memory appear to be linked to higher NAD+ levels in the hippocampus and cerebellum of cisplatin-treated mice.

NAD+ Boosts Cancer Therapy Sensitivity

Another study demonstrated that NAD+ production in cells reduces tumor growth. Their research found that supplementing with the NAD+ precursor nicotinamide mononucleotide (NMN) raised NAD+ levels and enhanced the efficiency of an immunotherapy treatment for cancers resistant to immunotherapy.

Using mice, the researchers discovered that reducing NAMPT, an enzyme involved in NAD+ synthesis boosted the activity of CD8+ T cells. T cell activation helped them fight cancer. NAD+ metabolism impacts CD8+ T cell activity against tumors. A rise in PD-L1 levels was shown to assist cancer cells to elude the immune system. On cancer cells, PD-L1 attaches to T cell PD-1 receptors, inhibiting their function. T cell weariness (loss of capacity to kill malignant cells) and immune evasion are caused by PD-L1 on cancer cells and PD-1 on T cells. Increased levels of NAMPT in tumor cells were linked to increased levels of PD-L1 protein on cancer cell surfaces and immune evasion.

According to this study, high levels of NAD+ promote the expression of PD-L1 on tumor cells, which leads to immune cell fatigue. Increasing NAD+ levels with its precursor NMN also increased tumor susceptibility to cancer treatment.


Aging is a key risk factor for many diseases including cancer, the concern is the enzyme called NAMPT which helps to make NAD+ is overexpressed in the number of malignancies and its presence has been related to tumor growth. So, cancer cells have also been discovered to contain high amounts of NAD+, and PARPs & Sirtuins are activated anytime there is DNA damage to recruiting the components of a DNA repair machine.

This relationship of PARPs & Sirtuins activity has been related to aggression as well as repression. This paradox has been related to PARPs’ & Sirtuins  role in DNA repair which may prevent accumulation, mutation, and cancer formation but may also aid cancer formation and survival when the tumor is developed. Summarizing all this, before the DNA damage is so damaged that it becomes cancerous, PARPs’ are great to repair it at this level. But when the damage has occurred beyond the repair level, PARPs’ are found to have protective activity for DNA damage.