Prophylactic Effects of NMN on Depressive-Like Behaviors
Introduction
According to the report by World Health Organization (WHO) in 2017, depression is the third leading cause of the global disease burden, with over 300 million people suffering from this disease worldwide, equivalent to approximately 4.4% of the world’s population. Depression is prone to recurrent episodes, posing a heavy burden on patients, families and society. Strikingly, nicotinamide mononucleotide (NMN) supplementation has been deemed as a novel approach to protect and prevent individuals at a risk of developing stress-induced depression.
About depression
Depression is a prevalent progressive psychiatric disorder, with main clinical symptoms of negative emotion (e.g. sadness, feelings of guilt or low self-worth), disturbed sleep or appetite, fatigue, poor concentration and loss of interest or pleasure. This disorder seriously reduces the patient's quality of life, which may eventually lead to self-harm or even suicide.The role of ATP level in the mPFC in regulating depressive-like behaviors
Adenosine triphosphate (ATP), an important neurotransmitter or neuromodulator, serves as a crucial cellular energy source and can be released by neurons and glial cells. Blocking ATP release can decrease neuronal excitability and ultimately lead to depressive-like behaviors. Mounting evidence has revealed a decreased extracellular ATP level in the medial prefrontal cortex (mPFC) of patients with depression and in mice that are susceptible to chronic stress. Hence, boosting the extracellular ATP level in the mPFC may exert antidepressant-like effects.
Prophylactic effects of NMN on CSDS-induced depressive-like behaviors
To induce rodent depressive-like behaviors, the chronic social defeat stress (CSDS) mouse model is established herein. Notably, both the 2-week intraperitoneal (i.p.) injection and 3-week oral gavage of NMN prior to CSDS exposure dose-dependently elevate nicotinamide adenine dinucleotide (NAD+) biosynthesis and extracellular ATP level in the mouse mPFC, and prevent the development of depressive-like behaviors of mice. Moreover, prophylactic NMN treatment also prevents the deficiency of ATP-mediated GABAergic transmission and the increase of excitability in mPFC neurons projecting to the lateral habenula (LHb).
Conclusion
Prophylactic effects of NMN against CSDS-induced depressive-like behaviors may be achieved by the preservation of both NAD+ biosynthesis and extracellular ATP level in the mPFC, opening up new clues for the formulation of anti-depressant strategies.Reference
[1] Deng J, Tong X, Huang Y, et al. Prophylactic nicotinamide mononucleotide (NMN) mitigates CSDS-induced depressive-like behaviors in mice via preserving of ATP level in the mPFC. Biomed Pharmacother. 2024;176:116850. doi:10.1016/j.biopha.2024.116850
[2] World Health Organization. Depression and Other Common Mental Disorders: Global Health Estimates. Geneva: World Health Organization, 2017
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