Sobriety and Satiety: Is NAD+ the Answer?

Braidy, Nady; Villalva, Maria D.; Eeden, Sam van

doi:10.3390/antiox9050425

Cited by 12 publications

(9 citation statements)

References 203 publications

(241 reference statements)

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“…In addition, there is intense interest in pharmaceutical approaches to alleviate mitochondrial dysfunction after CA (15,16). NAD + has been used in IV form since the early 1990s to significantly lessen withdrawal from a variety of drugs and alcohol (17). NAD + has been reported to have potent neuroprotective effects against ischemic neuronal injury and traumatic brain injury (18)(19)(20)(21).…”

mentioning

confidence: 99%

Exogenous Nicotinamide Adenine Dinucleotide Attenuates Postresuscitation Myocardial and Neurologic Dysfunction in a Rat Model of Cardiac Arrest

Xiao

Zhang

et al. 2021

Critical Care Medicine

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To investigate the therapeutic potential and underlying mechanisms of exogenous nicotinamide adenine dinucleotide + on postresuscitation myocardial and neurologic dysfunction in a rat model of cardiac arrest.DESIGN: Thirty-eight rats were randomized into three groups: 1) Sham, 2) Control, and 3) NAD. Except for the sham group, untreated ventricular fibrillation for 6 minutes followed by cardiopulmonary resuscitation was performed in the control and NAD groups. Nicotinamide adenine dinucleotide + (20 mg/kg) was IV administered at the onset of return of spontaneous circulation. SETTING:University-affiliated research laboratory. SUBJECTS:Sprague-Dawley rats. INTERVENTIONS:Nicotinamide adenine dinucleotide + . MEASUREMENTS AND MAIN RESULTS:Hemodynamic and myocardial function were measured at baseline and within 4 hours following return of spontaneous circulation. Survival analysis and Neurologic Deficit Score were performed up to 72 hours after return of spontaneous circulation. Adenosine triphosphate (adenosine triphosphate) level was measured in both brain and heart tissue. Mitochondrial respiratory chain function, acetylation level, and expression of Sirtuin3 and NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 9 (NDUFA9) in isolated mitochondrial protein from both brain and heart tissue were evaluated at 4 hours following return of spontaneous circulation. The results demonstrated that nicotinamide adenine dinucleotide + treatment improved mean arterial pressure (at 1 hr following return of spontaneous circulation, 94.69 ± 4.25 mm Hg vs 89.57 ± 7.71 mm Hg; p < 0.05), ejection fraction (at 1 hr following return of spontaneous circulation, 62.67% ± 6.71% vs 52.96% ± 9.37%; p < 0.05), Neurologic Deficit Score (at 24 hr following return of spontaneous circulation, 449.50 ± 82.58 vs 339.50 ± 90.66; p < 0.05), and survival rate compared with that of the control group. The adenosine triphosphate level and complex I respiratory were significantly restored in the NAD group compared with those of the control group. In addition, nicotinamide adenine dinucleotide + treatment activated the Sirtuin3 pathway, down-regulating acetylated-NDUFA9 in the isolated mitochondria protein. CONCLUSIONS:Exogenous nicotinamide adenine dinucleotide + treatment attenuated postresuscitation myocardial and neurologic dysfunction. The responsible mechanisms may involve the preservation of mitochondrial complex I respiratory capacity and adenosine triphosphate production, which involves the Sirtuin3-NDUFA9 deacetylation.

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confidence: 99%

Exogenous Nicotinamide Adenine Dinucleotide Attenuates Postresuscitation Myocardial and Neurologic Dysfunction in a Rat Model of Cardiac Arrest

Xiao

Zhang

et al. 2021

Critical Care Medicine

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“…However, a plausible mechanism has been posited. Nicotinamide adenine dinucleotide (NAD + ) is essential for the dehydrogenation of acetylaldehyde, which is essential for alcohol metabolism ( 29 ). Sirtuin5 (SIRT5), which is an NAD + -dependent enzyme, can trigger deacetylation and upregulate the CPS1 activity ( 30 ).…”

Section: Discussionmentioning

confidence: 99%

A 36-year-old Man with Repeated Short-term Transient Hyperammonemia and Impaired Consciousness with a Confirmed <i>Carbamoyl Phosphate Synthase 1</i> Gene Monoallelic Mutation

et al. 2022

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A 36-year-old man experienced severely impaired consciousness twice after drinking because of hyperammonemia. No abnormal blood tests were found other than ammonia levels. However, magnetic resonance imaging showed atrophy of the brain parenchyma. One the second occasion, the patient suffered severe impairment of consciousness, and because of seizures and glossoptosis, mechanical ventilation was started. Urea cycle disorders (UCDs) were assumed to be involved. Genetic testing revealed a monoallelic mutation of the carbamoyl phosphate synthase 1 gene. When transient hyperammonemia of unknown cause occurs repeatedly in adults, an active investigation for UCDs should be conducted.

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“…Although further studies are needed to conclusively determine the impact of SARS-CoV-2-mediated NAD+ depletion in PACS pathogenesis, preclinical and clinical data has suggested that supplementation with NAD+ or its analogs may accelerate PACS recovery. 55 - 59 Moreover, there is one ongoing pilot study with NAD+ investigating its effect on reducing fatigue in PACS. 60 Despite the evidence supporting NAD+ supplementation as potential PACS therapy, considerably more information about the safety, efficacy and potential long-term sequel of IV NAD+ administration is required to claim a therapeutic effect in PACS patients.…”

Section: Rationale For Nad+ Intravenous Administration Therapy For Pa...mentioning

confidence: 99%

Rationale for Nicotinamide Adenine Dinucleotide (NAD+) Metabolome Disruption as a Pathogenic Mechanism of Post-Acute COVID-19 Syndrome

Block

Kuo

2022

Clin Med�Insights�Pathol

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Many acute COVID-19 convalescents experience a persistent sequelae of infection, called post-acute COVID-19 syndrome (PACS). With incidence ranging between 31% and 69%, PACS is becoming increasingly acknowledged as a new disease state in the context of SARS-CoV-2 infection. As SARS-CoV-2 infection can affect several organ systems to varying degrees and durations, the cellular and molecular abnormalities contributing to PACS pathogenesis remain unclear. Despite our limited understanding of how SARS-CoV-2 infection promotes this persistent disease state, mitochondrial dysfunction has been increasingly recognized as a contributing factor to acute SARS-CoV-2 infection and, more recently, to PACS pathogenesis. The biological mechanisms contributing to this phenomena have not been well established in previous literature; however, in this review, we summarize the evidence that NAD+ metabolome disruption and subsequent mitochondrial dysfunction following SARS-CoV-2 genome integration may contribute to PACS biological pathogenesis. We also briefly examine the coordinated and complex relationship between increased oxidative stress, inflammation, and mitochondrial dysfunction and speculate as to how SARS-CoV-2-mediated NAD+ depletion may be causing these abnormalities in PACS. As such, we present evidence supporting the therapeutic potential of intravenous administration of NAD+ as a novel treatment intervention for PACS symptom management.

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Sobriety and Satiety: Is NAD+ the Answer?

Cited by 12 publications

References 203 publications

Exogenous Nicotinamide Adenine Dinucleotide Attenuates Postresuscitation Myocardial and Neurologic Dysfunction in a Rat Model of Cardiac Arrest

Exogenous Nicotinamide Adenine Dinucleotide Attenuates Postresuscitation Myocardial and Neurologic Dysfunction in a Rat Model of Cardiac Arrest

A 36-year-old Man with Repeated Short-term Transient Hyperammonemia and Impaired Consciousness with a Confirmed <i>Carbamoyl Phosphate Synthase 1</i> Gene Monoallelic Mutation

Rationale for Nicotinamide Adenine Dinucleotide (NAD+) Metabolome Disruption as a Pathogenic Mechanism of Post-Acute COVID-19 Syndrome

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