What if you could truly turn back time and heal your cells from within?
Nicotinamide Adenine Dinucleotide (NAD) is a metabolic co-enzyme that structures, repairs, and is an essential component of energy production (mitochondrial function). As we grow older, certain genes can be triggered that accelerate degenerative aging processes. This can result in symptoms such as chronic fatigue, loss of mental clarity, depression, stress, anxiety, and various other chronic illnesses. NAD is critical and every cell in our body needs it. This coenzyme is heavily involved in DNA repair and cell repair, responsible for turning off those genes that accelerate degenerative aging, essential for maintaining neurotransmitter levels for proper functioning of the brain.
Researchers investigating brain health and longevity have found NAD+ is an essential coenzyme that promotes cellular regeneration. Studies have found replenishing cellular levels of NAD+ can repair DNA, protect brain cells from damage, reduce inflammation and turn on enzymes that help prevent aging.
Intravenous NAD+ has been used since the 1960s to help individuals detoxify from alcohol and opioid dependencies. In the last ten years, NAD+ has been more widely used to help detoxify from other types of chemical dependencies, including benzodiazepines, methadone, suboxone, methamphetamines and stimulants.
Many chronic conditions, including chronic fatigue syndrome, neurodegenerative disease and mental health disorders have been linked to cellular dysfunction and dysregulation. NAD+ therapy may help reduce the symptoms of many chronic conditions, and may help individuals suffering from chronic conditions regain their vitality and strength.
What Is NAD+?
We have several built-in systems for fixing errors in our DNA, and these systems need NAD+.
This family of proteins, which requires NAD+, keeps the cell in homeostasis under conditions of stress and governs longevity in lower organisms.
The liver does a lot of important metabolic work, like breaking down fats for energy and keeping blood sugar in balance, all of which requires NAD+.
A form of communication in the cell — needed for muscle contraction, cell growth, and neurotransmission — that depends on the coenzyme NAD+.
Our sleep and wake cycle, and everything it entails, depends on NAD+.
NAD+ is a key player in making ATP, the source of energy in the cell.
Stem Cell Maintenance
Organs depend on stem cells for regular maintenance, and NAD+ is necessary for having a healthy number of functioning stem cells.
Unfolded Protein Response
The shape of a protein determines its function. NAD+ helps to make sure the proteins are ‘folded’ into the correct shape.
Our genes get turned on and off (a process called “expression”) constantly in response to conditions like nutrition and stress. This requires NAD+.
Why is NAD important?
Chronic Illness is a medical condition that affects millions of people. These conditions typically do not have a cure and are managed through medication and lifestyle changes. For many individuals this often leads to depression, stress and hopelessness. Increasing NAD+ had been show to dramatically reduce symptoms of illness by boosting the body’s natural cell repair.
What does NAD+ do?
Scientists have shown that NAD+ significantly decreases as we age, so it’s beneficial to replenish NAD+ levels so your body can function at optimal levels. NAD therapy is both a natural and safe form of treatment that generates cellular energy. It is an activated form of vitamin B3 that has a number of potential benefits for patients.
NAD+ is involved in these roles throughout the body.
1. Replenishes balance of neurotransmitters in the brain.
2. Optimizes mitochondrial function in brain.
3. Improves mental clarity and cognitive function (focus and concentration).
4. Accelerates recovery of psycho-emotional issues following treatment of chronic conditions.
5. Helps the cells convert food into energy by acting as an electron transporter during cell metabolism.
6. Support the activation of PARPs (Poly ADP ribose polymerase), which detect and repair damaged DNA.
7. Gene expression: Your body has a class of proteins called sirtuins that help regulate certain metabolic pathways and genetic expressions. Sirtuins are NAD-dependent and the more sirtuin activity, the better for health and longevity. Increased sirtuin activity can help increase metabolism, decrease inflammation, extend cell life, and prevent neurodegeneration.
8. Activates cell signaling: research is revealing that NAD and ATP may alert the immune response when the cell is under stress or when there is inflammation.
Who can benefit from NAD+?
Since NAD+ is such a powerful and prolific molecule in the body, high dose IV therapy can be helpful for many different conditions including:
- Substance Abuse
- Sleep Disorders
- Brain Injury
- Chronic Pain
- Chronic Traumatic Encephalopathy (CTE)
- Neurodegeneration Disease
- Chronic Fatigue
- Chronic Migraine Headaches
At the end of treatment with NAD+ therapy, clients have generally reported the following benefits:
Focus and concentration
Enhanced sense of purpose
Craving of substances
NAD+ Treatment Process
At VitamedIV, every client has an individualized protocol based on the condition. The first step in the process is to have an assessment prior to treatment, where a patient’s medical history and current health status will be reviewed. Once reviewed by our medically trained staff and under the supervision of our doctor, clients will then be able to start treatment. NAD+ Therapy involves high dose intravenous infusion that goes straight into the bloodstream and provides the best form of absorption.
All of our treatments are outpatient procedures, and a course of NAD+ typically require 4 – 10 (or more) sessions to ensure complete results. This treatment is not a cure but provides you with a journey to life-changing results.
Our NAD+ formula is compounded by a state-of-the-art, FDA-regulated facility that can only be found in a small number of medical offices in the world and requires special licensing and training. It is used both intravenously and as a nasal spray.
Nad+ Detox – What to Expect
At NAD+ Detox Clinic, the comfort and well-being of our patients is paramount. Everything within the clinic has been considerately designed to ensure that the NAD+ experience is as relaxing as possible. By carrying out the treatment in a calm, tranquil environment, our patients will not only benefit from the end results of NAD+, they also enjoy the process of getting there.
How do I prepare for an NAD+ infusion?
Prior to visiting the clinic, it is advantageous to have eaten. We also recommend bringing lunch or suitable snacks with you. Tea, coffee and soft drinks are readily available in the clinic throughout the day.
It is advisable to wear loose comfortable clothing to ensure that you are relaxed whilst undergoing the treatment. There is wi-fi available, so feel free to bring any electronic devices, plus any books or iPods that you may wish to use during your therapy.
What happens when I come to the clinic?
When you arrive at the clinic, you will have a thorough consultation with our doctor. During this consultation, the doctor will talk through your medical history with you and assess your suitability for NAD+.
With this information, the doctor will then be able to draw up a unique program that is personalized to suit your requirements. This will include the prescribing of any additional medication and supplements.
Once the consultation is complete, you will be introduced to your supporting nurse who will settle you into the IV Treatment Room. The nurse will check your vital signs and ensure that you are comfortable, before attaching you to the intravenous drip and begin the treatment.
Does the process differ according to the condition being treated?
NAD+ is used to treat many different conditions, and each individual patient will clearly have their own personal requirements. Whilst the dose and timescale of the therapy may vary from patient to patient, the process of how the actual NAD+ intravenous infusion is administered is the same for everyone, regardless of their condition.
How long will the NAD+ therapy take?
The length of each NAD+ infusion will vary from patient to patient. You will be advised on the specifics of your own personal therapy during your consultation. It is worth noting that different people can tolerate different drip rates, which will also factor into how long each individual session will take. As a general rule, you should expect to spend the full day at the clinic, to ensure that you have allocated enough time to undergo the full treatment.
Does the treatment hurt?
Aside from the initial insertion of the cannula, NAD+ treatment is pain-free. Occasionally, a patient may experience minor discomfort, in the form of tension in the stomach or slight pressure in the neck, but this can be immediately rectified by simply slowing the drip rate of the NAD+.
How will I feel after the treatment?
As soon as the intravenous drip is disconnected, you will be 100% back to normal. Unlike other treatments, there is no need to lie down or take it easy after the treatment is finished and you will be able to resume all day-to-day activities.
How soon will I feel/see the benefits of NAD+?
Every individual is different, and will respond to the treatment in their own time. Patients generally experience the benefits of NAD+ after the second or third infusion, however some patients have reported feeling a positive change after their very first infusion.
How many NAD+ infusions will I need?
Again, each patient will have different requirements, and you will be advised thoroughly on this during your consultation. An average course of treatment generally takes between 3 – 5 infusions. Patients are strongly recommended to have booster infusions, between 1-3 months after the initial course of treatment, to maintain the positive results.
Are there any side effects?
One of the many positives of NAD+ treatment is that there are no side effects, aside from the possibility of slight discomfort during the treatment itself.
Is it approved by the FDA?
Because NAD+ is a vitamin supplement and naturally produced by the human body, the FDA has not found reason to assess NAD+ therapy.
NAD & CANCER:
1. Loss of SIRT2 leads to axonal degeneration and locomotor disability associated with redox and energy imbalance.
2. Aldehyde dehydrogenase 1A1 increases NADH levels and promotes tumor growth via glutathione/dihydrolipoic acid-dependent NAD+ reduction.
3. Meta-analysis of SIRT1 expression as a prognostic marker for overall survival in gastrointestinal cancer.
4. SIRT6 inhibitors with salicylate-like structure show immunosuppressive and chemosensitizing effects.
(cite: https://www.ncbi.nlm.nih.gov/pubmed/28958848 )
5. Tyrosine Phosphorylation of Lactate Dehydrogenase A Is Important for NADH/NAD+ Redox Homeostasis in Cancer Cells ▿
( http://mcb.asm.org/content/31/24/4938.short )
6. Reactive Oxygen Species Produced by NAD(P)H Oxidase Inhibit Apoptosis in Pancreatic Cancer Cells*
( http://www.jbc.org/content/279/33/34643.short )
7. Association of the NAD(P)H:quinone Oxidoreductase 609C→T Polymorphism with a Decreased Lung Cancer Risk
8. Pharmacological Inhibition of Nicotinamide Phosphoribosyltransferase (NAMPT), an Enzyme Essential for NAD+ Biosynthesis, in Human Cancer
METABOLIC BASIS AND POTENTIAL CLINICAL IMPLICATIONS*
9. NAD(P)H and Collagen as in Vivo Quantitative Fluorescent Biomarkers of Epithelial Precancerous Changes
( http://cancerres.aacrjournals.org/content/62/3/682.short )
10. Subcellular Localization of NAD(P)H:quinone Oxidoreductase 1 in Human Cancer Cells
( http://cancerres.aacrjournals.org/content/62/5/1420.short )
11. The NAD+-dependent Histone Deacetylase SIRT6 Promotes Cytokine Production and Migration in Pancreatic Cancer Cells by Regulating
( http://www.jbc.org/content/287/49/40924.short )
12. Bilirubin decreases nos2 expression via inhibition of NAD (P) H oxidase: implications for protection against endotoxic shock in rats
( http://www.fasebj.org/content/19/13/1890.short )
13. SIRT1, metabolism and cancer
( http://journals.lww.com/co-oncology/Abstract/2012/01000/SIRT1,_metabolism_and_cancer.13.aspx )
14. NAD + -linked 15-hydroxyprostaglandin dehydrogenase (15-PGDH) behaves as a tumor suppressor in lung cancer
15. A Lack of a Functional NAD(P)H:Quinone Oxidoreductase Allele Is Selectively Associated with Pediatric Leukemias That Have MLL Fusions
( http://cancerres.aacrjournals.org/content/59/16/4095.short )
16. Clinical significance of a NAD(P)H: quinone oxidoreductase 1 polymorphism in patients with disseminated peritoneal cancer receiving intraperitoneal
hyperthermic chemotherapy with mitomycin C
( http://journals.lww.com/jpharmacogenetics/Abstract/2002/01000/Clinical_significance_of_a_NAD_P_H__quinone.5.aspx )
17. Altered metabolism in cancer
( https://bmcbiol.biomedcentral.com/articles/10.1186/1741-7007-8-88 )
18. NAD(P)H:quinone oxidoreductase-dependent risk for colorectal cancer and its association with the presence of K-ras mutations in tumors
( https://academic.oup.com/carcin/article/21/10/1813/2908713/NAD-P-H-quinone-oxidoreductase-dependent-risk-for )
19. The SIRT1 Deacetylase Suppresses Intestinal Tumorigenesis and Colon Cancer Growth
( http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0002020 )
20. 15-Hydroxyprostaglandin Dehydrogenase Is Down-regulated in Colorectal Cancer
( http://www.jbc.org/content/280/5/3217.short )
21. NAD(P)H:Quinone Oxidoreductase 1 Deficiency Increases Susceptibility to Benzo(a)pyrene-induced Mouse Skin Carcinogenesis
( http://cancerres.aacrjournals.org/content/60/21/5913.short )
22. An NQO1- and PARP-1-mediated cell death pathway induced in non-small-cell lung cancer cells by β-lapachone
( http://www.pnas.org/content/104/28/11832.short )
NAD AND PTSD
1. Metabolic syndrome, somatic and psychiatric comorbidity in war veterans with post-traumatic stress disorder: Preliminary findings ( https://
2. Serotonin, tryptophan metabolism and the brain-gut-microbiome axis
( http://www.sciencedirect.com/science/article/pii/S0166432814004768 )
3. Stress and glucocorticoid receptor transcriptional programming in time and space: Implications for the brain–gut axis
( http://onlinelibrary.wiley.com/doi/10.1111/nmo.12706/full )
4. Glucocorticoid “Programming” and PTSD
( http://onlinelibrary.wiley.com/doi/10.1196/annals.1364.027/full )
5. Tissue Metabolism of Glucocorticoids: New Controls of Cognitive Function and the Stress Response
( https://link.springer.com/chapter/10.1007/4-431-29567-4_11 )
6. Tissue Metabolism of Glucocorticoids: New Controls of Cognitive Function and the Stress Response
( https://link.springer.com/chapter/10.1007/4-431-29567-4_11 )
7. Microbiome, inflammation, epigenetic alterations, and mental diseases
( http://onlinelibrary.wiley.com/doi/10.1002/ajmg.b.32567/full )
8. THE NORADRENALINE-ADRENALINE-AXIS OF THE FIGHT-OR-FLIGHT EXHIBITS OXYTOCIN AND SEROTONIN ADAPTIVE RESPONSES
( https://search.proquest.com/openview/f544a2eb3adbb2a699dffb2db1064a79/1?pq-origsite=gscholar&cbl=2034862 )
9. ( https://books.google.com/books?
10. SARM1 activation triggers axon degeneration locally via NAD+ destruction
( http://science.sciencemag.org/content/348/6233/453 )
11. The Role of Glutamate in Anxiety and Related Disorders
12. Oxidative Stress in the Progression of Alzheimer Disease in the Frontal Cortex
( https://academic.oup.com/jnen/article/69/2/155/2917186/Oxidative-Stress-in-the-Progression-of-Alzheimer )
13. Resveratrol as a Therapeutic Agent for Neurodegenerative Diseases
( https://link.springer.com/article/10.1007/s12035-010-8111-y )
14. Neonatal endotoxin exposure modifies the acoustic startle response and circulating levels of corticosterone in the adult rat but only following
( http://www.sciencedirect.com/science/article/pii/S0022395607002130 )
15. Critical role of NADPH oxidase in neuronal oxidative damage and microglia activation following traumatic brain injury
( http://journals.plos.org/plosone/article/figures?id=10.1371/journal.pone.0034504 )
NAD and addiction
1. Operant Behavior and Alcohol Levels in Blood and Brain of Alcohol-Dependent Rat
( http://onlinelibrary.wiley.com/doi/10.1111/j.1530-0277.2009.01051.x/full )
2. Role of diacetyl metabolite in alcohol toxicity and addiction via an electron transfer and oxidative stress
( https://link.springer.com/article/10.1007/s00204-004-0602-z )
3. 1H-Nuclear magnetic resonance-based metabolomic analysis of brain in mice with nicotine treatment
( https://bmcneurosci.biomedcentral.com/articles/10.1186/1471-2202-15-32 )
4. Isoquinolines, beta-carbolines and alcohol drinking: Involvement of opioid and dopaminergic mechanisms
( https://link.springer.com/article/10.1007/BF01952025 )
5. Substance-specific and shared transcription and epigenetic changes in the human hippocampus chronically exposed to cocaine and alcohol
( http://www.pnas.org/content/108/16/6626.short )
NAD and anxiety/ depression
1. SIRT1 Activates MAO-A in the Brain to Mediate Anxiety and Exploratory Drive
( http://www.sciencedirect.com/science/article/pii/S0092867411013742 )
2. The Biological Underpinnings of Mood Disorders Interact with Early Trauma, Sexual Abuse and Neuroticism: Implications for Psychiatric Classification
3. Diagnostic and predictive metabolite patterns for disorders affecting the brain and nervous system
( https://www.google.com/patents/US20160209428 )
4. Glucocorticoids, Stress, and Fertility
( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3547681/ )
5. Role of Sirtuins in Linking Metabolic Syndrome with Depression.
( https://www.ncbi.nlm.nih.gov/pubmed/27065808 )
6. Pharmacological targeting of redox regulation systems as new therapeutic approach for psychiatric disorders: A literature overview.
( https://www.ncbi.nlm.nih.gov/pubmed/26995306 )
7. ( multiple related articles ) Sleep fragmentation induces cognitive deficits via nicotinamide adenine dinucleotide phosphate oxidase-dependent
pathways in mouse.
( https://www.ncbi.nlm.nih.gov/pubmed/21868506 )
( https://www.ncbi.nlm.nih.gov/pubmed/28185898 )
( https://www.ncbi.nlm.nih.gov/pubmed/28093238 )
( https://www.ncbi.nlm.nih.gov/pubmed/26481044 )
( https://www.ncbi.nlm.nih.gov/pubmed/25596911 )
( https://www.ncbi.nlm.nih.gov/pubmed/24184921 )
( https://www.ncbi.nlm.nih.gov/pubmed/25401165 )
8. Chronic Fatigue[Nicotinamide adenine dinucleotide (NADH) in patients with chronic fatigue syndrome].
9. Exploring the therapeutic space around NAD+
( http://jcb.rupress.org/content/199/2/205 )
10. Role of Nicotinamide in DNA Damage, Mutagenesis, and DNA Repair
( https://www.hindawi.com/journals/jna/2010/157591 )
11. Genome-Wide and Gene-Based Association Studies of Anxiety Disorders in European and African American Samples
( http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0112559 )
12. Levels of Nicotinamide Adenine Dinucleotide and Reduced Nicotinamide Adenine Dinucleotide in Facultative Bacteria and the Effect of Oxygen
( http://jb.asm.org/content/111/1/24 )
NAD and longevity
1. The NAD+/sirtuin pathway modulates longevity through activation of mitochondrial UPR and FOXO signaling
( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3753670/ )
2. NAD+ Shown to Reverse Aging Biomarkers
( http://www.lifeextension.com/Magazine/2016/7/NAD-Shown-to-Reverse-Aging-Biomarkers/Page-01 )
3. The anti-aging pill
( https://www.technologyreview.com/s/534636/the-anti-aging-pill/ )
4. Scientists unveil a giant leap for anti-aging
( https://www.sciencedaily.com/releases/2017/03/170323141340.htm )
5. NAD Precursor NMN Improves DNA Repair in Mice
( https://www.fightaging.org/newsletter/ )
6. Antioxidants and Free Radical Scavengers for the Treatment Of Stroke, Traumatic Brain Injury and Aging
( http://www.ingentaconnect.com/content/ben/cmc/2008/00000015/00000004/art00009 )
7. The NAD+ precursor nicotinamide riboside enhances oxidative metabolism and protects against high-fat diet induced obesity
( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3616313/ )
8. Intracellular nicotinamide adenine dinucleotide promotes TNF-induced necroptosis in a sirtuin-dependent manner
( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4815976/ )
9. Nicotinamide adenine dinucleotide suppresses epileptogenesis at an early stage
( https://www.nature.com/articles/s41598-017-07343-0 )
10. Protecting Axonal Degeneration by Increasing Nicotinamide Adenine Dinucleotide Levels in Experimental Autoimmune Encephalomyelitis
( http://www.jneurosci.org/content/26/38/9794 )
11. Emerging therapeutic roles for NAD+ metabolism in mitochondrial and age-related disorders
( https://clintransmed.springeropen.com/articles/10.1186/s40169-016-0104-7 )
12) Stimulation of Nicotinamide Adenine Dinucleotide Biosynthetic Pathways Delays Axonal Degeneration after Axotomy
( http://www.jneurosci.org/content/26/33/8484/tab-figures-data )
13) Effect of nicotinamide mononucleotide on brain mitochondrial respiratory deficits in an Alzheimer’s disease-relevant murine model
( https://bmcneurol.biomedcentral.com/articles/10.1186/s12883-015-0272-x )
14) Oxidative stress and brain aging: is zinc the link?
( https://link.springer.com/article/10.1007/s10522-006-9045-7 )
NAD and Performance
1. Simultaneous extraction and reverse-phase high-performance liquid chromatographic determination of adenine and pyridine nucleotides in human
red blood cells
( http://www.sciencedirect.com/science/article/pii/0003269785904051 )
2. Identification of NAD interacting residues in proteins
( https://bmcbioinformatics.biomedcentral.com/articles/10.1186/1471-2105-11-160 )
3. Extracellular NAD+ Is an Agonist of the Human P2Y11 Purinergic Receptor in Human Granulocytes*
( http://www.jbc.org/content/281/42/31419.short )
4. Alcohol:NADGraphic Oxidoreductase Is Present in Rat Liver Peroxisomes (*)
( http://www.jbc.org/content/270/1/37.short#fn-1 )
5. Coupling of histone deacetylation to NAD breakdown by the yeast silencing protein Sir2: Evidence for acetyl transfer from substrate to an NAD
( http://www.pnas.org/content/98/2/415.short )
6. Methanol Production via Bioelectrocatalytic Reduction of Carbon Dioxide: Role of Carbonic Anhydrase in Improving Electrode Performance
( http://esl.ecsdl.org/content/14/4/E9.short )
7. The Effect of Antioxidant Supplementation on Fatigue during Exercise: Potential Role for NAD+(H)
( http://www.mdpi.com/2072-6643/2/3/319/htm )
8. Towards Recyclable NAD(P)H Regeneration Catalysts
( http://www.mdpi.com/1420-3049/17/8/9835/htm )
9. The Proposed Effects of Nicotinamide Adenine Dinucleotide (NAD) Supplementation on Energy Metabolism
( http://pubs.sciepub.com/ajssm/3/5/3/index.html )
10. B Vitamins and the Brain: Mechanisms, Dose and Efficacy—A Review
( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4772032/ )
11. The Effects of Nicotinamide Adenine Dinucleotide (NAD) on Brain Function and Cognition (NAD)
( https://clinicaltrials.gov/ct2/show/NCT02942888 )
12. Does Oral Coenzyme Q10 Plus NADH Supplementation Improve Fatigue and Biochemical Parameters in Chronic Fatigue Syndrome?
( http://online.liebertpub.com/doi/full/10.1089/ars.2014.6181 )
13. Aspects of Tryptophan and Nicotinamide Adenine Dinucleotide in Immunity: A New Twist in an Old Tale
( http://pubmedcentralcanada.ca/pmcc/articles/PMC5476425/ )
14. Kinetic Analysis of Bifidobacterial Metabolism Reveals a Minor Role for Succinic Acid in the Regeneration of NAD+ through Its Growth-Associated
( http://aem.asm.org/content/72/8/5204.short )
15. Alkaline extraction and reverse-phase high-performance liquid chromatography of adenine and pyridine nucleotides in human platelets
( http://www.sciencedirect.com/science/article/pii/0003269787902855 )
16. Beta-Lapachone, a Modulator of NAD Metabolism, Prevents Health Declines in Aged Mice
( http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0047122 )
17. New biotechnological perspectives of a NADH oxidase variant from Thermus thermophilus HB27 as NAD+-recycling enzyme
( https://bmcbiotechnol.biomedcentral.com/articles/10.1186/1472-6750-11-101 )
18. Mitochondria-Driven Changes in Leaf NAD Status Exert a Crucial Influence on the Control of Nitrate Assimilation and the Integration of Carbon
and Nitrogen Metabolism
( http://www.plantphysiol.org/content/139/1/64.short )
19. Quantitative evaluation of yeast’s requirement for glycerol formation in very high ethanol performance fed-batch process
( https://microbialcellfactories.biomedcentral.com/articles/10.1186/1475-2859-9-36 )
20. The Ferredoxin:NAD+ Oxidoreductase (Rnf) from the Acetogen Acetobacterium woodii Requires Na+ and Is Reversibly Coupled to the Membrane
( http://www.jbc.org/content/288/44/31496.short )
21. Cerebrospinal fluid levels of inflammation, oxidative stress and NAD+are linked to differences in plasma carotenoid concentrations
( https://jneuroinflammation.biomedcentral.com/articles/10.1186/1742-2094-11-117 )
22. INHIBITION OF MITOCHONDRIAL RESPIRATION BY SODIUM NITROPRUSSIDE AND THE MECHANISM OF CYANIDE LIBERATION
( https://academic.oup.com/bja/article/49/12/1239/286079/INHIBITION-OF-MITOCHONDRIAL-RESPIRATION-BY-SODIUM )
NAD and traumatic brain injury
1. Study of Generalized Anxiety Disorder in Traumatic Brain Injury
( http://imsear.li.mahidol.ac.th/handle/123456789/181868 )
2. Alpha-synuclein immunoreactivity is present in axonal swellings in neuroaxonal dystrophy and acute traumatic brain injury
( https://search.proquest.com/openview/ed34ebdbe6b261c4d0fdf99ceb9bffbf/1?pq-origsite=gscholar&cbl=40718 )
3. Metabolic Crisis without Brain Ischemia is Common after Traumatic Brain Injury: A Combined Microdialysis and Positron Emission Tomography
( http://journals.sagepub.com/doi/abs/10.1038/sj.jcbfm.9600073 )
4. Mitochondrial Dysfunction and Calcium Perturbation Induced by Traumatic Brain Injury
( http://online.liebertpub.com/doi/abs/10.1089/neu.1997.14.23 )
5. Identification of poly-ADP-ribosylated mitochondrial proteins after traumatic brain injury
( http://onlinelibrary.wiley.com/doi/10.1111/j.1471-4159.2007.05114.x/full )
6. Neuroprotection for traumatic brain injury: translational challenges and emerging therapeutic strategies
( http://www.sciencedirect.com/science/article/pii/S0165614710001689 )
7. Local Administration of the Poly(ADP-Ribose) Polymerase Inhibitor INO-1001 Prevents NAD+ Depletion and Improves Water Maze Performance
after Traumatic Brain Injury in Mice
( http://online.liebertpub.com/doi/abs/10.1089/neu.2007.0305 )
8. used twice) Antioxidants and Free Radical Scavengers for the Treatment Of Stroke, Traumatic Brain Injury and Aging
( http://www.ingentaconnect.com/content/ben/cmc/2008/00000015/00000004/art00009 )
9. (major) Pharmacologic Inhibition of Poly(ADP-Ribose) Polymerase Is Neuroprotective Following Traumatic Brain Injury in Rats
( http://online.liebertpub.com/doi/abs/10.1089/089771501750170912 )
10. Bench-to-bedside review: Apoptosis/programmed cell death triggered by traumatic brain injury
( https://ccforum.biomedcentral.com/articles/10.1186/cc2950 )
11. Omega-3 Fatty Acids Supplementation Restores Mechanisms that Maintain Brain Homeostasis in Traumatic Brain Injury
( http://online.liebertpub.com/doi/abs/10.1089/neu.2007.0313 )
12. Age-dependent reduction of cortical contusion volume by ketones after traumatic brain injury
( http://onlinelibrary.wiley.com/doi/10.1002/jnr.20633/full )
13. Mice Lacking Catalase Develop Normally but Show Differential Sensitivity to Oxidant Tissue Injury*
( http://www.jbc.org/content/279/31/32804.short )
14. Attenuation of brain edema and spatial learning deficits by the inhibition of NADPH oxidase activity using apocynin following diffuse traumatic
brain injury in rats
( https://www.spandidos-publications.com/mmr/7/1/327 )
15. Erythropoietin Prevents Secondary Brain Injury Induced by Cortical Lesion in Mice: Possible Involvement of Nrf2 Signaling Pathway
( http://www.annclinlabsci.org/content/41/1/25.short )
16. GPI 6150 Prevents H2O2 Cytotoxicity by Inhibiting Poly(ADP-ribose) Polymerase
( http://www.sciencedirect.com/science/article/pii/S0006291X00938166 )
17. Interactions between SIRT1 and MAPK/ERK regulate neuronal apoptosis induced by traumatic brain injury in vitro and in vivo
( http://www.sciencedirect.com/science/article/pii/S0014488612002816 )
18. The Contribution of the Blood Glutamate Scavenging Activity of Pyruvate to its Neuroprotective Properties in a Rat Model of Closed Head Injury
( https://link.springer.com/article/10.1007/s11064-007-9548-x )
19. Physiologic progesterone reduces mitochondrial dysfunction and hippocampal cell loss after traumatic brain injury in female rats
( http://www.sciencedirect.com/science/article/pii/S0014488605003493 )
20. Effect of indomethacin pretreatment on acute mortality in experimental brain injury
( http://thejns.org/doi/abs/10.3171/jns.1989.71.4.0565 )