New Research Supports Niacin For Parkinsons Disease Treatment
New research1 further supports the use of Niacin in the treatment and long-term management of Parkinsons Disease . Parkinsons disease occurs when dopaminergic neurons in the substantia nigra are lost the loss of dopamine causes the neurological manifestations of PD. This loss of dopaminergic function can have various etiologies, but as Dr. Miguel Martins, lead researcher of the study points out,
in some hereditary cases, the main problem is unhealthy mitochondria.
The role of dysfunctional mitochondria in the pathogenesis of PD has been explained before2, as a cascade of events which includes cellular insult leading to a decreased membrane potential and more permeable transitional pores. The increased pore permeability, in turn, leads to a depletion of NAD+ and ultimately cell death.
Trial Shows Increasing Brain Nad+ Improves Parkinsons
In clinical study, Norwegian researchers show that supplementation with NAD+ precursor NR improves underlying defects of Parkinsons disease.
Key Points:
- NR supplementation increases brain NAD+ levels and reduces brain activity in regions typically active in patients with Parkinsons disease.
- Changes in brain patterns following NR supplementation were strongly correlated with improved physical performance.
- NR activates genes that repress Parkinsons disease drivers: oxidative stress, mitochondrial dysfunction, and brain inflammation .
Outstanding Questions And Future Perspectives
Recent studies on animals and human clinical trials have expanded our understanding of NAD+ and NAD+-dependent enzymes in neuroplasticity, brain aging, and neurodegenerative disorders. Emerging evidence suggests NAD+ depletion in brain cells is common during aging and is accentuated in many neurodegenerative disorders including AD, PD, HD, and ALS, and that NAD+ augmentation inhibits pathological features in animal models of these disorders . Emerging findings are revealing a critical role for NAD+ in neural resilience and in the molecular mechanisms of the hallmarks of brain aging. Although NAD+ depletion occurs in vulnerable neuronal populations in several major neurodegenerative diseases, it remains to be established whether impaired NAD+-dependent processes occur upstream and/or downstream of the specific proteopathic lesions that define each of the neurodegenerative diseases .
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Nad For Addiction Treatment
There is considerable interest in making NAD available for the treatment of addiction, but there is a lack of published evidence showing that this therapy is effective.
One provider claims:
It has been determined that the excessive use of drugs and alcohol will deplete the bodys natural stores of NAD. Because of this, the brain cannot receive the same energy it usually would from breaking down food. NAD Therapy floods the brain with the co-enzyme to replenish its stores, providing 4 key effects.
- It flushes out all of the drugs that are still in the users system.
- It reduces withdrawal effects, which can be extremely difficult and uncomfortable to tolerate.
- It curbs the cravings for alcohol and Opioids and lessens the pain of withdrawal, making recovery easier physically and mentally.
- It allows the body to produce energy more naturally, without a crash or jitters like Caffeine and sugar or the negative effects that come with other substances.
From an investigation into NAD marketing conducted by NPR in 2019:
There is no published evidence to show that NAD therapy has any benefit in the treatment of addiction. But that hasnt stopped an industry from flourishing:
Clinical Trials Of Nir Light:
Intracerebral NIR 670 nm implanted device
The Clinical Trial for Near Infrared Endoventricular Illumination is taking place in France and is being conducted by one of the pioneers in deep brain stimulation surgery. In this trial, a device is implanted in the brain that emits NIR light.
Transcranial and intranasal NIR stimulation
This trial is testing two other delivery methods of NIR light a helmet with light sources and intranasal delivery.
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How Nad Therapy Can Help Parkinsons Disease
Parkinsons disease neurological deterioration and the arising motor dysfunction are triggered by the formation of Lewy body and the death of dopaminergic neuronal within the substantia nigra. Impaired function of the mitochondrial and incorrect cellular metabolism of the reactive oxygen species are the two factors known to cause apoptosis which is related to PD.
What is Parkinsons Disease?
Parkinsons disease is the world second largest neurodegenerative illness among older adults. It is characterized by motor functionality disturbances such as bradykinesia, muscular rigidity, and resting tremors.
The part of the brain responsible for motor control releases a compound known as nicotinamide adenine dinucleotide which is said to ease PA symptoms. In a mouse study of the disease, it has also been clinically proven to reduce the neurons that produce dopamine. NAD is a substance that activates the action of an enzyme.
Research shows that the causative mechanism of Parkinsons disease involves inactive mitochondria, genetics, and oxidative stress. These then trigger an imbalance between the ability of the cells to detoxify free radicals and the production of free radicals. The cellular and the molecular changes that occur destroy dopamine-producing neurons. This is the nerve cell that dies in PA.
Studies show that NAD is crucial in the metabolism of healthy cellular redox and the production of energy in the mitochondrial.
Case Study on NAD Therapy
The Rodent Model
Summary
Gene Therapies Targeting Mitochondrial Dysfunction In Parkinsons Disease
Gene therapy entails the treatment of disease via delivery of a transgene that either replaces or corrects a defective gene or is generally supportive of cells in the disease environment . Gene therapy vectors can be either viral or non-viral .
Autosomal recessive mutations in the PRKN gene cause loss of function or inactivation of the parkin protein . Overexpression of PRKN has been shown to have a protective effect against numerous cellular insults . For example, overexpression of wild type parkin in a transgenic mouse model was shown to alleviate MPTP-induced dopaminergic neurodegeneration via protection of mitochondria and decreased striatal alpha-synuclein . Furthermore, recombinant AAV vector-mediated intranigral delivery of parkin prevented motor deficits and dopaminergic cell loss in a chronic MPTP-minipump mouse model of PD .
Loss of function mutations in PINK1 can also lead to autosomal recessive PD . Removal of Drosophila PINK1 homologue function leads to male sterility, apoptotic muscle degeneration, defects in mitochondrial morphology and increased sensitivity to multiple stressors including oxidative stress. In a portion of PINK1 mutants, expression of human PINK1 in the Drosophila testes restores male fertility and normal mitochondrial morphology .
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Nad Treatment For Alzheimers Disease
If you are a loved one is struggling with Alzheimers disease call us at to get an assessment and see if Dr. Milgram can help with an NAD infusion.
Alzheimers disease is defined as a chronic neurodegenerative disease that is associated with loss of memory, coordination, and spatial awareness, among other things.
NAD is essential to living and is found in every cell of all living things. There is much more NAD in the bodies of babies and growing adults. Declining NAD is due to the inability of our cells to recycle NAD, or to synthesize new NAD. This decline is associated with Alzheimers.
Available Light Therapy Devices
Because light therapy delivered via the eyes or the skin has minimal side effects, multiple light-emitting devices have already been designed, marketed, and are available for purchase without FDA approval.
These white light and red-light devices are currently marketed for treatment of depression, chronic pain, wrinkles, wound healing, acne, and sleep improvement. There are no white light or red-light therapy devices yet on the market that are designed and marketed specifically for Parkinsons disease.
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Past Data On Light Therapy For Parkinsons Disease
Many studies of light therapy in animal models of PD have supported the testing of light therapy in people with PD.
There have been nine completed clinical trials so far. Seven investigated white light, one investigated blue light, and one investigated NIR light, and each selected a set of variables to utilize in conducting the clinical trial. The white light trials tested intensities ranging from 1000-10,000 lux and duration of light exposure ranging from 30 minutes to 1.5 hours. The trials also varied when the light stimulation was presented either in the morning , in the evening or twice daily.
Although the trials were small, all of them showed promising results as it related to improvement of various PD symptoms.
Trial: Case series 2007Light parameters: 1000-1500 Lux for 1-1.5 hours, one hour prior to sleep# of patients: 12Results: Improvement in various motor and non-motor symptoms: Willis and Turner
Light parameters: Transcranial and intra-oral infrared light # of patients: 22Results: Montreal cognitive assessment remained stable over the 4 weeks of treatment. There were some trends to improvement in fine motor tasks, but did not reach statistical significance: Bullock-Saxton, et alReference:
Ask Your Nad Therapy Provider These Questions
- Ask Your NAD Therapy Provider These Questions
NAD stands for Nicotinamide Adenine Dinucleotide. NAD is very effective in eliminating drug withdrawal and cravings. Additionally, it is effective for improving neurocognitive impairments like brain fog, dementia, Parkinsons disease, chronic headaches and some types of neuropathic pain. Because NAD programs require a substantial investment of both time and money, Ive put together a short checklist of questions to ask your prospective NAD program.
Its not as simple as just getting an infusion and going home, although many providers think it is. Like any specialized area of medicine, you want to be under the care of someone with an area of expertise in the field and in the medications used to treat these conditions.
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Iv Nad And Parkinsons
Intravenous Administration of Nicotinamide Adenine Dinucleotide Alleviates Tremors Associated With Parkinsons Disease: A Case Report.
*L. RUTHERFORD1, S. L. BROOM2, T. OLDS1,3, R. F. MESTAYER1,3, P. NORRIS-MESTAYER11Springfield Wellness Center, Springfield, LA 2Dept Psychology, William Carey Univ., Hattiesburg, MS 3NAD Research, Inc., Springfield, LA
Introduction
A number of pharmacological agents currently exist for treating symptoms associated with Parkinsons Disease , however these drugs are not optimal because they typically target dopamine reuptake in depleted dopaminergic systems. Nicotinamide Adenine Dinucleotide is present in all cells and serves a vital role in cell and mitochondrial function in fact, disruption or depletion of NAD+ is associated with a number of disease states, including those associated with dopaminergic dysfunction. Clinicians in Springfield, LA previously developed an intravenous administration protocol of NAD+ for a patient experiencing symptoms associated with PD. Subsequent observation of a rapid and sustained reduction of Parkinsons symptoms were noted such as gait rigidity, slurred speech, shuffle steps, cognitive impairment and tremors. This previous case study provides rationale for further describing and quantifying the positive effects of IV BR+NAD on symptoms associated with PD.
Methods
Acknowledgements
Thank you to Springfield Wellness Center for providing the setting and clinical staff in support for this project.
Nad+ Synthesis In Cells
Nicotinamide adenine dinucleotide is a fundamental molecule in health and disease, as it is central to several cellular bioenergetic functions. NAD+ is synthesized via three major pathways, including de novo biosynthesis, the Preiss-Handler pathway, and the salvage pathway . While the aspartate pathway is the de novo NAD+ pathway in most photosynthetic eukaryotes, the kynurenine pathway is the only de novo NAD+ synthetic pathway in mammals. The kynurenine pathway starts with the catabolism of the amino acid tryptophan that is converted via two steps to the intermediate kynurenine, which can generate NAD+, kynurenic acid, or xanthurenic acid . The kynurenine pathway modulates neuronal functions as it is involved in the synthesis of two fundamental neuro-transmitters as well as regulates N-methyl-D-aspartate receptor activity and free radical production . The kynurenine pathway exhibits double-edged sword effects on neurons with both neuroprotective metabolites and neurotoxic intermediates, including 3-hydroxykynure-nine that generates free radicals, 3-hydroxyanthranilic acid , and quinolinic acid . While kynurenic acid is an NMDA receptor antagonist, quinolinic acid is an NMDA receptor agonist . The ambient levels of these metabolites are determined by different enzymes, which in the brain are preferentially localized in microglia and astrocytes, suggesting necessary glial cell-neuron communication .
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Overview Of Parkinsons Disease
Parkinsons is a neurodegenerative movement disorder whose symptoms progressively worsen over time. A broad spectrum of drugs have been developed to treat Parkinsons symptoms, with dismal success rates.
Parkinsons affects the central nervous system, causing cellular damage in the brain that leads to a severe drop in dopamine levels. Dopamine is an important chemical neurotransmitter that helps to deliver messages between the brain and the body, governing movement.
Early symptoms of Parkinsons disease include:
- A slight tremor in one hand
- Shrinking handwriting
- Sleep disrupted with night terrors and violent thrashing
- Reduced balance
- rinary and fecal incontinence
- nability to perform activities of daily living like dressing, bathing, and eating
As Parkinsons approaches its end game, palliative care and hospice with pain management are the final treatment approaches.
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Mutation Of Parp Rescues Mitochondrial Dysfunction Of Pink1 Mutants
Depletion of cellular NAD+ levels has been linked to enhanced oxidative stress, which causes activation of the NAD+-consuming PARP enzymes . We have previously shown that Drosophila parkin mutants have increased levels of the oxidative stress markers methionine sulfoxide and homocysteine, a marker of oxidative stress and a metabolite that generates reactive oxygen species upon auto-oxidation, respectively .
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Clinical Trials Of White Light:
Bright vs dim light
Bright light therapy is being compared to dim red-light therapy delivered twice daily. Outcome measures include an assessment of excessive daytime sleepiness and a general scale of non-motor symptoms in PD.
SunRay light boxes
This trial will also compare bright white vs. dim red light stimulation, with light to be administered via the SunRay light box. Outcome measures include assessment of sleep and fatigue.
DayVia lamp
This trial will compare bright light vs control light. The outcome measures will be United Parkinson Disease Rating Scale scores.
Within the DB RCT for Specialized Phototherapy trial, double-blinded and randomized comparing the Celeste device to a control light. PDQ 39, a measurement of quality of life, will be the primary outcome measure. Other endpoints will be UPDRS scores of motor and non-motor symptoms. This trial has not started yet.
Parkinsons Disease Is A Neurodegenerative Disorder
If someone you love has been diagnosed with a neurodegenerative disease, this can be difficult to process. Neurodegenerative disorders can be overwhelming, seeming to strip someone of his or her identity. Even though your loved one is physically there, he or she might change so much that he or she is difficult to recognize. One of the most common neurodegenerative disorders is called Parkinsons Disease.
When someone you love has Parkinsons Disease, this can erode the fabric of who that person is. In this manner, Parkinsons Disease has an impact on not only the individual with the diagnosis but also his or her family members and friends. Therefore, it is important to understand how Parkinsons Disease manifests as well as some of the common symptoms.
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What Does Parkinsons Disease Look Like
If someone you love has been diagnosed with Parkinsons Disease, this can present in a variety of ways. Parkinsons Disease impacts the neurons in the brain. Nerves are responsible for carrying motor signals from the brain to the rest of the body. Then, nerves carry signals regarding pain, temperature, and pressure back to the brain for processing.
As Parkinsons Disease progresses, it damages the nerves in the brain. This can lead to symptoms such as:
- Tremors: Patients with Parkinsons Disease usually develop tremors and shakes that start in one part of the body and progress elsewhere. One of the most common symptoms is called a pill-rolling tremor, where the person appears to be rubbing a pill between the thumb and index finger.
- Bradykinesia: This means that Parkinsons Disease leads to slow movements. Simple tasks become time-consuming. It might be hard to walk, get out of a chair, and take the stairs.
- Rigidity: People with Parkinsons Disease notice that their muscles become rigid. This can lead to chronic pain and flexibility issues.
- Poor Balance: Over time, people with Parkinsons Disease will have issues with their posture. They may become stooped, which can lead to serious balance problems.Writing Issues: Because simple tasks become difficult, people with Parkinsons Disease often notice that their writing becomes small and difficult to read.
Nr Affects Genes Linked To Oxidative Stress Mitochondrial Dysfunction And Brain Inflammation
Since oxidative-induced injury drives Parkinsons disease progression, investigators wanted to see if NR affected any genes responsible for combating oxidative stress. By looking at messenger RNA molecules, intermediate templates for protein formation, Brakedal and colleagues noticed significantly higher levels of the gene KLF2, which upon activation, turns on another protein that serves to guard against oxidative damage. Moreover, this finding demonstrates NRs ability to block one of the key players that promote Parkinsons disease progression.
NR activates genes that hinder Parkinsons disease promoters
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Nad Therapy For Parkinsons Disease Treatment
NAD therapy can restore your brains levels of the chemical nicotinamide adenine dinucleotide. Usually, every cell in your body produces this chemical. However, for various reasons, your NAD levels may drop. This is important because NAD helps sustain some of your bodys most important functions. That includes the automatic repair of damaged DNA. It also includes controlling your metabolism and the rate at which you age. Low levels of NAD may interfere with these essential processes. During NAD therapy, you receive IV doses of nicotinamide adenine dinucleotide. The amount of the chemical supplied in these doses is high enough to produce a therapeutic effect.
Parkinsons disease is associated with low NAD levels. If you receive NAD therapy during the early stages of the disease, you can reverse this deficit. The net effect is often a slowdown in the progression of Parkinsons. In turn, this slowdown helps you limit your symptoms for as long as possible.
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What Does Nad+ Do
NAD+ stands for Nicotinamide Adenine Dinucleotide, and is an essential molecule found in every cell of your body. It is a coenzyme of Vitamin B3 , which means its a small helper molecule that binds to a protein molecule in order to activate an enzyme. Enzymes are responsible for over 5,000 different biochemical reactions throughout the body and NAD+participates in more reactions than any other vitamin-derived molecule.
Gene Expression
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