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Does Restore Gold Work For Parkinson’s Disease

How Parkinsons Disease Affects Your Brain

Keith is now enjoying retirement with Restore Gold

Weve already covered the macro-level concepts as it regards how Parkinsons works, but everyday consumers and researchers alike need to learn the underlying mechanisms involved in both a healthy and Parkinsons-affected brain in order to appreciate how therapeutic agents like cannabidiol can help.

How Your Brain Is Supposed to Work

The billions of nerve cells in your brain use cable-like extensions called axons to transmit impulses from one neuron to the next.

When an outgoing impulse or message reaches the end of an axon, it approaches a gap between the sending and receiving nerves known as the synapse.

The impulse is then ferried across the synapse by a specific chemical messenger, or neurotransmitterdopamine in this instance.

Once the dopamine accomplishes its job of getting the impulse across the synapse to the receiving neuron, it is broken down by enzymes.

How Your Brain Works with Parkinsons Disease

In the case of PD, the cells that produce dopamine die off for an unknown reason.

When the dopamine deficiency reaches 80 percent, the more readily recognizable symptoms of tremors and rigidity begin to manifest as communication between neurons is seriously impaired.

The immune system activates microglia in response to the rampant destruction of dopamine-producing cells microglia are a type of immune cell that cause inflammation and further damage to neurons when overstimulated.

How does cannabidiol counteract these harmful developments, you might be wondering?

Anticholinergics For Early On

The first pharmacological agents used in PD therapy were anticholinergic drugs. They reduce the activity of acetylcholine by acting as antagonists at choline receptors, hoping to restore the balance between dopamine and acetylcholine levels that was disturbed by PD. These drugs have largely been replaced by L-DOPA and other centrally acting dopaminergic agonists, but they still remain available for use in the treatment of PD. Benztropine, biperiden, diphenhydramine, ethopropazine, orphenadrine, procyclidine, and trihexyphenidyl are included in this therapeutic class of drugs, though there is little pharmacokinetic information available on them because of their low plasma drug concentrations. Typically, anticholinergic drugs have a greater role in tremor-predominant PD and can be a monotherapy in early stages, but are usually done in adjunct with L-DOPA or other prescribed medications.

The Search For Biomarkers And Neuroprotective Therapies: Future Challenges In Pd

The therapeutic approaches discussed so far highlight the progress that has been made toward the development of symptomatic PD therapies. However, one of the most important challenges PD researchers and physicians have faced has not been successfully overcome, ie, the discovery of biomarkers that could predict disease onset, and, thus, guide the use of neuroprotective treatments. Knowing that PD motor symptoms develop only when the dopaminergic denervation of the striatum has reached 7080%, and that as much as 50% of SNc dopaminergic neurons are lost, the identification of such biomarkers is absolutely essential for the effective use of neuroprotective therapies that could alter the progression and course of the disease. The current lack of such markers most likely explains the numerous disappointing failures of neuroprotective clinical trials that have been completed during the past 10 years .

There are many potential biomarkers and early nonmotor clinical signs of PD that are currently being considered in combination to identify at-risk PD patients . In the final section of this review, we will discuss the current status of knowledge of each of these approaches, and critically examine their limitations in their application toward early PD diagnosis.

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How Many People Are Affected By Parkinsons Disease

The Parkinsons Foundation reports that 60,000 Americans are diagnosed with PD annually, and the total number of diagnosed people is approaching one million nationally and ten million globally.

Also of note is the diseases affinity for men, who are affected at one and a half times the rate that women are.

Though researchers havent been able to find a cure, they use large-scale prevalence studies to determine who has the disease, where it is most concentrated, and how resources can be best distributed.

Depending on the precise area of the brain affected and the progression of the disease, PD sufferers can experience an entire spectrum of symptoms beyond movement issues.

Basics Of Parkinsons Disease

Does Restore Gold Work For Parkinson

Parkinsons disease , or paralysis agitans, is a common neurodegenerative condition, which typically develops between the ages of 55 and 65 years. This disease was first named and described by James Parkinson in 1817. The progression of this disease is gradual and prolonged. It has a plausible familial incidence, although the estimates of these occurrences are low and usually sporadic. This disease is organized into two classifications: genetic and sporadic. Genetic PD follows Mendelian inheritance. Sporadic PD, which accounts for about 90% of all Parkinsons cases, is a more complex category in which the pathogenic mechanisms that underlie it are not yet fully understood. Nonetheless, it is known that the byzantine interactions of genetic and environmental influences play roles in the determination of sporadic PD. Several subtypes of PD exist. Each has its own set of causative factors and susceptibilities, pathology, and treatment courses. General risk factors, symptoms, and pathology will be discussed first, before addressing some of the subtypes.

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Parkinsons Disease Symptoms Of Dementia

Up to one-third of people living with Parkinsons disease experience dementia, according to the Parkinsons Disease Foundation. Problems with dementia may include trouble with memory, attention span, and what is called executive function the process of making decisions, organizing, managing time, and setting priorities.

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How Can I Submit A Review For The Restore Gold

Only those who are verified buyers of Restore Gold can submit a review. After purchasing a Restore Gold, review requests are sent to customers periodically by an independent company we chartered to collect reviews from our customers. This ensures accurate and honest reviews from those who have actually purchased our products. At three months, six months, and twelve months, we also send out surveys to collect anonymous data about ones experience with Restore Gold.

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What Is Revive Tcm Gold

Revive TCM Gold is a natural libido enhancement formula and, like other enhancement supplements, also contain extracts of natural herbal medicine. It is said to be derived from Ancient Traditional Chinese Medicine and used as a treatment for decreased libido in both men and women. It also brings back the balance between body hormones that usually deteriorate as people grow older.

Problem #3 Neural Inflammation And Oxidation

He took Restore Gold and then things began to happen with his Parkinson’s

Inflammatory responses contribute to the perpetuation of neurodegeneration in Parkinsonss disease. The brain contains immune cells called microglia, which are known to be activated in Parkinsons disease . Upon activation, microglia release inflammatory cytokines that can spread to nearby healthy neurons and cause degeneration. Dopaminergic neurons in the substantia nigra, the brain region most affected by Parkinsons disease, express receptors for an inflammatory cytokine called Tumor Necrosis Factor-alpha , which suggests that excess TNF-alpha released by nearby activated microglia may damage nigral dopaminergic cells.

Elevated cytokines in the brain of those with Parkinsons disease is a consequence of neurodegeneration . In experimental models, exposure to the neurotoxin MPTP leads to death of dopaminergic neurons. Interestingly, in monkeys, inflammation is increased even years after initial exposure to MPTP . This suggests that inflammation, once initiated, has long-term consequences in Parkinsons disease.

As dopaminergic cells succumb to either environmentally or genetically induced mitochondrial dysfunction, they release free radicals. These free radicals then activate nearby microglial cells, which in turn, excrete inflammatory cytokines that bind to and damage nearby dopaminergic neurons. This positive feedback loop may continue over years or even decades and slowly contribute to the loss of dopaminergic neurons that leads to Parkinson symptoms .

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The Next Stages Of Therapeutic Development

It is clear that the therapeutics discussed in this review have emerged out of an increasingly well-grounded knowledge of the circuits underlying BG function and the role of neurotransmitters and neural regulation in these circuits . Consequently, while L-Dopa remains the mainstay of treatment, the major advances are coming from directing treatments to modify other aspects of BG circuit function. While many of these non-dopaminergic treatments may not erase the need for DA replacement strategies, they may support the use of these therapies through the reduction in L-Dopa dose, improvement of motor symptoms, and/or reducing LIDs.

We have only focused on the new wave of treatments that have shown promise in animal models and that have also gone to human clinical trials, however, efforts to identify ever more viable therapeutic targets continues. Notable developments in animal models in this area include histamine H3 antagonists which, in addition to their non-motor effects, are able to improve L-Dopa-induced motor effects dopamine uptake inhibitors, which potentiate the efficacy of L-Dopa and conserved dopamine neurotrophic factor , which has demonstrated neuroprotective properties and rescue of motor deficits . This, together with efforts directed to address the basic mechanisms and causes of PD, our increased understanding of genetics, and recent extensive efforts to develop new biomarkers that should in turn improve clinical trials, provides a great basis for optimism.

Complementary And Alternative Therapies

DO NOT try to treat Parkinson disease with alternative therapies alone. Used with conventional medications, complementary and alternative therapies may help provide some relief of symptoms and slow progression of the disease. Some CAM therapies may interfere with certain medications, so work with your physician to find the safest, most effective CAM therapies for you.

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Can Restore Gold Delay Or Pause My Parkinsons Progression

We collect data and feedback from those that take Restore Gold for at least three months. Restore Gold has now been available for nearly five years. This has yielded some interesting observations. Some of our longest customers are noting observations in either substantially delaying Parkinsons progression or the pausing of Parkinsons progression. This is also true for some of us with Parkinsons at WHP. Whether Restore Gold is pausing or slowing Parkinsons progression in these individuals is difficult to tell as at least five years is necessary to properly discern between a substantial slowing or pausing. We would encourage reading some of our verified reviews for more on this subject.

The Ingredients In Restore Gold

Get Involved

There are no shortage of problems in the substantia nigra for those with Parkinsons. For decades, Parkinsons research experts have searched in vain for a magical natural or drug compound to address all issues in the Parkinsons patient with no practical success. However, in doing so, many compounds have been discovered that have found support for possibly addressing either mitochondrial dysfunction, alpha-synuclein aggregation, neural inflammation, or neural oxidation.

Researchers have known about many of these compounds for years, but for the first time certain compounds have been hand picked to be compounded together in one convenient capsule, called Restore Gold.

Following each ingredient, you can follow the links to the scientific journals that contain Parkinsons disease related research.


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Parkinsons Sufferers Offer Tips For Those Struggling With Symptoms

Despite Parkinsons Disease affecting around 1 million people in the US alone, the degenerative disease can be difficult to live with. We Have Parkinsons, one of the growing support and research groups in the US dedicated to helping those live with the disease, has offered those who may feel isolated and struggling with daily tasks tips for living with their illness.

The first port of call for sufferers is to ask for help. Many feel that seeking help is a sign of weakness, but as Parkinsons becomes more well-known, many individuals are much more informed and educated on the topic, meaning theyre often more sympathetic to those suffering.

Speaking about the illness, Jon Sherman, CEO, from We Have Parkinsons, said, Not long ago, not an awful lot was known about Parkinsons, but as treatments have developed, and more people with Parkinsons have spoken about their experiences, there is a growing awareness of the disease. As a result, friends, family and colleagues increasingly will know how to help those struggling. Therefore, anyone who may be struggling with new symptoms, or those whose quality of life is gradually deteriorating, will often find that asking loved ones and even strangers for help can be a huge support.

To find out more about We Have Parkinsons, and read the reviews of Restore Gold, the groups innovative product that has been easing Parkinsons symptoms, visit the website:

What Will A Cure For Parkinson’s Look Like

Parkinson’s varies so much from person to person. There are over 40 symptoms of Parkinsons. Tremor. Pain. Hallucinations. Everyones experience is different.

Because of this, there may not be a single ‘cure’.

Instead, we may need a range of different therapies to meet the needs of the individual and their specific form of the condition.

This mix may include treatments, therapies and strategies that can:

  • slow or stop the progression of the condition
  • replace or repair lost or damaged brain cells
  • control and manage particular symptoms
  • diagnose Parkinson’s at the earliest possible stage.

And this could involve medical treatments, such as drugs and surgical approaches, as well as lifestyle changes, for example to diet and exercise.

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Box 2 Dopamine Replacement Therapy

There is no evidence that the long-term use of LD is toxic for dopaminergic neurons thus LD remains the first drug of choice for most PD patients, even at early stages of the disease.

Dyskinesias are the most common motor side effect associated with chronic LD treatment, but are not as prevalent following dopamine receptor agonist therapy.

The use of dopamine receptor agonists is often complicated by the development of major autonomic and psychiatric side effects that outweigh the therapeutic benefits of these drugs on motor symptoms.

The development of new delivery methods that attenuate fluctuations of circulating dopaminergic drugs may reduce the development of dyskinesias and other dopamine therapy-mediated side effects.

Side effects of dopamine replacement therapies

On the other hand, because retroperitoneal, pericardial, and pleuropulmonary fibrosis have been associated with the use of ergot derivatives , the use of this specific group of dopamine-related drugs as treatment for PD was ended, and pergolide in particular was removed from the market.

Sustained levels of circulating dopaminergic drugs: a key to reduce motor fluctuations and dyskinesias

Vitamins For Parkinson’s Disease

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Verywell / Michela Buttignol

Apart from traditional pharmaceutical treatments, if you have Parkinsons disease, your doctor may recommend vitamins with antioxidant properties. While it is best to get these from food sources as part of a healthy, balanced diet, some people need to take supplements. These vitamins include:

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Possible Mechanisms Of Adverse Effects

L-DOPA also seems to act through non-canonical modes of action besides its well-known effect as a DA precursor. These effects could involve not only the striatum, considered the established target area for the actions of DA, but also other nuclei of the basal ganglia circuits. For example, it has been recently reported that L-DOPA has dual effects on nigral dopaminergic neurons . An early effect is associated with a membrane depolarization and is reduced by an -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor antagonist. A late phase of the excitation is not mediated by glutamate receptors but is sensitive to carbidopa, a dopa-decarboxylase inhibitor, demonstrating its dependence on the conversion of L-DOPA to DA. These dual excitatory effects are associated with an intracellular calcium increase and they might influence the survival of the dopaminergic neurons as well as the release of DA from the residual axon terminals.

According to this hypothesis, serotonin terminals, which lack an efficient reuptake machinery to control synaptically released DA, can contribute to abnormal pulsatile stimulation of DA receptors that causes aberrant responses to long-term L-DOPA treatment. In this regard, L-DOPA-induced plasticity of the striatal serotonin innervation might represent an important factor underlying abnormal presynaptic DA dynamics contributing to the development of LIDs.

Therapeutics For Nonmotor Symptoms Of Pd

Nonmotor symptoms are very common in PD and often result in significant disability and decrease in quality of life of these patients, often more so than the motor features . The key nonmotor symptoms of PD are listed in . Unfortunately, most of these symptoms, which in some cases can occur at early stages of the disease, years prior to the appearance of motor deficits, are often poorly recognized by the clinicians and remain inadequately managed. Nonmotor symptoms are classified under four main categories: neuropsychiatric, sleep, autonomic, and sensory. Many of these symptoms, which are unresponsive, exacerbated, or even induced by conventional PD therapy, are very prevalent, affecting the vast majority of patients, most particularly those who survive for many years with the disease . For these reasons, nonmotor symptoms have become one of the greatest challenges to the current clinical management of PD. There have been a small number of placebo-controlled trials of treatment for specific PD nonmotor symptoms , but this field remains largely unexplored and will deserve significant attention in the years to come. Treatments of hallucinations psychosis, depression, and dementia have received the greatest attention in recent years because they occur in such a large proportion of PD patients.

Table 3 Nonmotor Symptoms of Parkinson’s Disease

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Antioxidants: Vitamin C And E Mediterranean Diet

Since there is evidence relating oxidative damage of nerve cells to PD, some researchers are studying antioxidants:

  • A 2002 study focused on the potential antioxidant Coenzyme Q10 , which is believed to play an important role in mitochondria health. Mitochondria are the powerhouses of a cell. Some scientists think that abnormalities of mitochondrial function may play a role in PD.

In 2011, a large clinical trial studying the potential benefits of CoQ10 on reducing the progression of early PD was stopped because a mid-study analysis suggested that there was no improvement in the people taking CoQ10 in comparison to those receiving treatment. Researchers decided that continuing the study would have shown an extremely low likelihood of CoQ10 showing any benefit in delaying the progression of early PD.

Scientists have also examined Vitamin E, Vitamin C and health foods to evaluate oxidative properties. Vitamin E can fight damage in the brain caused by free radicals and has been suggested to lower the risk of PD. However, researchers conducted an extensive and thorough study more than 10 years ago and failed to find any evidence that Vitamin E slows the progression of PD or manages symptoms. Since Vitamin E has few side effects, many people with PD continue to take it in high doses of 400 IU or more.

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