Neurological Parkinson’s

Investigating the Potential of Antioxidant Supplements To Prevent Parkinson’s

The dreaded tremors and degenerative brain dysfunction of Parkinson’s disease are notoriously emotionally painful for patients and caretakers alike. Clinically, Parkinson’s disease is marked by highly variable symptoms like difficulties with voluntary motion and impaired executive functioning, which increase with intensity as the disease progresses. But patients may be suffering from Parkinson’s-related depression, anxiety, or cognitive dysfunction for years before a diagnosis is made, significantly diminishing quality of life before they are even aware of their condition. Once diagnosed, patients may have an explanation for their symptoms, but often struggle with difficult side effects of treatment that only delays the inevitable; there is no cure for Parkinson’s.

Due to the severe suffering Parkinson’s brings and the lack of curative treatment options, there is widespread interest amongst both patients and clinicians in preventing the condition from developing. At present, there are no pharmaceutical interventions which purport to prevent Parkinson’s. Nonetheless, several supplements have recently been investigated as potential methods of preventing or mitigating Parkinson’s disease. These supplements are still under intense research, but their early promise in helping patients protect their health and wellbeing is undeniable. Patients who want to take the initiative to prevent Parkinson’s disease rather than react after it has become established should follow these supplements closely and understand how they might be beneficial.

The Pathophysiology Of Parkinson’s and the Limits of Treatment

Parkinson’s disease is extraordinarily complex in terms of its pathophysiology and also its treatment strategies. This complexity stems from the disease’s protracted progression. The symptoms of Parkinson’s disease have a gradual onset because Parkinson’s slowly damages the patient’s brain, starting with the dopaminergic motor neurons. As dopaminergic motor neurons die, similarly afflicted neighboring neurons are unable to compensate for the absence of the dead cells and symptoms increase in severity.

As the disease progresses, patients lose voluntary control over many of their body’s movements; voluntary motion becomes more difficult while involuntary tremors and stereotyped motions become harder for the patient to suppress. At the same time, the dearth of dopaminergic neurons can produce significant psychological and cognitive effects, including depression, executive dysfunction, anxiety, apathy, and dementia. Eventually, controlling facial expressions becomes impossible, as does forming words properly due to the malfunctioning of the motor neurons responsible for moving the larynx and facial muscles. During this final stage, patients are confined to bed, having experienced extreme loss of functionality. If Parkinson’s remains untreated, it eventually becomes fatal as a result of extensive neuronal death.

Deaths caused solely by Parkinson’s are rare, however. Instead, Parkinson’s tends to increase risk of other health problems, often as the result of diminished motor control. For example, Parkinson’s patients highly vulnerable to falls and often struggle with basic self-care, such as feeding themselves. Nonetheless, with early detection and intervention using the current standard of treatment, patients who develop Parkinson’s can expect roughly 15 years between initial diagnosis and the need for constant medical aid. Patients who are untreated will experience more rapid progression of the disease, though the speed varies substantially from individual to individual. Significantly, while Parkinson’s progression can be drastically slowed with the right treatment regimen, no treatment can cause progression to entirely stop at this time. This underlines the need for adjunctive therapies that help preserve motor neurons.

The difficulty of treating Parkinson’s disease stems not only from the lack of curative therapies, but the fact that several of the most common pharmacological interventions cause lasting disability and an extensive number of intense side effects when they are used over the course of 10 or 15 years. These side effects range from the unpleasant dyskinesias in which the patient cannot halt involuntary movements to the deadly aggravation of Parkinson’s progression as the result of medication-induced dopamine secretion in the brain. Artificially prompting dopamine secretion to replace the natural dopamine secretion which is lost when dopaminergic neurons die due to Parkinson’s is effective at allaying symptoms for a time, which is why dopamine precursors or dopamine agonists are typically used after initial diagnosis. After extended courses of these medications, however, the brain adapts to the artificially increased concentrations of dopamine created by these drugs, diminishing responsiveness. At the same time, the brain has fewer dopaminergic neurons than ever, as they have continued to die over the course of treatment. This combination causes Parkinson’s symptoms to worsen precipitously and typically heralds the introduction of the next line of treatment.

The second line of treatment is anticholinergic drugs. Anticholinergics antagonize the acetylcholine receptors on neurons, preventing acetylcholine from interacting with the cell. When acetylcholine can’t interact with neurons, the neurons don’t transmit their acetylcholine-prompted signals as frequently or as strongly. This is important because cholinergic neurotransmission tends to also actuate dopaminergic neurotransmission. In other words, the second line of treatment tries to dampen neurological processes which utilize dopaminergic neurons indirectly. In contrast to the first line drugs, anticholinergics carry a brutal side effect profile which includes confusion, hallucination, blurry vision, decreased kidney function, dry mouth, and delirium. As a result, these drugs often incur a large penalty on the patient’s quality of life.

The difficult conditions of treatment for Parkinson’s, in addition to the disease itself, underline the necessity of effective prevention, but at present, there are only a very limited number of prevention strategies. Studies indicate that getting plentiful exercise during the peak risk years and drinking coffee appear to be associated with a lower risk of developing Parkinson’s. But these methods are not universally effective, and data regarding their efficacy is sparse. Thus, for patients who wish to try to prevent Parkinson’s or its progression, the current standard of treatment is woefully insufficient. Thanks to an emerging body of research, however, several new nutritional supplements may soon offer critical new options for patients.

The Potential Preventive Effect of Curcumin

Preventing Parkinson’s requires a novel therapeutic approach to the disease’s mechanism, supporting the preservation of dopaminergic motor neurons and dopaminergic activity. The chemical called curcumin, a biologically active compound isolated from turmeric, is one such promising avenue. In recent years, curcumin has been the focus of intense scientific inquiry owing to its confirmed diverse impact on cells, including powerful antioxidant activity. It is this antioxidant activity that may enable curcumin to slow the rate of dopaminergic neuron death caused by Parkinson’s.

Neurons are highly sensitive to environmental changes and the body produces many different chemicals designed to keep their environment stable. However, a multitude of factors constantly disrupts this stability. One of the most common threats to homeostasis is reactive oxygen species (ROS), the remainders of metabolic reactions which remain circulating within the cell. As their name implies, ROS react with cellular machinery like enzymes and DNA, preventing those pieces of machinery from doing their job with normal efficiency and causing cellular damage, otherwise known as oxidative stress, as a result.

Researchers believe that high levels of oxidative stress exist in the brains of Parkinson’s patients. In fact, the neurological level of oxidative stress is considered one of the major contributors to dopaminergic cell death and, thus, the disease’s progression. As such, antioxidants like curcumin are promising because they can potentially help healthy cells stay healthy by relieving some of the burden of defending against oxidative stress. Spending less energy on defending against oxidative stress would also benefit cells suffering from Parkinsonian-related degeneration, which means the treatment would be effective in both prevention and in treatment. Indeed, research into curcumin for Parkinson’s prevention is still in its nascent stages, but there is early evidence that it may offer these protective benefits.

In a 2012 experiment conducted in rats, a group of researchers led by Dr. Xi-Xun at the Medical College of Qingdao University in China found that a curcumin-based supplement could partially restore neuronal dopamine concentrations after an artificial induction of Parkinsonian symptoms. The researchers used three groups of rats: one group of rats was set aside as a control, and the other two groups were given 6-OHDA to trigger the development of irreversible Parkinson’s symptoms. 6-OHDA causes damage to dopaminergic motor neurons by creating extreme levels of oxidative stress. Then, one of the groups with Parkinson’s symptoms was given a curcumin-based supplement for 24 days. Measuring the concentrations of dopamine in the rat brains, the researchers found that the rats given the curcumin supplement had an average of 1 nanogram of dopamine per gram of tissue in their brains. The rats with Parkinson’s that hadn’t received the supplement exhibited an average of 0 detectable dopamine. In comparison, healthy control rats had around 6 nanograms of dopamine per gram of tissue. In a clinical setting, the difference between one nanogram of dopamine per gram of tissue and none whatsoever is difficult to overstate. Even if dopamine concentrations are very low, neurons can adapt to the low level by downregulating their receptors and can continue to perform dopaminergic neurotransmission, albeit at a reduced rate. If dopamine is entirely absent, there is no way for neurons to adapt and maintain a semblance of their prior pattern of neurotransmission; the rats without any dopamine in their brains were likely catatonic or brain dead at the time of dissection. These results indicate that curcumin might be an effective adjunct treatment for Parkinson’s disease and, potentially, act as prevention; because Parkinson’s is degenerative, taking a curcumin supplement might slow the disease’s progression to a point where its symptoms do not become noticeable over the patient’s lifetime.

While hard data regarding the efficacy of curcumin in a preventative role remains forthcoming, curcumin supplements are already widely available to purchase. Most patients who take these supplements find that the supplements are easy to tolerate, with transient nausea being the most common side effect reported. However, given that this research will take some time to develop, patients may want to use more than one supplement to optimize any benefits.

Exploring the Benefits of Glutathione

Aside from curcumin, there is another chemical which may revolutionize Parkinson’s prevention: the antioxidant molecule called glutathione. Glutathione (GSH) is naturally produced by cells to help control their level of oxidative stress. Much like with curcumin, glutathione can be thought of as a molecular sponge which absorbs ROS so that they can be discharged safely in a controlled environment where they can’t cause damage. Because glutathione is already a tool that the body uses to prevent oxidative stress damage, it has enormous potential as a Parkinson’s therapy.

In a healthy body, cells constantly recycle glutathione such that there is always some glutathione on hand that is ready to accept ROS and thus prevent damage. However, in people with Parkinson’s disease, this may not be the case. An early post-mortem study into the role of glutathione in Parkinson’s patients found stark differences between patients with Parkinsonian pathology and healthy controls. Healthy people had between 92.8 and 12.6 micrograms of glutathione for every gram of brain tissue in the dopaminergic neuronal tracts that the researchers examined. Furthermore, only 2% of the detected glutathione molecules were carrying ROS. In contrast, patients with Parkinson’s disease had between 49.3 and 4.6 micrograms of glutathione per gram of tissue, and between 50 to 100% of glutathione molecules were laden with ROS. This may mean that lower levels of glutathione are correlated with worse Parkinson’s symptoms; with certainty, this finding means that patients with Parkinson’s exhibit high levels of oxidative stress in their brains. Additionally, the prevalence of ROS-laden glutathione molecules in the Parkinson’s patients indicates that their neurons may have been incapable of clearing all of the ROS, which likely led to high rates of cell death. Though the researchers declined to speculate regarding the causes of the disparity between the healthy participants and the patients with Parkinson’s, other researchers have picked up where they left off in an attempt to learn more.

While the cause of Parkinson’s and the impact of oxidative stress remains unclear, there is evidence which suggests glutathione plays a role. Significantly, researchers have found that a drop in neuronal glutathione concentrations is one of the earliest biochemical signs of Parkinson’s and that glutathione depletion can be partially remedied pharmacologically. At present, scientists believe that patients who exhibit naturally high levels of glutathione have vastly improved neuronal survival; some have gone as far as to suggest glutathione as a treatment for Parkinson’s in and of itself. As such, it is possible that glutathione may offer a protective effect against the development and progression of the condition.

Clinical data on patients using glutathione supplements to prevent Parkinson’s or slow progression remains lacking, but it is an area of active investigation. Preliminary clinical trials have shown that glutathione is well-tolerated for current Parkinson’s patients, laying the groundwork for ongoing investigations regarding its efficacy. Patients seeking to prevent Parkinson’s may increase their chances of success with the help of a glutathione supplement provided that they utilize other proven preventative measures like exercise.

A Novel Combination Therapy For Parkinson’s?

Preventing Parkinson’s or slowing its progression is still an imprecise science even with the canonical pharmaceutical interventions. Currently available data, however, suggests that glutathione and curcumin are both promising supplements for those interested in optimizing their health, particularly when used in concert; researchers have shown in vitro that curcumin can work in conjunction with glutathione such that neurons are doubly protected. Curcumin appears to induce glutathione localization, with research indicating that glutathione levels were 64% higher in cells which received curcumin than those which did not. Indeed, while human clinical trials of both compounds are still forthcoming, the early evidence indicates that future therapies will likely operate in groups to maximize their effectiveness.

If patients are interested in using curcumin and glutathione supplements to prevent or slow Parkinson’s disease, it is likely safe to do so. There is no data which indicates the therapies are any more dangerous in conjunction than they are individually or that either of the therapies is dangerous when used as indicated. Furthermore, both therapies should be safe to use in conjunction with the first and second lines of pharmacological treatments for Parkinson’s, though patients should consult with their clinicians to be certain that no other interactions apply. Notably, it’s very difficult to assess the efficacy of preventative interventions. Patients taking curcumin or glutathione should remain vigilant regarding changes in their health, and remain in consultation with their physician to achieve the best possible outcome.

Foundational Medicine Review covers cutting-edge research related to innovative treatment strategies for neurological disorders, including Parkinson’s disease. Join our mailing list for more insight and analysis sent right to your inbox.

Works Cited

Du XX, Xu HM, Jiang H, Song N, Wang J, et al. 2012. Curcumin protects nigral dopaminergic neurons by iron-chelation in the 6-hydroxydopamine rat model of Parkinson’s disease. Neuroscience Bulletin. 28(3):253-258. https://link.springer.com/article/10.1007/s12264-012-1238-2

Harish G, Venkateshappa C, Mythri RB, Dubey SK, Mishra K, et al. 2010. Bioconjugates of curcumin display improved protection against glutathione depletion mediated oxidative stress in a dopaminergic neuronal cell line: Implications for Parkinson’s disease. Bioorganic and Medicinal Chemistry. 18(7):2631-2638. https://www.sciencedirect.com/science/article/pii/S0968089610001501

Martin HL and Teismann P. 2009. Glutathione—a review on its role and significance in Parkinson’s disease. FASEB Journal. 23(10). https://www.fasebj.org/doi/abs/10.1096/fj.08-125443

Mischley LK, Leverenz JB, Lau RC, Polissar NL, Neradilek MB, et al. 2015. A randomized, double-blind phase I/IIa study of intranasal glutathione in Parkinson’s disease. Movement Disorders. 12:1696-1701. https://www.ncbi.nlm.nih.gov/pubmed/26230671

Mythri B and Bharath S. 2012. Curcumin: a potential neuroprotective agent in Parkinson’s disease. Current Pharmaceutical Design. 18(1):91-99. https://www.ingentaconnect.com/content/ben/cpd/2012/00000018/00000001/art00012

Nirenberg MJ. 2013. Dopamine agonist withdrawal syndrome: implications for patient care. Drugs and Aging. 30(8):587-592. https://www.ncbi.nlm.nih.gov/pubmed/23686524

Poewe W. 2006. The natural history of Parkinson’s disease. Journal of Neurology. 253(7):VII2-VII6. https://www.ncbi.nlm.nih.gov/pubmed/17131223

Sian J, Dexter DT, Lees AJ, Daniel S, Agid Y, et al. 1994. Alterations in glutathione levels in Parkinson’s disease and other neurodegenerative disorders affecting basal ganglia. Annals of Neurology. 36(3):348-355. https://onlinelibrary.wiley.com/doi/abs/10.1002/ana.410360305

Smeyne M and Smeyne RJ. 2013. Glutathione metabolism and Parkinson’s disease. Free Radical Biology and Medicine. 62:13-25. https://www.sciencedirect.com/science/article/pii/S0891584913002062

Sofic E, Lange KW, Jellinger K, and Riederer P. 1992. Reduced and oxidized glutathione in the substantia nigra of patients with Parkinson’s disease. Neuroscience Letters 42:128-130. https://epub.uni-regensburg.de/25427/1/langekw9.pdf

Sveinbjornsdottir S. 2016. The clinical symptoms of Parkinson’s disease. Journal of Neurochemistry. 139(Suppl 1):318-324. https://www.ncbi.nlm.nih.gov/pubmed/27401947

Related Articles

oxidative stress supplement

Why Glutathione May Be the Best Oxidative Stress Supplement

GABA supplement side effects

GABA Supplement Side Effects Remain Largely Unknown


Follow Us
facebook facebook facebook


Sponsored Advertisement

RECENT POSTS
oxidative stress supplement
Why Glutathione May Be the Best Oxidativ...
curcumin for weight loss
Research Supports Using Curcumin for Wei...
GABA supplement side effects
GABA Supplement Side Effects Remain Larg...
Investigating the Potential of Antioxida...
Contact Us

You are now leaving Foundational Medicine Review

The following abstracts and articles were not written by Foundational Medicine Review. The authors of these abstracts and articles did not write the material with the intention of promoting a particular brand of nutritional supplement.

Foundational Medicine Review is providing a link to this information from our website to assist you in expanding your knowledge of complementary and alternative medicine, including various possible uses of nutritional supplements.

You will be redirected to

Click the link above to continue or CANCEL