Neurological Parkinson’s

Supplements for Parkinson’s Disease: Considering Quercetin as a Treatment Option

supplements for Parkinson's

For patients, one of the most challenging aspects of a Parkinson’s disease diagnosis is the uncertainty. The progress of the disease differs significantly between patients, so it is difficult to predict the timing of the stages and the severity of the symptoms. Moreover, patients and practitioners have to contend with the fact that the existing pharmacological treatments are insufficient for addressing all concerns: they vary in their effectiveness for individual patients, and most only offer relief for the motor symptoms of Parkinson’s disease. That leaves a wide range of nonmotor symptoms untreated, including sleep problems, cognitive impairment, depression, sialorrhea, and hypotension. Traditional pharmacological therapies also often have side effects that interfere with a patient’s quality of life. Because of these issues, more scientists are looking to nutritional factors that may aid in the effective management of Parkinson’s disease. One of the dietary supplements that has emerged as a viable possibility is quercetin.

Quercetin is plant pigment that is commonly found in vegetables, fruits, flowers, and herbs. As a flavonoid, it is well-recognized for its anti-inflammatory and antioxidant effects, and it continues to draw the attention of the research community as more studies establish connections between antioxidant supplements and neuroprotection against Parkinson’s disease. While clinical trials are still lacking, there have been several promising in vitro and animal model studies, which cumulatively suggest that there are multiple mechanisms through which a quercetin supplement may benefit Parkinson’s disease patients.

The Early Evidence for Quercetin as an Effective Supplement for Parkinson’s Disease Management

One of the early animal studies indicating that a quercetin supplement could benefit Parkinson’s disease patients was published in the journal Neuroscience Letters in 2011. The researchers wanted to know whether taking quercetin might have an effect on dopamine levels in rat models of Parkinson’s disease, based on the fact that one of the most effective pharmacological treatments for Parkinson’s disease is levodopa—a chemical precursor to dopamine that is designed to combat declining levels of dopamine, which interfere with the patient’s ability to control their body movements and contribute to a variety of non-motor symptoms. Indeed, after 14 days of quercetin treatment, the levels of quercetin in the rat models had increased significantly, along with the levels of enzymes involved in key antioxidant processes that could provide neuroprotection. Importantly, these observations were also associated with increased neuron survival in the rats. Thus, the researchers were able to conclude that taking quercetin could aid in both the reduction of oxidative damage and neuronal loss associated with Parkinson’s disease.

The Link Between Quercetin Supplementation and Autophagy

More recently, in 2016, a group of scientists from Tanta University in Egypt conducted an animal model study that established a link between quercetin and another neurochemical pathway associated with Parkinson’s disease: autophagy. Autophagy refers to the cell’s metabolism of its own tissues. In scientific circles, this cellular process has traditionally been associated with starvation, but scientists are increasingly recognizing its importance for neuronal homeostasis. Autophagy removes damaged organelles and aggregated proteins in brain cells that contribute to neurodegeneration, and it can even contribute to oxidative processes that stress the endoplasmic reticulum (a key cell organelle) to the point where a cell undergoes apoptosis (programmed cell death). Thus, a supplement that combats dysfunctional autophagy in Parkinson’s disease patients could potentially help slow the onset and progress of the disease.

To explore the possibility that quercetin could play such a role, the researchers treated rat models of Parkinson’s disease with quercetin for four weeks. After the trial period, the researchers used DNA fragmentation to examine changes in gene expression, and they used histopathological analysis to assess observable changes in rat tissue. Like the researchers who conducted the early study in 2011, they found that quercetin supplementation resulted in higher levels of dopamine and antioxidant enzymes. In addition, they observed increases in the levels of several key autophagy-associated proteins, including Beclin-1 and C/EBP homologous protein (CHOP). Notably, they also reported significant declines in the behavioral impairments displayed by the rat models of Parkinson’s disease. Based on these results, the authors were able to draw three conclusions: that quercetin could improve the functioning of the autophagy pathway, that it could reduce the risk of ER stress-induced apoptosis by acting as an antioxidant, and that it could ameliorate some of the known symptoms of Parkinson’s disease.

The Protective Effects of Coffee Against Parkinson’s Disease: Caffeine or Quercetin?

It is important to note that quercetin is not the only compound that has been proposed as a possible alternative to traditional pharmacological therapy for Parkinson’s disease. Over the last decade, a combination of epidemiological studies and preclinical studies have associated the consumption of coffee with a lower risk of neurodegenerative diseases, including Parkinson’s disease. That’s great news for coffee drinkers, but scientists and supplement developers have been more interested in determining the specific component of coffee that offers neuroprotection. Many scientists immediately pointed to caffeine, suggesting that the compound could aid in the management of some of the motor symptoms of Parkinson’s disease due to its effects on dopaminergic pathways. Indeed, caffeine can play a role similar to that of certain traditional pharmacological therapies that effectively treat certain motor symptoms of Parkinson’s disease. However, many of these studies failed to explain the associations between coffee-drinking and the effects of caffeine on non-motor symptoms of Parkinson’s disease.

In 2016, a group of researchers from the Kinsmen Laboratory of Neurological Research at The University of British Columbia proposed an alternative to the caffeine hypothesis: that it was the quercetin in the coffee, not the caffeine, that was truly reducing the risk for Parkinson’s disease. To explore this idea, the researchers examined how a number of different coffee components—including quercetin, caffeine, flavones, and chlorogenic acid—affected cell models of neurodegenerative disease.Through a series of in vitro studies, they found that quercetin could reduce neurotoxicity by preventing damage to DNA, lipids, and proteins. This resulted in an increase in glutathione, a key compound that is known to protect against oxidative damage in Parkinson’s disease. While treatment with caffeine did provide minor benefits, they were minimal compared to the significant impacts of quercetin. Thus, the researchers concluded that it is the quercetin—not the caffeine—that is the major neuroprotective component in coffee.

Acting on the Preliminary Evidence

For patients and practitioners, there’s no denying that studies on quercetin as a supplement for Parkinson’s disease are still in their infancy. However, given that most traditional pharmacological treatments may not be effective for all patients—and generally fail to address non-motor symptoms at all—trying quercetin as a supplement in a highly bioavailable form may be a viable consideration when developing a treatment strategy. The evidence supporting their efficacy in the lab is strong, and it will be exciting to see how these results translate to clinical studies in the future.

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Works Cited

Connolly BS, Lang AE. 2014. Pharmacological treatment of Parkinson disease: A review. JAMA. 311(16):1670-83. https://www.ncbi.nlm.nih.gov/pubmed/24756517

El-Horany HE, El-Latif RN, El Batsch MM, Emam MN. 2016. Ameliorative effect of quercetin on neurochemical and behavioral deficits in rotenone rat model of Parkinson’s disease: Modulating autophagy (quercetin on experimental Parkinson’s disease). 2016. Journal of Biochemical and Molecular Toxicology. 30(7):360-9. https://www.ncbi.nlm.nih.gov/pubmed/27252111

Haleagrahara N, Siew CJ, Mitra NK, Kumari M. 2011. Neuroprotective effect of bioflavonoid quercetin in 6-hydroxydopamine-induced oxidative stress biomarkers in the rat striatum. Neuroscience Letters. https://www.ncbi.nlm.nih.gov/pubmed/21704673

Lee M, McGeer EG, McGeer PL. 2016. Quercetin, not caffeine, is a major neuroprotective component in coffee. Neurobiology of Aging. 46:113-23. https://www.ncbi.nlm.nih.gov/pubmed/27479153

Maday S. 2016. Mechanisms of neuronal homeostasis: Autophagy in the axon. Brain Research. 1649(PtB):143-50. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5045311/

Mischley LK, Lau RC, Bennett RD. 2017. Role of diet and nutritional supplements in Parkinson’s disease progression. Oxidative Medicine and Cellular Longevity. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5610862/

Prediger RD. 2010. Effects of caffeine in Parkinson’s disease: From neuroprotection to the management of motor and non-motor symptoms. Journal of Alzheimer’s Disease. 20(Suppl 1):S205-20. https://www.ncbi.nlm.nih.gov/pubmed/20182024

Smeyne M, Smeyne RJ. 2013. Glutathione metabolism and Parkinson’s disease. Free Radical Biology and Medicine. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3736736/

Weber CA, Ernst ME. 2006. Antioxidants, supplements, and Parkinson’s disease. Annals of Pharmacotherapy. 40(5):935-8. https://www.ncbi.nlm.nih.gov/pubmed/16622156

Yao L, Yao J, Han C, Yang J, Chaudhry MT et al. 2016. Quercetin, inflammation, and immunity. Nutrients, 8(3):167. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4808895/

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