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What is Parkinson’s disease?

Parkinson’s disease (PD) is a progressive disease of the nervous system that results in gradual loss of control over muscle movements (motor function).1,2 It is characterized by tremors (rapid shaking of the hands or head) when resting, slow movements, and rigidity. These symptoms get more severe as the disease progresses. Non-motor symptoms of PD include constipation, disordered sleep, dementia, and depression.3

In PD, certain nerve cells in the brain that produce dopamine begin to disappear for reasons that are not fully understood. Dopamine is a chemical messenger molecule with many functions in the brain, including muscle movement and feelings of motivation and reward. When the dopamine-producing nerve cells die, levels of dopamine decrease. This causes brain activities related to muscle movement to stop working properly.3

In 2010, approximately 630,000 to 1,000,000 people in the U.S., or 0.3% of the general population, had PD. These numbers are expected to double by 2040.4 Parkinson’s disease affects twice as many men as women, and mostly those over 50.5

What are common symptoms?

Parkinson’s disease symptoms can be both physical or mental, and usually start out very mild and progress slowly. Physical symptoms may begin on only one side. Often, the first symptom of PD is a trembling of one hand when sitting still that disappears when the arm is moved. Some common physical symptoms are (in order of frequency)1,2,3:

  • Stiff, rigid, or frozen muscles
  • Slow movements
  • Tremors when resting
  • Poor posture and balance
  • Tiredness
  • Pain

Mental symptoms affect quality of life and may include (in order of frequency)1,3:

  • Mood changes
  • Cognitive decline
  • Sleep disturbance
  • Constipation and other gastrointestinal disorders
  • Autonomic dysfunction
  • Depression
  • Psychosis
  • Dementia
a condition in which the autonomic nervous system does not work correctly, causing malfunctions in the heart, bladder, intestines, sweat glands, pupils, and blood vessels.

What are the causes?

The cause of PD is not well understood but is most likely related to a patient’s genes and environment. In the early stages of PD, dopaminergic cells degenerate throughout the nervous system. The first PD motor symptoms appear after the midbrain has already experienced a significant decrease in dopamine neurons, which regulate voluntary movement, mood, stress, and other brain functions.6,7

In PD, abnormal deposits of altered brain proteins (e.g. 𝛼-synuclein) form. These deposits are known as Lewy bodies (LB). LB presence is the key sign necessary for the diagnosis of PD, although the build up of LB may develop relatively late in the disease. However, the presence of LB can only be confirmed through a brain autopsy after death. Current methods for PD diagnosis include assessment of dementia symptoms, biomarkers in blood and spinal fluid, and brain imaging.8

A person’s family history and environment are strong risk factors for PD. Because our cells already deteriorate as we get older, age is also a definitive risk factor.6,7

Environmental factors that could be PD risk factors include6,7:

  • Exposure to pesticides
  • High dairy consumption
  • Sedentarism
  • Low intake of antioxidants

Genetic risks believed to be risk factors for PD development are6:

  • Aging
  • Family history
  • Male sex
  • European ancestry
  • Pre-existing medical conditions:
    • Anxiety disorders
    • Depression
    • Loss of sense of smell and taste
    • Sleep behavior disorders
are neurons that release dopamine, a neurotransmitter that sends signals to other nerve cells. Dopamine also affects motor control and helps regulate hormone release.

How does this topic relate to my microbiome?

Recent studies have linked microbial dysbiosis to neurodegenerative disorders, such as PD, Alzheimer’s disease, and multiple sclerosis. Recurrent microbial infections also increase the probability of developing these disorders.9 Because gastrointestinal dysfunction is often detected several years before the onset of PD, one hypothesis is that the disease begins in the gut and spreads to the brain through the vagus nerve and spinal cord.9,10,11

Microbial signals from the gut are thought to trigger neuro-inflammatory responses. When the gut microbiota from PD patients are transplanted into mice, these mice develop symptoms very similar to PD patients.12The way that the gut microbiota respond to intestinal inflammation may alter function of the brain protein 𝛼-synuclein, causing these proteins to aggregate in the nervous system and the disease to develop.11

Helicobacter pylori infections and small intestinal bacterial overgrowth (SIBO) can increase the severity of PD motor symptoms, so curing these infections can improve symptoms.13,14

Some studies show that the fecal microbiota of patients with PD contains less Prevotella – which is known to promote a healthy intestinal environment – and more Enterobacteriaceae.15 Other studies found decreased Eubacterium biforme and Faecalibacterium prausnitzii, and higher amounts of Akkermansia muciniphila, Bifidobacterium, and Enterobacteriaceae.16,17,18,19

Which diseases/topics are related to Parkinson’s disease?

Parkinson’s disease is related to other neurodegenerative diseases, such as3,5:

  • Alzheimer’s Disease
  • Dementia
  • Huntington’s disease
  • Motor neuron diseases
  • Multiple sclerosis
  • Multiple system atrophy

Many comorbidities have been associated with PD, including (in order of relevancy)20:

  • Type 2 diabetes
  • Depression
  • Anemia
  • Cancer
  • Gastrointestinal dysfunction and constipation

Other, less associated comorbidities are2020:

  • Cognitive impairment
  • Hypertension
  • Hyposmia
  • Restless leg syndrome
  • Sleep disorders
is a condition describing partial or total loss of the sense of smell.

How can I take action?

Early detection and treatment of PD can prevent or delay its progression. If you notice any sign of PD symptoms, consult your healthcare provider. Depending on how far the disease has progressed, different treatments might be recommended, such as (in order of frequency)21:

  • Dopamine agonists
  • Supplements such as coenzyme Q10, creatine, and vitamin D
  • Regular physical activity
  • Drugs to help with gait and balance
  • Physiotherapy to improve tremors and other physical symptoms

Though limited, recent studies suggest that taking probiotics, prebiotics, and synbiotics may help manage and prevent PD by boosting the immune system, improving gut dysbiosis and gastrointestinal tract functioning, and protecting the brain and nerves. Taking probiotics, prebiotics, and synbiotics may also reduce common symptoms of the disease. Common probiotics that may help treat PD are Lactobacillus, Enterococcus, and Bifidobacterium species, while common prebiotics include galacto-oligosaccharides (GOS) and fructo-oligosaccharides (FOS).22

are drugs that activate dopamine receptors, and are mainly used to treat low dopamine conditions, such as PD.


1. Politis, M., Wu, K., Molloy, S., Bain, P. G., Chaudhuri, K. R., & Piccini, P. (2010). Parkinson’s disease symptoms: The patient’s perspective. Movement Disorders, 25(11), 1646–1651.

2. Rana, A. Q., Kabir, A., Jesudasan, M., Siddiqui, I., & Khondker, S. (2013). Pain in Parkinson’s disease: Analysis and literature review. Clinical Neurology and Neurosurgery, 115(11), 2313–2317.

3. Elbaz, A., Carcaillon, L., Kab, S., & Moisan, F. (2016). Epidemiology of Parkinson’s disease. Revue Neurologique, 172(1), 14–26.

4. Kowal, S. L., Dall, T. M., Chakrabarti, R., Storm, M. V., & Jain, A. (2013). The current and projected economic burden of Parkinson’s disease in the United States. Movement Disorders, 28(3), 311–318.

5. Gooch, C. L., Pracht, E., & Borenstein, A. R. (2017). The burden of neurological disease in the United States: A summary report and call to action. Annals of Neurology, 81(4), 479–484.

6. Shulman, J. M., De Jager, P. L., & Feany, M. B. (2011). Parkinson’s Disease: Genetics and Pathogenesis. Annual Review of Pathology: Mechanisms of Disease, 6(1), 193–222.

7. Wirdefeldt, K., Adami, H.-O., Cole, P., Trichopoulos, D., & Mandel, J. (2011). Epidemiology and etiology of Parkinson’s disease: a review of the evidence. European Journal of Epidemiology, 26(S1), 1–58.

8. McKeith, I. G., Boeve, B. F., Dickson, D. W., Halliday, G., Taylor, J.-P., Weintraub, D., … Kosaka, K. (2017). Diagnosis and management of dementia with Lewy bodies. Neurology, 89(1), 88–100.

9. Ghaisas, S., Maher, J., & Kanthasamy, A. (2017). Gut microbiome in health and disease: linking the microbiome- gut-brain axis and environmental factors in the pathogenesis of systemic and neurodegenerative diseases. Pharmacol Ther, 52–62.

10. Mulak, A., & Bonaz, B. (2015). Brain-gut-microbiota axis in Parkinson’s disease. World Journal of Gastroenterology, 21(37), 10609–10620.

11. Mukherjee, A., Biswas, A., & Das, S. K. (2016). Gut dysfunction in Parkinson’s disease. World Journal of Gastroenterology, 22(25), 5742–5752.

12. Sampson, T. R., Debelius, J. W., Thron, T., Janssen, S., Shastri, G. G., Ilhan, Z. E., … Mazmanian, S. K. (2016). Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson’s Disease. Cell, 167(6), 1469–1480.e12.

13. Fasano, A., Bove, F., Gabrielli, M., Petracca, M., Zocco, M. A., Ragazzoni, E., … Bentivoglio, A. R. (2013). The role of small intestinal bacterial overgrowth in Parkinson’s disease. Movement Disorders, 28(9), 1241–1249.

14. Tan, A. H., Mahadeva, S., Marras, C., Thalha, A. M., Kiew, C. K., Yeat, C. M., … Lim, S.-Y. (2015). Helicobacter pylori infection is associated with worse severity of Parkinson’s disease. Parkinsonism & Related Disorders, 21(3), 221–225.

15. Scheperjans, F., Aho, V., Pereira, P. A. B., Koskinen, K., Paulin, L., Pekkonen, E., … Auvinen, P. (2015). Gut microbiota are related to Parkinson’s disease and clinical phenotype. Movement Disorders, 30(3), 350–358.

16. Unger, M. M., Spiegel, J., Dillmann, K.-U., Grundmann, D., Philippeit, H., Bürmann, J., … Schäfer, K.-H. (2016). Short chain fatty acids and gut microbiota differ between patients with Parkinson’s disease and age-matched controls. Parkinsonism & Related Disorders, 32, 66–72.

17. Bedarf, J. R., Hildebrand, F., Coelho, L. P., Sunagawa, S., Bahram, M., Goeser, F., … Wüllner, U. (2017). Functional implications of microbial and viral gut metagenome changes in early stage L-DOPA-naïve Parkinson’s disease patients. Genome Medicine, 9(1), 39.

18. Hill-Burns, E. M., Debelius, J. W., Morton, J. T., Wissemann, W. T., Lewis, M. R., Wallen, Z. D., … Payami, H. (2017). Parkinson’s disease and Parkinson’s disease medications have distinct signatures of the gut microbiome. Movement Disorders, 32(5), 739–749.

19. Heintz-Buschart, A., Pandey, U., Wicke, T., Sixel-Döring, F., Janzen, A., Sittig-Wiegand, E., … Wilmes, P. (2018). The nasal and gut microbiome in Parkinson’s disease and idiopathic rapid eye movement sleep behavior disorder. Movement Disorders, 33(1), 88–98.

20. Santiago, J. A., Bottero, V., & Potashkin, J. A. (2017). Biological and clinical implications of comorbidities in Parkinson’s disease. Frontiers in Aging Neuroscience, 9(DEC), 1–16.

21. Fox, S. H., Katzenschlager, R., Lim, S. Y., Barton, B., de Bie, R. M. A., Seppi, K., … Sampaio, C. (2018). International Parkinson and movement disorder society evidence-based medicine review: Update on treatments for the motor symptoms of Parkinson’s disease. Movement Disorders, 00(00), 1–19.

22. Perez-Pardo, P., Kliest, T., Dodiya, H. B., Broersen, L. M., Garssen, J., Keshavarzian, A., & Kraneveld, A. D. (2017). The gut-brain axis in Parkinson’s disease: Possibilities for food-based therapies. European Journal of Pharmacology, 817(March), 86–95.