PQQ’s Protective Roles in Parkinson’s Disease

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PQQ’s Protective Roles in Parkinson’s Disease
Juanita Enogieru, MS

Parkinson’s disease is a degenerative disorder of the the dopamine-producing neurons (nerve cells) in a region of central nervous system (CNS). It occurs when the brain called the substantia nigra become damaged or die. When the neurons are impaired, they produce less dopamine, leading to the inability to control body movements.1,2

Emerging research provides evidence that inflammation, oxidative damage to the neurons that control movement, and malfunctioning mitochondria play a role in the neurodegenerative aspect of the disease.3,4 Furthermore, Parkinson’s disease is associated with the accumulation of a protein known as alpha-synuclein that can be toxic. Accumulation of this protein can cause an increase in toxin accumulation in the mitochondria, leading to damage that disrupts mitochondrial function and may lead to the death of neurons. Alpha-synuclein also triggers inflammatory changes that contribute to cell death. These effects may be involved in producing Parkinson’s disease symptoms.5

Pyrroloquinoline quinone (PQQ) is a powerful antioxidant nutrient that may be promising for managing Parkinson’s disease progression.4,6 Human clinical studies should be conducted to further investigate the benefits of PQQ for individuals with Parkinson’s disease.

How can oxidative stress lead to Parkinson’s disease?

Various biochemical processes in the body can lead to the production of free radicals, such as the creation of cellular energy using oxygen. The body utilizes an endogenous antioxidant defense system to remove free radicals from the body. Oxidative stress can arise when there is a disturbance in the balance between the production of free radicals, also known as reactive oxygen species (ROS), and antioxidant defenses.7

As oxidative damage can lead to neuron death, it is a critical factor in neurodegenerative diseases and is an underlying factor in Parkinson’s disease progression.8,9

Many Parkinson’s disease strategies focus on reducing oxidative stress. Preclinical studies have shown PQQ to be a potent antioxidant that can protect neurons from oxidative damage.4,6,10 In fact, one cell study showed that after cells were exposed to a toxin that induces oxidative damage, PQQ effectively scavenged superoxide (a reactive oxygen species), protected cells from death and prevented fragmentation of the DNA.10

How is mitochondrial dysfunction linked to Parkinson’s disease progression?

Mitochondria are organelles that produce energy, known as adenosine triphosphate, or ATP. ATP is used for many processes in the body, including neurological and muscular function for movement. When mitochondria are damaged or destroyed, cells do not function properly. An important feature of mitochondrial dysfunction is a decrease in the number of mitochondria, as well as inefficient energy production due to decreased functionality.11 Furthermore, mitochondria are vulnerable to damage from oxidative stress. Mutations in certain genes linked to familial cases of Parkinson’s disease impact mitochondrial processes, function and integrity. The changes seen with these mutations are strongly associated with an increase in mitochondrial dysfunction in dopaminergic cells of the substantia nigra.9

In addition to PQQ’s ability to lower levels of oxidative stress, PQQ is also noted for supporting the growth of new mitochondria through gene activation.12-14 PQQ further supports mitochondria by activating genes that fix damaged DNA, as mitochondria have poor DNA repair systems.15 In an animal model of Parkinson’s, PQQ prevented mitochondrial dysfunction and exerted neuroprotective effects.16

What is alpha-synuclein’s part in Parkinson’s disease?

Another hallmark of Parkinson’s disease is the formation of Lewy bodies and Lewy neurites, which are primarily made up of alpha-synuclein.17 Alpha-synuclein sounds like a space station in a sci-fi movie, but it is a protein found abundantly in the brains of Parkinson’s patients.

Misfolded alpha-synuclein proteins form abnormal aggregates (clumps) of protein fibrils in nerve cells. Specific forms of alpha-synuclein can accumulate to levels that contribute to neurodegeneration. Over time, clumps of alpha-synuclein may increase to a point where they spread and contribute to Parkinson’s disease progression. In Parkinson’s disease, oxidative stress is noted as being a potential contributor to protein fibril formation.18

Preclinical studies have demonstrated that PQQ can prevent the development of protein fibrils by attaching to a specific region on the alpha-synuclein molecule.19-21As such, PQQ is being explored as a potential candidate for the prevention of Parkinson’s disease progression.

The bottom line

It has been estimated that the number of individuals in North America with Parkinson’s disease will rise to approximately 930,000 in 2020 and 1,238,000 in 2030 based on the US Census Bureau population projections.22 PQQ’s ability to scavenge free radicals, inhibit the formation of alpha-synuclein aggregates and offer well-rounded support of mitochondrial health may make it an important nutrient for improving quality of life for those with Parkinson’s disease.

About the author: Juanita Enogieru is a nutritionist and Life Extension Wellness Specialist working with the community to build healthy and balanced nutritional habits. While pursuing an education in medicine and attempting to help her body heal, it became apparent that there was a gap in medical practices with regard to nutrition and an abundance of misinformation about balanced nutritional practices. After obtaining a Bachelor’s Degree in Health Education from the University of Florida, she worked with non-profit organizations to deliver nutrition education to community members. Wanting to learn more about nutrition and how herbs could be used to help the body heal, she pursued a Master’s Degree in Dietetics and Nutrition and shortly after began working with Life Extension. With the understanding that everyone has a unique biochemical individuality, it is vital to address each individual based on their specific needs and biochemical make-up. Her mission now is to offer guidance, support and education to individuals based on balanced nutritional insights that address the mind, body and spirit.


  1. National Institute on Aging. Parkinson’s Disease. https://www.nia.nih.gov/health/parkinsons-disease. Accessed 10/16/2019.
  2. Parkinson’s Foundation. What is Parkinson’s? https://www.parkinson.org/understanding-parkinsons/what-is-parkinsons. Accessed 10/16/2019.
  3. Hassanzadeh K, Rahimmi A. Oxidative stress and neuroinflammation in the story of Parkinson’s disease: Could targeting these pathways write a good ending? Journal of cellular physiology. 2018;234(1):23-32.
  4. Zhang Q, Chen S, Yu S, et al. Neuroprotective effects of pyrroloquinoline quinone against rotenone injury in primary cultured midbrain neurons and in a rat model of Parkinson’s disease. Neuropharmacology. 2016;108:238-251.
  5. Stefanis L. alpha-Synuclein in Parkinson’s disease. Cold Spring Harb Perspect Med. 2012;2(2):a009399.
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  8. Liu C, Fang J, Liu W. Superoxide dismutase coding of gene polymorphisms associated with susceptibility to Parkinson’s disease. J Integr Neurosci. 2019;18(3):299-303.
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  10. Hara H, Hiramatsu H, Adachi T. Pyrroloquinoline quinone is a potent neuroprotective nutrient against 6-hydroxydopamine-induced neurotoxicity. Neurochemical research. 2007;32(3):489-495.
  11. Nicolson GL. Mitochondrial Dysfunction and Chronic Disease: Treatment With Natural Supplements. Integrative medicine (Encinitas, Calif). 2014;13(4):35-43.
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  13. Saihara K, Kamikubo R, Ikemoto K, Uchida K, Akagawa M. Pyrroloquinoline Quinone, a Redox-Active o-Quinone, Stimulates Mitochondrial Biogenesis by Activating the SIRT1/PGC-1alpha Signaling Pathway. Biochemistry. 2017;56(50):6615-6625.
  14. Stites T, Storms D, Bauerly K, et al. Pyrroloquinoline quinone modulates mitochondrial quantity and function in mice. The Journal of nutrition. 2006;136(2):390-396.
  15. Zhang Q, Zhang J, Jiang C, Qin J, Ke K, Ding F. Involvement of ERK1/2 pathway in neuroprotective effects of pyrroloquinoline quinine against rotenone-induced SH-SY5Y cell injury. Neuroscience. 2014;270:183-191.
  16. Lu J, Chen S, Shen M, et al. Mitochondrial regulation by pyrroloquinoline quinone prevents rotenone-induced neurotoxicity in Parkinson’s disease models. Neurosci Lett. 2018;687:104-110.
  17. Meade RM, Fairlie DP, Mason JM. Alpha-synuclein structure and Parkinson’s disease – lessons and emerging principles. Mol Neurodegener. 2019;14(1):29.
  18. Xu L, Pu J. Alpha-Synuclein in Parkinson’s Disease: From Pathogenetic Dysfunction to Potential Clinical Application. Parkinsons Dis. 2016;2016:1720621.
  19. Kobayashi M, Kim J, Kobayashi N, et al. Pyrroloquinoline quinone (PQQ) prevents fibril formation of alpha-synuclein. Biochemical and biophysical research communications. 2006;349(3):1139-1144.
  20. Kim J, Harada R, Kobayashi M, Kobayashi N, Sode K. The inhibitory effect of pyrroloquinoline quinone on the amyloid formation and cytotoxicity of truncated alpha-synuclein. Mol Neurodegener. 2010;5:20.
  21. Kim J, Kobayashi M, Fukuda M, et al. Pyrroloquinoline quinone inhibits the fibrillation of amyloid proteins. Prion. 2010;4(1):26-31.
  22. Marras C, Beck JC, Bower JH, et al. Prevalence of Parkinson’s disease across North America. NPJ Parkinsons Dis. 2018;4:21.

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