Mike Rucker, Ph.D.

PQQ and disease

Michael Rucker

Regarding PQQ and Parkinson’s disease:

PQQ and Parkinson’s disease, regrettably, there are no clinical studies that been done to date to directly address whether PQQ is effective in the treatment of Parkinson’s disease. Although you can find these assertions on suspect nutritional supplement-oriented blogs and websites, there is no real proof PQQ will help. There are some promising treatment options that help better regulate dopamine, PQQ is not one of them. That said, there are a number of basic studies that appear promising, which suggest pyrroloquinoline quinone may be beneficial in slowing or altering the progression of Parkinson’s disease.




What is currently known about PQQ and Parkinson’s disease?

In studies using experimental animal models, PQQ does interact with the neurotransmitter systems. It appears to be a neuroprotective (also see the post, PQQ, glutamate, nitric oxide and N-methyl-D-aspartic acid receptors). PQQ could potentially protect against neurotoxicity induced by compounds that promote or produce Parkinson-like symptoms in laboratory animals. Moreover, PQQ in chemical assays inhibits the aggregation of alpha-synuclein, a process that is associated with the progression to Parkinson’s disease. Pyrroloquinoline quinone also seems to protect nerve cells by blocking new amyloid beta molecular structures from forming before they can cause cellular damage akin to what is observed in Parkinson’s disease. Although these observations are promising, questions nevertheless remain regarding how direct and specific the actions of PQQ are as they relate to altering the functions of alpha-synuclein and amyloid beta, if and when they are abnormally aggregated.

Regarding PQQ and HIV:

[QUESTION FROM READER:] This one may hit you from left field, but I landed on your website after researching mitochondrial toxicity and mutations caused by the HIV medication AZT, Ziduvodine, Lamuvidine, and Combivir. I was put on post-exposure prophylaxis, a 3 drug course, and have been unwell ever since with muscular and neuropathy problems.  After extensive MRI, EMG, and 40 or 50 blood tests all being normal, I have returned to the possibility that I experienced mitochondrial damage while on those toxic medications. I am wondering if PQQ would play any role in *replacing* the damaged mitochondria with new, healthy mitochondria?  Is that even how it works with DNA and Mitochondria?  Does it die, and cycle in new healthy versions? Can new versions be created, and eventually outnumber the damaged versions?  As my current goal is to undo or replace the damage done by the drugs I was prescribed. My understanding is the damaged mitochondria can replicate with new damaged mitochondria and thus causing ongoing problems, and possible mitochondrial disease. My symptoms have gradually worsened since the medications, and match exactly with mitochondrial disease.  I guess it all comes down to whether or not damaged mitochondria can eventually be filtered out of the system entirely. This is all predicated on the assumption I don’t have a genetic birth mutation and this is drug-induced.

HIV medications and mitochondrial function antiretroviral therapy are improving the life expectancy for those with HIV infections, but there is also the potential for serious side effects associated with the medications used for HIV treatment. The current attempts to monitor such negative drug effects have focused on mitochondrial toxicity.  For example, increased apoptosis (the process of cell death that is related to or caused by a decrease in functioning mitochondria) has been demonstrated both in vitro and in vivo to occur in association with exposure to various antiretroviral drug classes.

Currently, there are no studies that link PQQ to the amelioration of HIV drug side effects.  However, there are papers that suggest some promise for biofactors, such as resveratrol and various bioflavonoids (e.g., J Neurovirol. 2012;18:445-55 and Molecular Medicine Reports 2011; 4: 151-155). The average life span of a cell depends on what type of cell it is. There are approximately 200 types of cells in the average adult human body. The average cell life span varies:

For comparison, mitochondria are normally replaced in most cells at reasonably rapid rates (days in contrast to weeks or months).  Their numbers and functional capacity can increase or be altered in a relationship by a number of factors – for example, exercise and reduced food intake (to promote the combustion of adipose tissue) are prime factors.  Given that many of the positive effects of pyrroloquinoline quinone related to mitochondria occur by mechanisms similar to those for resveratrol and to some degree the bioflavonoids and PQQ appear to influence mitochondria by well-established pathways, analogous to current speculations regarding other biofactors, one guess might be that it could potentially be helpful. However, this would only be a guess.

Regarding PQQ and Guillain–Barré syndrome:

Guillain–Barré syndrome can occur with rapid onset and result in severe muscle weakness due to damage to the peripheral nervous system.  In some individuals, the symptoms may occur in as little as two to three days.  Physiologic functions can be altered ranging from breathing to muscle weakness (usually beginning in the feet and hands).  The current view is that Guillain–Barré syndrome may be considered an autoimmune disease and represents immune dysfunction caused by an attack on the peripheral nerves and damage to the myelin sheet.

Whether compounds such as PQQ would be of any benefit, unfortunately, there is nothing in the current medical literature that would support and/or allow one to make that assertion at this time.  No nutritional supplements per se have been shown to have much value, except for strategies to deal with iatrogenic-related eating behaviors such as poor food intake (induced inadvertently by standard medical treatments for Guillain-Barre syndrome).  Amantadine (trade name Symmetrel) has been shown to have some benefit, but it has to be administered with a number of caveats and its exact mechanism of action is not clear.  Information found in recent summaries regarding approaches to diseases with peripheral neuropathy as a component may be of some additional help (e.g. Interventions for fatigue in peripheral neuropathy, Cochrane Database Syst Rev. 2014; 12: CD008146).

Sources & further reading about PQQ and Parkinson’s disease:

Sources & further reading about PQQ and HIV:

Sources & further reading about Guillain–Barré syndrome:

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