PQQ & Parkinson’s Disease

There have been very positive reports in the area of PQQ and Parkinson’s. A number of studies have shown that pyrroloquinoline quinone (PQQ) could be beneficial in slowing down or altering the progression of Parkinson’s disease. Life Extention published this: “A mounting body of evidence points to PQQ as a potent intervention in Alzheimer’s and Parkinson’s disease.

Both are triggered by accumulation of abnormal proteins that initiate a cascade of oxidative events resulting in brain cell death.” But it has to be noted that they sell a synthetic PQQ product. PQQ prevents development of alpha-synuclein, the protein responsible for Parkinson’s disease. It also protects nerve cells from the oxidizing ravages of the Alzheimer’s-causing amyloid-beta protein.

A 2010 study revealed that PQQ could prevent formation of amyloid-beta molecular structures. These effects were traced to three distinct biochemical mechanisms described in the sidebar above. PQQ regulates a recently discovered gene called DJ-1. As with PGC-1α and CREB, DJ-1 is intrinsically involved in cell function and survival. It has been shown to prevent cell death by combating intensive antioxidant stress and is of particular importance to brain health and function.DJ-1 damage and mutation have been conclusively linked to the onset of Parkinson’s disease and other neurological disorders.

In spite of the positive reviews where some medical blogs, writers and researchers are referring to PQQ specifically as a cure for Parkinson’s, it should be noted there is still an absence of clinical studies which specifically address whether PQQ can be used as an effective treatment of the Parkinson’s disease. So while we are referring to the fact that these studies are out there and we are encouraged greatly by them, it would still be somewhat unscrupulous to say it is a cure or treatment.

What we know so far is that in studies using experimental animal models, PQQ does interact with the neurotransmitter systems. PQQ appears to be a neuro-protective and possibly it can protect against neurotoxicity induced by compounds which promote or produce Parkinson-like symptoms in the animal laboratory setting. Furthermore, Pyrroloquinoline quinone in chemical assays inhibits the aggregation of alpha-synuclein, a process that is associated with the progression to Parkinson’s disease.

PQQ also seems to protect nerve cells by blocking new amyloid beta molecular structures from forming before they have a chance to cause cellular damage much like that which is observed in Parkinson’s disease. As promising as these observations seems to be and all of the above having been said, there are still questions remaining about how specific and how direct the actions of PQQ might be as it relates to altering the functions of alpha-synuclein and amyloid beta, if and when they are abnormally aggregated.

These are the studies Life Extention specifically referred to in there references to PQQ helping Parkinson’s:

Taira T, Saito Y, Niki T, Iguchi-Ariga SM, Takahashi K, Ariga H. DJ-1 has a role in antioxidative stress to prevent cell death. EMBO Rep. 2004 Feb;5(2):213-8.

Kobayashi M, Kim J, Kobayashi N, et al. Pyrroloquinoline quinone (PQQ) prevents fibril formation of alpha-synuclein. Biochem Biophys Res Commun. 2006 Oct 27;349(3):1139-44.

Mitsumoto A, Nakagawa Y. DJ-1 is an indicator for endogenous reactive oxygen species elicited by endotoxin. Free Rad Res. 2001; 35(6):885-93.

Nunome K, Miyazaki S, Nakano M, Iguchi-Ariga S, Ariga H. Pyrroloquinoline quinone prevents oxidative stress-induced neuronal death probably through changes in oxidative status of DJ-1. Biol Pharm Bull. 2008 Jul;31(7):1321-6.

Zhong N, Xu J. Synergistic activation of the human MnSOD promoter by DJ-1 and PGC-1alpha: regulation by SUMOylation and oxidation. Hum Mol Genet. 2008 Nov 1;17(21):3357-67.

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