This Is MS Multiple Sclerosis Knowledge & Support Community

Hi everyone,

I was wondering if anyone had heard from, or even tried, pyrroloquinoline quinone (PQQ). It is supposed to help stimulate the generation of new mitochondria.

Thanks,
brm

I too would like to find out if anyone has taken it. It looks to be an inexpensive supplement.

http://pyrroloquinoline-quinone.com/pqq ... upplement/

Discussion of PQQ and Parkinson's
http://www.lef.org/magazine/mag2011/feb ... PQQ_01.htm

Bump

Just read more on PQQ's support for mitochondria. Still interested. Maybe I should just buy some?

http://emediahealth.com/2011/04/10/low- ... -patients/

http://optimalhealthresource.wordpress. ... in-health/

http://pen.sagepub.com/content/early/20 ... 2.full.pdf

http://www.healthpalace.ca/pure-encapsu ... -capsules/

PN

If you decide to take it make sure to report back on how it worked for you. I'm always in need of more energy. I hope it works.

No, I haven't taken it but after reading all of the links in this thread, I find it pretty intriguing myself. It's supposed to be abundant in plant sources so if you don't want to pop another pill, maybe that's a more natural way to boost your PQQ. I wonder if something doesn't interfere with it's absorption...

I'm about to cross a topic line again....it could be helpful to minimize reperfusion/CCSVI damage too. A multi-tasker! There is a lot more info at that wiki link.
http://en.wikipedia.org/wiki/Pyrroloqui ... sen1994-40

PQQ protects brain cells against oxidative damage following ischemia-reperfusion injury—the inflammation and oxidative damage that result from the sudden return of blood and nutrients to tissues deprived of them by stroke.[40

The study cited ...
http://www.sciencedirect.com/science/ar ... 2294903751

The putative essential nutrient pyrroloquinoline quinone is neuroprotective in a rodent model of hypoxic/ischemic brain injury
F.E. Jensen, *, G.J. Gardner*, A.P. Williams*, P.M. Gallop§, E. Aizenman∥, P.A. Rosenberg*
* Department of Neurology , Enders 260, Children's Hospital, 300 Longwood Avenue and Harvard Medical School, Boston, MA 02115, U.S.A.
§ Laboratory of Human BiochemistryEnders 260, Children's Hospital, 300 Longwood Avenue and Harvard Medical School, Boston, MA 02115, U.S.A.
∥ Department of Neurobiology, University of Pittsburgh School of Medicine, PA 15261, U.S.A.
http://dx.doi.org/10.1016/0306-4522(94)90375-1, How to Cite or Link Using DOI

Abstract
Pyrroloquinoline quinone is a ubiquitous redox cofactor and putative essential nutrient in mammals. Pyrroloquinoline quinone has recently been demonstrated to depress N-methyl-d-rasparate induced electrical responses and is neuroprotective in vitro. In addition, pyrroloquinoline quinone has been demonstrated to act as a free radical scavenger in mammalian tissues. In this study, we demonstrate a neuroprotective effect of pyrroloquinoline quinone in an in vivo cerebral hypoxia/ischemia model in the rodent. Significant reduction in infarct size resulted from pyrroloquinoline quinone pretreatment and also when pyrroloquinoline quinone was administered following induction of hypoxia/ischemia. The neuroprotective effect was not dependent on change in core or cranial temperatures, as there was no difference between temperature measurements in pyrroloquinoline quinone-treated and vehicle-treated controls. No changes in electroencephalographie activity were observed at neuroprotective doses. These findings suggest that pyrroloquinoline quinone may represent a novel class of quinoid reagents of potential use in the treatment of neurological disorders that involve excitotoxicity.

This study demonstrates a protective effect of the novel essential nutrient pyrroloquinoline quinone on brain injury in a rodent model of cerebral hypoxia/ischemia. Pyrroloquinoline quinone was neuroprotective when administered before and even after the insult, and did not appear to have significant neurobehavioral side effects. Pyrroloquinoline quinone represents a new class of agents with potential use in the therapy of stroke.

So, who's going to take this stuff and report back?

OK. I've stirred the pot so I'll go first. I've seen a PQQ+CoQ but I'm already taking CoQ. I will research and come up with a short list.

P

Just to follow up: I've been taking 10mg PQQ and 120mg Q10 twice daily for about 6 months now.

Unfortunately I can't say that I've noticed anything that can be called an improvement.

Cheers,
brm

Just pinging this thread to see if anybody else has tried PQQ since?

Recent article at: http://www.lef.org/newsletter/2014/0124 ... humans.htm

"... A significant decline in post-treatment C-reactive protein and interleukin-6 levels occurred indicating a decrease in the inflammatory response. The researchers also documented alterations in urinary metabolites that indicated improvements in mitochondrial efficiency...."

I tried one capsule pqq for just a couple of days. I had to stop taking it to isolate the cause of some weirdness (it wasn't pqq) so I don't have any feedback based on long term experience or inflammation really (currently on a rituxan vacation from inflammation). I can say it gave me a mild energy/mental acuity boost that wasn't unnatural feeling like caffeine. I don't know if that phenomena would continue or if it would occur if I were in an inflammatory state. I'm guessing not based on others' experience.

Give it a try and see for yourself??

These abstracts seems to show it reduces one of the key destructive neuron processes in MS -Glutmate neurotoxicity.

http://home.ix.netcom.com/~jdalton/ms-two-stages.pdf (glutamate MS info)



Neurochem Res. 2013 Aug;38(8):1661-71. doi: 10.1007/s11064-013-1068-2. Epub 2013 May 18.

Pyrroloquinoline quinine protects rat brain cortex against acute glutamate-induced neurotoxicity.

Zhang Q, Ding M, Cao Z, Zhang J, Ding F, Ke K.
Abstract

To investigate possible protective effects of pyrroloquinoline quinone (PQQ) on the rat cortex with glutamate injection and to understand the mechanisms linking the in vivo neuroprotection of PQQ. Adult Sprague-Dawley rats received glutamate injection into the rat cortex. Terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling assay was performed to observe influences of co-treatment with PQQ (simultaneous injection with PQQ and glutamate) on neural cell apoptosis in the rat cortex. The production of reactive oxygen species (ROS) in the rat cortex was detected by flow cytometry using 2',7'-dichlorofluorescin diacetate labeling, and the activity of superoxide dismutase, glutathione and malondialdehyde was respectively determined. Real time quantitative RT-PCR and Western blot were applied to measure the mRNA and protein expressions of Nrf1, Nrf2, HO-1 and GCLC in the rat cortex. Western blot was used to detect the phosphorylation of Akt and GSK3β in the rat cortex. Co-treatment with PQQ protected neural cells in the rat cortex from glutamate-induced apoptosis. PQQ decreased the ROS production induced by glutamate injection. PQQ increased the mRNA and protein expressions of Nrf2, HO-1 and GCLC and the phosphorylation of Akt and GSK3β in the cortex of glutamate-injected rats. PQQ could produce neuroprotective effects on the rat cortex. The antioxidant properties of PQQ and PQQ-induced activation of Akt/GSK3β signal pathway might be responsible for the in vivo neuroprotection of PQQ.


PMID: 23686346 [PubMed - in process]

http://www.sciencedirect.com/science/ar ... 8X11000524 (full text)



Toxicol Appl Pharmacol. 2011 Apr 1;252(1):62-72. doi: 10.1016/j.taap.2011.02.006. Epub 2011 Feb 12.

The neuroprotective action of pyrroloquinoline quinone against glutamate-induced apoptosis in hippocampal neurons is mediated through the activation of PI3K/Akt pathway.

Zhang Q, Shen M, Ding M, Shen D, Ding F.
Abstract

Pyrroloquinoline quinone (PQQ), a cofactor in several enzyme-catalyzed redox reactions, possesses a potential capability of scavenging reactive oxygen species (ROS) and inhibiting cell apoptosis. In this study, we investigated the effects of PQQ on glutamate-induced cell death in primary cultured hippocampal neurons and the possible underlying mechanisms. We found that glutamate-induced apoptosis in cultured hippocampal neurons was significantly attenuated by the ensuing PQQ treatment, which also inhibited the glutamate-induced increase in Ca²+ influx, caspase-3 activity, and ROS production, and reversed the glutamate-induced decrease in Bcl-2/Bax ratio. The examination of signaling pathways revealed that PQQ treatment activated the phosphorylation of Akt and suppressed the glutamate-induced phosphorylation of c-Jun N-terminal protein kinase (JNK). And inhibition of phosphatidylinositol-3-kinase (PI3K)/Akt cascade by LY294002 and wortmannin significantly blocked the protective effects of PQQ, and alleviated the increase in Bcl-2/Bax ratio. Taken together, our results indicated that PQQ could protect primary cultured hippocampal neurons against glutamate-induced cell damage by scavenging ROS, reducing Ca²+ influx, and caspase-3 activity, and suggested that PQQ-activated PI3K/Akt signaling might be responsible for its neuroprotective action through modulation of glutamate-induced imbalance between Bcl-2 and Bax.

Copyright © 2011 Elsevier Inc. All rights reserved.

PMID: 21320517 [PubMed - indexed for MEDLINE]


jackD

P.S. It could also help lower nerve pain..

Eur J Pharmacol. 2012 Dec 15;697(1-3):53-8. doi: 10.1016/j.ejphar.2012.09.052. Epub 2012 Oct 12.

Effect of pyrroloquinoline quinone on neuropathic pain following chronic constriction injury of the sciatic nerve in rats.

Gong D, Geng C, Jiang L, Aoki Y, Nakano M, Zhong L.
Abstract

Pyrroloquinoline quinone PQQ is a naturally occurring redox cofactor that acts as an essential nutrient, antioxidant, and redox modulator. PQQ has been demonstrated to oxidize the redox modulatory site of N-methyl-d-aspartic acid (NMDA) receptors.

Such agents are known to be neuroprotective in experimental stroke models. However, there is not report about the therapeutic effect of PQQ on neuropathic pain. We tested the effects of oral administration of PQQ on neuropathic pain of rats with chronic constriction injury (CCI) of the sciatic nerve.

The repeated oral administration of PQQ (20 and 40mg/kg, once a day for 4 weeks, from day 1 after the injury) attenuated both thermal and mechanical hyperalgesia, and also attenuated the muscle atrophy.

The anti-hyperalgesic activity of PQQ was associated with a significant reduction of pro-inflammatory mediators such as tumor necrosis factor alpha (TNF-α) and lipid peroxide malondialdehyde (MDA) levels.

In the present investigation, PQQ is shown to have analgesic effect which was found in the first time, probably through reducing the release of pro-inflammatory mediator and inhibiting oxidative stress.

Copyright © 2012 Elsevier B.V. All rights reserved.

Potential Benefits of Taking a PQQ Supplement and/or Increasing Pyrroloquinoline Quinone Intake

http://michaelrucker.com/sandbox/pqq/supplement/