PQQ Reduces Brain AgingJuly 2018
By Brian Parker
Scientists have uncovered further evidence about the abilities of PQQ (pyrroloquinoline quinone) to help support the brain.
Generating excitement are three distinct ways that PQQ reduces brain aging including:
- Improved brain blood flow1,2
- Reduced neurotoxicity3-6
- Protection against sugar damage.7
A study published in 2017 demonstrates that a formulation containing PQQ reduced evidence of Alzheimer’s disease in the laboratory animal model.4
What you need to know
- Cognitive decline and dementia take a lifetime to develop, but can rob an individual of a lifetime of memories in just a few years.
- Many different processes contribute to cognitive decline, most of which are preventable if addressed far enough in advance.
- PQQ is showing tremendous promise at fighting age-related brain dysfunction.
- Studies show that PQQ acts on at least three different dementia-producing processes: neurotoxicity, declining brain blood flow, and glucose-induced vascular damage.
- Many of these beneficial effects can be traced back to PQQ’s ability to boost mitochondria, the cell’s energy factories that are particularly important for healthy brain function.
- Taking 20 mg of PQQ is recommended for keeping these cognition-threatening processes at bay and slowing the age-related decline in cognitive function.
How PQQ Powers Better Brain Function
The human brain uses more energy than any other organ in the body.
We devote 20%-25% of all energy to supporting brain function.8
This energy production is powered by mitochondria, the energy factories that convert food into the cellular fuel that powers our entire body.9
With age, some mitochondria tend to die off, and the ones that are left don’t function as well.10 This results in an energy crisis that can have a devastating impact on brain function.
PQQ has been shown to reduce brain aging by helping existing mitochondria work more efficiently—and to promote the formation of new mitochondria.
Neurotoxicity Damages the Brain
Brain cells are damaged by chronic exposure to toxins, even at low doses.
Some toxins come from outside the body. For example, heavy metals, bacterial toxins, and environmental poisonings are all possible factors in neurodegenerative diseases like Parkinson’s.11-14
Other brain-damaging toxins form within the body. These include the abnormal proteins (like tau and beta-amyloid) that accumulate in brain tissue and contribute to the destruction of brain cells in senile disorders.4,15,16 The neurotransmitter glutamate is known to cause excitotoxic damage to brain cells with aging.3,16,17
A 2017 animal study has now demonstrated that PQQ can help prevent the neurotoxicity that is so damaging to the brain.
Protecting Against Senile Pathologies
In a mouse model of Alzheimer’s disease, mice were given a formulation containing PQQ and other ingredients (green tea, blueberry powder and extract, carnosine, vitamin D, and grapeseed extract) for 12 weeks. The researchers then compared their behavioral and neurological progress with similar, but unsupplemented, animals.4
The supplemented mice experienced benefits over their unsupplemented counterparts, including reduced motor deficits and reduced cognitive impairment. They also learned significantly faster and had better recall.4
When the researchers examined the mice’s brains, they found significantly smaller deposits of toxic proteins in the brains of the supplemented animals indicative of protection against neurotoxicity.4
There were also compelling indications of improved mitochondrial efficiency in the supplemented mice. This was evidenced by raised levels of ATP (energy) and oxygen utilization, and less oxidative stress, which damages mitochondria.4
Overall, this study shows that PQQ, along with other ingredients, may contribute to beneficial effects on motor and cognitive function, largely through improving mitochondrial function and reducing toxic proteins in the brain.4
These findings add considerably to previous work done with a mouse model of Parkinson’s disease. In this study, PQQ restored mitochondrial function in damaged brain cells and prevented brain-cell loss—effects that reduced the abnormal movements associated with Parkinson’s.5
There’s also evidence that PQQ can prevent glutamate-induced neurotoxicity in brain cells in culture, helping to quell the storm of chemical stresses that such “excitotoxicity” produces.3,6
Together, these studies highlight PQQ’s ability to interfere with brain cell toxicity and restore normal function.
PQQ Restores Brain Blood Flow
Because of the brain’s constant energy requirements, it demands a substantial share of blood.
However, as we age, conditions like atherosclerosis, endothelial dysfunction, and other blood-vessel changes blunt blood flow to the brain. This can affect cognitive function, while leaving us vulnerable to acute loss of blood flow, which can result in a stroke.
Two human studies published in 2016 demonstrate that supplementing with PQQ has beneficial effects on brain blood flow and cognitive function.
In one randomized, placebo-controlled clinical trial, 41 healthy elderly subjects took 20 mg of PQQ/day or a placebo.2 Then they were tested for both cognitive function and brain blood flow using sophisticated near-infrared spectrometry.
After 12 weeks, the people taking PQQ experienced improvements in their working memory and in their ability to retain focus on tasks in the face of distractions. These benefits were likely produced by a PQQ-induced increase in brain blood flow to the relevant parts of the brain.2
A follow-up study demonstrated that taking 20 mg of PQQ every day for 12 weeks boosted blood flow to the right prefrontal cortex. This is the area of the brain devoted to higher cognitive functions.
In addition, oxygen utilization in that area was significantly higher in supplemented people, a clear demonstration that PQQ was boosting energy extraction to fuel the improved cognitive performance.1
These studies highlight the importance of PQQ in improving brain blood flow as an important step in slowing cognitive decline with aging.
PQQ Protects Brain Tissue From Sugar Damage
People with type II diabetes have an increased risk of developing Alzheimer’s disease. The connection is so strong that many scientists now refer to Alzheimer’s as “type III diabetes.”15
This is partly because chemical activity associated with increased glucose levels has now been directly tied to the formation of the toxic tau and beta-amyloid proteins associated with Alzheimer’s and other neurodegenerative diseases.15
But sugar-induced damage takes place in many people, which means that non-diabetic individuals are at risk for neurodegeneration related to the harmful effects of chronic glucose exposure.18,19
One of the most destructive effects of sugar on brain function is its impact on brain blood vessels. Long-term glucose exposure damages cells in the vessel lining (the endothelial layer) that are responsible for modulating blood flow and pressure.20,21
A recent study has indicated that PQQ may protect against glucose-induced endothelial dysfunction in the brain.7
To determine this, researchers treated cultured brain endothelial cells with concentrated sugar solutions, which reduced the cells’ ability to survive. Sugar exposure caused many cells to undergo programmed cell death (apoptosis), while raising the levels of reactive chemical stressors within cells.7 This is critical because the loss of brain cells plays a role in neurodegenerative diseases.22,23
When PQQ was added to these sugar-laden endothelial cell cultures, there was:
- Reversal of cell damage
- Prevention of apoptosis
- Reduced formation of chemical stressors
Most of these beneficial effects could be traced to improvements in the function, and even the number, of mitochondria within endothelial cells.7
It is already known that PQQ can boost the production of new energy-producing mitochondria (this is called mitochondrial biogenesis). This study advances our knowledge of PQQ in this arena, and shows that such protection affords insurance against the sugar-induced vessel damage that can contribute to declining brain function.
PQQ is emerging as an important brain-protective nutrient. Studies now show that PQQ can protect brain tissue against toxic assault (neurotoxicity) from inside and outside the body.
PQQ boosts brain blood flow, in a direct counterattack on blood flow restrictions imposed by aging blood vessels.
PQQ can also limit the glucose-induced damage to brain blood vessels, a major contributor to dementia and other forms of cognitive decline.
Supplementing with 20 mg of PQQ is recommended for keeping these cognition-threatening processes at bay and slowing age-related decline in cognitive function.
If you have any questions on the scientific content of this article, please call a Life Extension® Wellness Specialist at 1-866-864-3027.
- Nakano M, Murayama Y, Hu L, et al. Effects of Antioxidant Supplements (BioPQQ) on Cerebral Blood Flow and Oxygen Metabolism in the Prefrontal Cortex. Adv Exp Med Biol. 2016;923:215-22.
- Itoh Y, Hine K, Miura H, et al. Effect of the Antioxidant Supplement Pyrroloquinoline Quinone Disodium Salt (BioPQQ) on Cognitive Functions. Adv Exp Med Biol. 2016;876:319-25.
- Guan S, Xu J, Guo Y, et al. Pyrroloquinoline quinone against glutamate-induced neurotoxicity in cultured neural stem and progenitor cells. Int J Dev Neurosci. 2015;42:37-45.
- Sawmiller D, Li S, Mori T, et al. Beneficial effects of a pyrroloquinolinequinone-containing dietary formulation on motor deficiency, cognitive decline and mitochondrial dysfunction in a mouse model of Alzheimer’s disease. Heliyon. 2017;3(4):e00279.
- 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;108:238-51.
- Zhou X, Chen Q, Hu X, et al. Pyrroloquinoline quinone prevents MK-801-induced stereotypical behavior and cognitive deficits in mice. Behav Brain Res. 2014;258:153-9.
- Wang Z, Chen GQ, Yu GP, et al. Pyrroloquinoline quinone protects mouse brain endothelial cells from high glucose-induced damage in vitro. Acta Pharmacol Sin. 2014;35(11):1402-10.
- Belanger M, Allaman I, Magistretti PJ. Brain energy metabolism: focus on astrocyte-neuron metabolic cooperation. Cell Metab. 2011;14(6):724-38.
- McBride HM, Neuspiel M, Wasiak S. Mitochondria: more than just a powerhouse. Curr Biol. 2006;16(14):R551-60.
- Bratic A, Larsson NG. The role of mitochondria in aging. J Clin Invest. 2013;123(3):951-7.
- Cicero CE, Mostile G, Vasta R, et al. Metals and neurodegenerative diseases. A systematic review. Environ Res. 2017;159:82-94.
- Kovacic S, Pepeljnjak S, Petrinec Z, et al. Fumonisin B1 neurotoxicity in young carp (Cyprinus carpio L.). Arh Hig Rada Toksikol. 2009;60(4):419-26.
- Bradley WG, Mash DC. Beyond Guam: the cyanobacteria/BMAA hypothesis of the cause of ALS and other neurodegenerative diseases. Amyotroph Lateral Scler. 2009;10 Suppl 2:7-20.
- Shaw CA, Hoglinger GU. Neurodegenerative diseases: neurotoxins as sufficient etiologic agents? Neuromolecular Med. 2008;10(1):1-9.
- Zhang Y, Huang NQ, Yan F, et al. Diabetes mellitus and Alzheimer’s disease: GSK-3beta as a potential link. Behav Brain Res. 2017;339:57-65.
- Roher AE, Kokjohn TA, Clarke SG, et al. APP/Abeta structural diversity and Alzheimer’s disease pathogenesis. Neurochem Int. 2017;110:1-13.
- Miyamoto T, Stein L, Thomas R, et al. Phosphorylation of tau at Y18, but not tau-fyn binding, is required for tau to modulate NMDA receptor-dependent excitotoxicity in primary neuronal culture. Mol Neurodegener. 2017;12(1):41.
- Shah RC, Matthews DC, Andrews RD, et al. An evaluation of MSDC-0160, a prototype mTOT modulating insulin sensitizer, in patients with mild Alzheimer’s disease. Curr Alzheimer Res. 2014;11(6):564-73.
- Kuusisto J, Koivisto K, Mykkanen L, et al. Association between features of the insulin resistance syndrome and Alzheimer’s disease independently of apolipoprotein E4 phenotype: cross sectional population based study. Bmj. 1997;315(7115):1045-9.
- Du H, Li P, Wang J, et al. The interaction of amyloid beta and the receptor for advanced glycation endproducts induces matrix metalloproteinase-2 expression in brain endothelial cells. Cell Mol Neurobiol. 2012;32(1):141-7.
- Xiong F, Leonov S, Howard AC, et al. Receptor for advanced glycation end products (RAGE) prevents endothelial cell membrane resealing and regulates F-actin remodeling in a beta-catenin-dependent manner. J Biol Chem. 2011;286(40):35061-70.
- Gorman AM. Neuronal cell death in neurodegenerative diseases: recurring themes around protein handling. J Cell Mol Med. 2008;12(6a):2263-80.
- Ford L, Crossley M, Williams T, et al. Effects of Abeta exposure on long-term associative memory and its neuronal mechanisms in a defined neuronal network. Sci Rep. 2015;5:10614.