If you Google “mitochondria” and “neurodegeneration,” you’ll find hundreds of published studies linking the two. Mitochondria, the powerhouses of our cells cell, generate damaging reactive oxygen species (ROS) as byproducts of energy production. And the older mitochondria get, the less efficient they become. That means less energy, but more ROS damage—from within! Nowhere is this more apparent than in the aging brain.

The decay of mitochondria in brain cells is a primary factor of all neurodegenerative disorders, from Parkinson’s to dementia.1,2 This deadly process begins when free radicals inflict damage to nerve cells. But increased antioxidant intake by itself is not enough to halt this degenerative cascade. As one team of scientists stated in a study published in July 2011:

“Once the mitochondria are destabilized, cells are destined to commit suicide. Therefore, antioxidative agents alone are not sufficient to protect neuronal loss in many neurodegenerative diseases.”1

That is one reason why the neuroprotective activity of pyrroloquinoline quinone (PQQ) is making waves in some research circles.  PQQ appears to provide protection to the brain not only by guarding against oxidative assaultsand making old mitochondria more efficient but also by birthing new mitochondria. This process, called mitochondrial biogenesis, can prevent age-related cell death that accelerates brain degeneration.

In an animal model, researchers simulated the conditions of stroke by injecting glutamate into brain tissue.  High levels of ROS were produced as expected leading to widespread neuronal damage.  However, in the presence of PQQ much of this damage was avoided. 3

The researchers noted that PQQ did not merely decrease levels of ROS, but also led to the phosphorylation of two kinases, Akt and GSK3β. 3 These kinases possess a larger role in neuronal protection and metabolism indicating a more sustained regulatory impact on brain tissue.  These observations point to larger signaling functions possessed by PQQ and confirm another mechanism by which PQQ not only protects the brain during trauma but also during normal day-to-day rigors.

Studies like this one are important because they help researchers and consumers better understand the results of human research.  For example, it shines some light on how 20 mg/day PQQ given to aging individuals led to reversals in cognitive decline. It is important to not that in that study the effects were increased with co-administration of CoQ10, which also supports mitochondrial function.

 

References:

1. Facecchia K, Fochesato LA, Ray SD, Stohs SJ, Pandey S. Oxidative toxicity in neurodegenerative diseases: role of mitochondrial dysfunction and therapeutic strategies. J Toxicol. 2011;2011:683728. Epub 2011 Jul 14.

2. Martin LJ. Mitochondrial and cell death mechanisms in neurodegenerative diseases. Pharmaceuticals (Basel). 2010;3(4):839-915.

3. Neurochem Res. 2013 Aug;38(8):1661-71.