An article published on May 11, 2012 in the journal Science reports the outcome of research that suggests that the administration of vitamin K2 could reverse mitochondrial defects responsible for the symptoms of Parkinson's disease.
Mitochondria are organelles within the cells that function as power plants to provide energy for the cells' operation. Energy is generated via the transporting of electrons—a process that is disrupted in Parkinson's disease. This loss of energy production results in cell death, which interferes with communication between cells known as neurons, leading to such characteristic symptoms as tremors, muscle stiffness and lack of movement.
In their introduction to the article, neuroscientist Patrik Verstreken of the Flanders Institute for Biotechnology and his colleagues at Northern Illinois University note that "Vitamin K2 is best known as a cofactor in blood coagulation, but in bacteria it is a membrane-bound electron carrier. Whether vitamin K2 exerts a similar carrier function in eukaryotic cells is unknown."
For their research, the team used fruitflies that were genetically modified to have defects found in human Parkinson's disease patients that lead to decreased mitochondrial activity. While flies with mutated PINK1 or Parkin were flightless due to defects in their mitochondria, those that received vitamin K2 were better able to fly due to improved electron transport within the mitochondria that led to more energy being produced--a process similar to that elicited by ubiquinone. "Thus, mitochondrial dysfunction was rescued by vitamin K2 that serves as a mitochondrial electron carrier, helping to maintain normal ATP production," the authors conclude.
"It appears from our research that administering vitamin K2 could possibly help patients with Parkinson's," Dr Verstreken remarked. "However, more work needs to be done to understand this better."