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."
Source: http://www.lef.org
