Vit K can help Parkinson's patients
http://www.irishhealth.com/article.html?id=20679

[Posted: Fri 11/05/2012 www.irishhealth.com]

By Caoimhe Moore

Administration of vitamin K2 could restore movement in Parkinson's patients.

Research has shown using vitamin K2 to reverse the effects of one of the genetic malfunctions that can lead to Parkinson's has given hope to Parkinson's patients.

Neuroscientist Patrik Verstreken, associated with the research institute VIB and KU Leuven university in Belgium, used fruit flies to study the mutation of a specific genetic pathway which can lead to Parkinson's.

Parkinson's is a neurodegenerative disease and the exact cause is unknown. The symptoms include lack of movement, hesitant speech, tremors and muscle stiffness.

The pathway studied regulates mitochondria, which transports electrons to the cell, providing the cell with energy. Mutation of the pathway can significantly lower the energy supply to the cell.

Lack of energy in a cell has serious consequences - parts of the brain will start to die and neuron communication will be disrupted.

Verstreken and his team found that vitamin K2 improved electron transport in the mitochondria. This in turn led to improved energy production.

Dr Versgtreken said therefore, it appeared that administering vitamin K2 could possibly help patients with Parkinson's. However, more work needed to be done to understand this better.

The study found that fruit flies became paralyzed when the PINK1 and Parkin pathway was mutated. Once the flies were given vitamin K2 their flying ability improved.

This research, it is believed, could potentially provide hope for new treatments for Parkinson's patients.

The study was published in the journal Scienc

Science DOI: 10.1126/science.1218632
REPORT
Vitamin K2 Is a Mitochondrial Electron Carrier That Rescues Pink1 Deficiency
Melissa Vos1,2, Giovanni Esposito1,2, Janaka N. Edirisinghe3, Sven Vilain1,2, Dominik M. Haddad1,2, Jan R. Slabbaert1,2, Stefanie Van Meensel1,2, Onno Schaap1,2, Bart De Strooper1,2, R. Meganathan3, Vanessa A. Morais1,2, Patrik Verstreken1,2,*
+ Author Affiliations

1VIB Center for the Biology of Disease, 3000 Leuven, Belgium.
2K.U.Leuven, Center for Human Genetics and Leuven Research Institute for Neurodegenerative Diseases (LIND), 3000 Leuven, Belgium.
3Department of Biological Sciences, Northern Illinois University, DeKalb, IL 60115, USA.
↵*To whom correspondence should be addressed. E-mail: Patrik.verstreken@med.kuleuven.be
ABSTRACT

Human UBIAD1 localizes to mitochondria and converts vitamin K1 to vitamin K2. 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. We identified Drosophila UBIAD1/Heix as a modifier of pink1, a gene mutated in Parkinson’s disease that affects mitochondrial function. Here, we found that vitamin K2 was necessary and sufficient to transfer electrons in Drosophila mitochondria. Heix mutants showed severe mitochondrial defects that were rescued by vitamin K2, and, similar to ubiquinone, vitamin K2 transferred electrons in Drosophila mitochondria, resulting in more efficient adenosine triphosphate (ATP) production. Thus, mitochondrial dysfunction was rescued by vitamin K2 that serves as a mitochondrial electron carrier, helping to maintain normal ATP production.

http://www.sciencemag.org/content/ea....1218632.short