Summary of my Research so Far

Posted: March 1, 2013 in Uncategorized
Tags: , , , ,

Since it is Friday I figured I would give everyone a summary of where I am on my research. I have started really diving into the survival benefit of having Huntington’s Disease and have found some really good information that should help with developing an appropriate protocol. I will write a much more thorough report on this with accompanying studies in days to come. Still sifting through some details.

With that said the survival benefit of HD is a minimal risk of cancer and an ability to reproduce more. The reason for the decreased cancer risk is an increase in the tumor suppressant protein p53. Protein p53 actually has another role in the human body that was recently discovered. It suppresses glucose biosynthesis and consumption by inhibiting glucose-6-phosphate-dehydrogenase. G6PD is responsible for maintaining glutathione levels, a major antioxidant. It also plays a role in the biosynthesis of fatty acids. It is actually increased by insulin.

G6PD is also the rate limiting factor of the pentose phosphate pathway. This is a pathway used as an alternative to glycolysis. An end product of this pathway is ribose-5-phosphate. This is intriguing to me because the ribose-5-phosphate is a major player in the creation of nucleotides. Huntington’s Disease just so happens to be a nucleotide repeat disorder. This brought me to my next question which was does inhibiting ribose-5-phosphate result in an improvement in symptoms.

There has been research done here within the last year that looks promising for Huntington’s Disease as well as diseases of aging. One study suggested that modulating the levels of ribose-5-phosphate could serve as a treatment for aging as well as polyglutamine neurotoxicity (Wang, 2011). The CAG repeats in Huntington’s Disease are polyglutamine tracts.

Currently I am trying to understand more about the pentose phosphate pathway and how the inhibition of G6PD by an increase of protein p53 can potentially lead to an increase in ribose-5-phosphate. Maybe if we can interfere with these steps we can decrease the number of nucleotides being made? Also, maybe G6PD’s role in cell death may be why we see chorea present with the decrease in GABA in the basal ganglia? Below are references and anyone willing to help out I greatly appreciate it.

http://www.sciencedaily.com/releases/2011/03/110302142921.htm

http://www.ncbi.nlm.nih.gov/books/NBK22590/

http://www.rose-hulman.edu/~brandt/Chem330/HMP_Shunt.pdf

http://ajpcell.physiology.org/content/276/5/C1121.short

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