GAPDH-its role in glycolysis (cont)
Research has been conducted at Duke University Medical Center by James Burke searching for other proteins from the human brain that bind to stretches of glutamine and pull out GAPDH to try an answer the glutamine-repeat diseases. Burke found that proteins that bound to GAPDH were huntingtin and a protein that causes a neurodegenerative disease called dentatorubral-pallidolysian atrophy (DRPLA). A researcher at Harvard named Flint Beal found 3 years ago that monkeys injected with a drug that inhibits energy production (such as with GAPDH), developed a Huntington-like disease. Along with the research by Burke, it suggests that defective energy metabolism may cause neurodegenerative diseases. We can explain this using what we know of the brain and its structures. Unlike the tissues of the body which can get energy from fat, the brain relies on almost exclusively on glucose for energy. Because glucose must be processed by the enzymes of glycolysis form its energy to be harvested, interfering with a key enzyme like GAPDH could harm the brain neurons by stunting their energy production. So some of the latest research has been to look for a way to promote glycolysis and not to have the proteins bind to GAPDH, a key enzyme in this metabolic pathway. As one neurogeneticist from University of Pennsylvania said, "It may be one of the better leads on potential treatments for Huntington's Disease."
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