Hope In The Battle Against Alzheimer’s Disease
Almost fifty percent of people over the age of 85 have Alzheimer’s disease, an illness that is not considered part of the normal aging process by the U.S. National Institute on Aging. Statistics on the NIA website also reveal that there is no cure for the degenerative disease. Recently, according to scientists at University of York and Simon Fraser University in Burnaby, British Columbia, tricking the brain into halting the degeneration of neurons could be a dramatic step in finding a remedy for neurodegenerative diseases—especially Alzheimer’s disease. Research in the latest issue of Nature Chemical Biology looks at Alzheimer’s disease in relation to neurodegeneration involving the death of neurons. This harmful change can be attributed largely to the modification of helpful proteins like “tau.” When phosphates interact with the tau protein it disrupts the stability of neurons in the brain causing neurodegeneration. Professor Gideon Davies of York and Professor David Vocadlo of Simon Fraser took their knowledge of taupathies, or diseases caused by excessive modification of tau by phosphates, to a new level. With the trick of an enzyme inhibitor they produced called “thiazoline,” the world is one step closer to a remedy to ward off Alzheimer’s disease and other neurodegenerative diseases. By manipulating thiazoline, the professors were able to stop the phosphorylation of tau in animals by tricking the brain into positioning sugars on tau instead of the damaging phosphates. Though it is not yet a drug, the findings involving thiazoline serve as an optimistic step in blood-brain barrier research and the prevention of taupathies. “We hope that the work will evolve into new drugs to treat Alzheimer’s disease, although that is still many years off,” said Professor Davies. “The work highlights the synergy of studying the chemistry of enzymes in living cells.” More about Professor Davies and Vocadlo’s findings can be found in this months Nature Structural & Molecular Biology paper.