Reprinted with the kind permission of Life Extension.
October 1, 2018. A study reported in Cell Death & Disease revealed a previously unknown mechanism that may contribute to traumatic brain injury and Alzheimer’s disease. While a buildup of the protein amyloid-beta has been hypothesized to be the major driver of Alzheimer’s disease, the study suggests that another protein, after undergoing oxidation by free radicals, could be a causative factor.
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“Indeed, scientists have known for a long time that during aging or in neurodegenerative disease cells produce free radicals,” explained lead researcher Federico Sesti, who is a professor of neuroscience and cell biology at Rutgers Robert Wood Johnson Medical School. “Free radicals are toxic molecules that can cause a reaction that results in lost electrons in important cellular components, including the channels.”
Dr Sesti and colleagues determined that oxidation of a potassium channel known as KCNB1 results in a toxic buildup of this protein, leading to increased amyloid-beta production and damage to brain function. “The discovery of KCNB1’s oxidation/build-up was found through observation of both mouse and human brains, which is significant as most scientific studies do not usually go beyond observing animals,” Dr Sesti reported. “Further, KCBB1 channels may not only contribute to Alzheimer’s but also to other conditions of stress as it was found in a recent study that they are formed following brain trauma.”
Acting on the knowledge that oxidation of KCNB1 channels in traumatic brain injury and Alzheimer’s disease leads to activation of Src tyrosine kinases, the researchers tested the effects of the Src kinase inhibitor dasatinib in a mouse model of Alzheimer’s disease. “Our study shows that this drug and similar ones could potentially be used to treat Alzheimer’s, a discovery that leads the way to launching a clinical trial to test this drug in humans,” Dr Sesti concluded.