In a bid to try to understand what causes Alzheimer’s and traumatic brain injury, Federico Sesti, a professor of neuroscience and cell biology at Rutgers Robert Wood Johnson Medical School, undertook a recent study that looked at a new mechanism involving a non-amyloid-beta protein, a potassium voltage-gated channel called KCNB1. Oxidation causes KCNB1 channels to build up in a brain and become toxic to neurons and then encourage the production of amyloid-beta. In this study, the build-up of KCNB1 was much higher in brains affected by Alzheimer’s than in those not affected.
“Study of KCNB1 sheds some light on cause of Alzheimer's and traumatic brain injury“
Sesti said: “Scientists have known for a long time that during aging or in neurodegenerative disease cells produce free radicals. Free radicals are toxic molecules that can cause a reaction that results in lost electrons in important cellular components, including the channels. 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. 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. 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."