In a new study, Rutgers researchers discovered a new mechanism that may contribute to Alzheimer’s disease and traumatic brain injury.
The team now hope to launch a clinical trial to test the treatment in humans.
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.
Although what causes Alzheimer’s is unknown, a popular theory suggests a protein known as amyloid-beta slowly builds up a plaque in the brains of people with Alzheimer’s.
In the current study, the team looked at a new mechanism, which involves a non-amyloid-beta protein, a potassium channel referred to as KCNB1.
Under conditions of stress in a brain affected by Alzheimer’s, KCNB1 builds up and becomes toxic to neurons and then promotes the production of amyloid-beta.
The build-up of KCNB1 channels is caused by a chemical process commonly known as oxidation.
The study found that in brains affected by Alzheimer’s, the build-up of KCNB1 was much higher compared to normal brains.
The team suggests that 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.
In the cases of Alzheimer’s and traumatic brain injury, the build-up of KCNB1 is associated with severe damage to mental function.
As a result of this discovery, the team successfully tested a drug called Sprycel in mice. The drug is used to treat patients with leukemia.
The researchers suggest that their study shows that this drug and similar ones could potentially be used to treat Alzheimer’s, a discovery that leads the way to launch a clinical trial to test this drug in humans.
The lead author is Dr. Sesti.
The study is published in the journal Cell Death & Disease.
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Source: Cell Death & Disease.