Possible cause for Alzheimer s, traumatic brain injury identified
Thursday - September 27, 2018 2:44 pm ,
Category : HEALTH
New York Sep 27 (IANS) Researchers have identified a new mechanism that may contribute to Alzheimer s disease and traumatic brain injury hoping that the discovery may lead to effective treatment.
According to researchers from Rutgers University the causes of Alzheimer s is unknown. But a popular theory suggests a protein known as amyloid-beta slowly builds up a plaque in the brains of people with the disease.
The research 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.
"Indeed scientists have known for a long time that during aging or in neurodegenerative disease cells produce free radicals " said co-author Federico Sesti a professor at the varsity.
"Free radicals are toxic molecules that can cause a reaction that results in lost electrons in important cellular components including the channels " Sesti added.
The study published in the journal Cell Death and Disease found that in brains affected by Alzheimer s the build-up of KCNB1 was much higher compared to normal brains.
"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 " said Sesti.
"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 " Sesti added.
In the cases of Alzheimer s and traumatic brain injury the build-up of KCNB1 is associated with severe damage of mental function. As a result of this discovery the researcher successfully tested a drug called Sprycel in mice. The drug is used to treat patients with leukemia.
The research team now hopes to launch a clinical trial to test the treatment in humans.
--IANS vc/ksk/mr
According to researchers from Rutgers University the causes of Alzheimer s is unknown. But a popular theory suggests a protein known as amyloid-beta slowly builds up a plaque in the brains of people with the disease.
The research 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.
"Indeed scientists have known for a long time that during aging or in neurodegenerative disease cells produce free radicals " said co-author Federico Sesti a professor at the varsity.
"Free radicals are toxic molecules that can cause a reaction that results in lost electrons in important cellular components including the channels " Sesti added.
The study published in the journal Cell Death and Disease found that in brains affected by Alzheimer s the build-up of KCNB1 was much higher compared to normal brains.
"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 " said Sesti.
"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 " Sesti added.
In the cases of Alzheimer s and traumatic brain injury the build-up of KCNB1 is associated with severe damage of mental function. As a result of this discovery the researcher successfully tested a drug called Sprycel in mice. The drug is used to treat patients with leukemia.
The research team now hopes to launch a clinical trial to test the treatment in humans.
--IANS vc/ksk/mr
