Wednesday February 20, 2019

A Possible Cause For Alzheimer’s Finally Found: Researchers

In the cases of Alzheimer's and traumatic brain injury, the build-up of KCNB1 is associated with severe damage of mental function.

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alzheimer's, cholesterol
One hemisphere of a healthy brain (L) is pictured next to one hemisphere of a brain of a person suffering from Alzheimer disease. VOA

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.

Alzheimer's
Alzheimer’s disease. Wikipedia

“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.

 Alzheimer's
A lady suffering from Alzheimer’s. Flickr

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.

Also Read: A Majority of Children Die Due to Lack of Basic Healthcare Facilities: UN

The research team now hopes to launch a clinical trial to test the treatment in humans. (IANS)

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Researchers Identify New Mechanism to Prevent Alzheimer’s

The team next plans to test this approach in additional animal studies and eventually in human trials using small molecule inhibitors targeting eEF2K

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In Alzheimer's disease, patients start losing memory, Pixabay

Researchers have identified a novel mechanism and a potential new therapeutic target for Alzheimer’s disease (AD), says a new study on mice.

Alzheimer’s is characterised by profound memory loss and synaptic failure. Although the exact cause of the disease remains unclear, it is well established that maintaining memory and synaptic plasticity requires protein synthesis.

The function of the synapse is to transfer electric activity (information) from one cell to another.

“Alzheimer’s is such a devastating disease and currently there is no cure or effective therapy for it,” said Tao Ma, Assistant Professor at Wake Forest School of Medicine in the US.

A lady suffering from Alzheimer’s. Flickr

“All completed clinical trials of new drugs have failed, so there is clearly a need for novel therapeutic targets for potential treatments.”

For the study, the team has shown that AD-associated activation of a signaling molecule termed eEF2K leads to inhibition of protein synthesis.

Further, they wanted to determine if suppression of eEF2K could improve protein synthesis capacity, consequently alleviating the cognitive and synaptic impairments associated with the disease.

They used a genetic approach to repress the activity of eEF2K in Alzheimer’s mouse models.

Cognitive Impairment
Alzheimer’s disease patient Isidora Tomaz, 82, sits in an armchair in her house in Lisbon, Portugal. VOA

The findings, published in the Journal of Clinical Investigation, showed that genetic suppression of eEF2K prevented memory loss in those animal models and significantly improved synaptic function.

Also Read- Global Warming Could Change US Cities’ Climate by 2080- Study

“These findings are encouraging and provide a new pathway for further research,” said Ma.

The team next plans to test this approach in additional animal studies and eventually in human trials using small molecule inhibitors targeting eEF2K. (IANS)