Researchers at Tel Aviv University found a link between brain hyperactivity and Alzheimer's-related seizures Researchers at Tel Aviv University found a link between brain hyperactivity and Alzheimer's-related seizures Researchers at Tel Aviv University found a link between brain hyperactivity and Alzheimer's-related seizures. (Photo: Bangkokhappiness/Shutterstock)

Research finds link between brain hyperactivity and seizures in Alzheimer's patients

Tel Aviv University study focuses on the area of the brain that controls learning and memory.

Elevated brain activity can be linked to a higher risk of seizures in  Alzheimer's patients, according to new research published in the journal Cell Reports.

The research, led by Dr. Inna Slutsky of Tel Aviv University in collaboration with Professors Dominic Walsh of Harvard University and Ehud Isacoff of the University of California at Berkeley, answers long-unexplained questions in the study of Alzheimer's disease. Scientists knew patients with Alzheimer's were more likely to have seizures, but until now, they didn't know how or why.

To find those answers, researchers looked at the hippocampus, the area of the brain that controls learning and memory. It's also one of the first regions of the brain to suffer damage due to Alzheimer's. The team found that elevated activity in that area of the brain is linked with the early stages of the disease, signaled by memory loss and disorientation.

The amyloid precursor protein (APP) plays a key role in producing a protein fragment known as amyloid-beta, which is involved in the development and progression of Alzheimer's. APP also acts as a receptor for amyloid-beta.  Slutsky's team found that when the amyloid-beta protein binds to pairs of APP, a signaling cascade is triggered, resulting in elevated brain activity.

The research project was launched five years ago after the team discovered that the amyloid-beta protein is essential for the normal day-to-day transfer of information through the brain's nerve cell networks; previously, it was thought to be an exclusively toxic molecule. However, if the level of amyloid-beta is increased even slightly, it significantly impairs the transfer of information between neurons.

The team used a combination of high-resolution optical imaging, biophysical methods and molecular biology to examine APP-dependent signaling in neural cultures, brain slices and mouse models.

According to Slutsky, the next step is to pinpoint the precise location where the amyloid-beta binds to APP and understand exactly how it modifies the structure of the APP molecule. “If we can change the APP structure and engineer molecules that interfere with the binding of amyloid-beta to APP, then we can break up the process leading to hippocampal hyperactivity. This may help to restore memory and protect the brain,” she said.

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