The team found that an existing drug called rapamycin, initially developed as an immunosuppressant for organ transplant patients that suppresses signaling between neurons, was able to regulate the over-excited neurons in mouse models of AD and seizures, and preserve cognitive function, like memory and the ability to learn new things.
Previous research has shown similar brain activity in individuals with AD who experience epilepsy. Additionally, many individuals with AD have also experienced at least one seizure, and previous research has shown that these seizures cause a more rapid progression of the disease, and worsen cognitive impairment, like trouble with memory or learning. However, researchers have not been able to identify the underlying connections between AD and seizures.
“Experts used to believe that seizures were an unfortunate byproduct of the neurodegeneration that causes Alzheimer’s disease, but now we see that seizures are actually advancing the disease itself,” said the study’s co-senior author, Frances E. Jensen, MD, chair of Penn’s Department of Neurology. “Now that we have identified the mechanisms that cause neurons to get over-excited and lead to seizures that accelerate AD, we can explore therapies, like rapamycin, that can reverse the imbalance, and slow AD progression.”
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