Neuroscientists and medical researchers have known for a while that seizures can cause memory loss. This is especially relevant in patients who have neurological disorders like Alzheimer's disease (AD).
The build-up of beta-amyloid plaques, which is thought to be a significant factor in AD, can impact the brain in several ways. One is that brain tissue is broken down and memory loss happens when the neurons die off in this process. But that isn't what causes seizures in patients with Alzheimer's. Instead, it's the by-products of beta-amyloid that can cause a "cortical excitability" in neurons, causing them to misfire. A seizure is primarily a result of electrical activity being disrupted in the brain, and this excitability can result in seizures in some AD patients.
New research from a team at Baylor College of Medicine might have an answer to how these seizures impact memory loss, however. A recent research study conducted there and published in the journal Nature: Medicine uncovered a mechanism for this in an animal model and while it's early days, the team at Baylor thinks their results could be the way forward to treatments for cognitive deficits and memory loss
Dr. Jeannie Chin, assistant professor of neuroscience at Baylor College of Medicine was a co-author on the study, and she explained, "It's been hard to reconcile how infrequent seizures can lead to persistent changes in memory in patients with Alzheimer's disease. To solve this puzzle, we worked with a mouse model of Alzheimer's disease focusing on the genetic changes that seizures might trigger in the memory center of the brain, the hippocampus, that could lead to loss of memory or other cognitive deficits."
In the neural networks of the brain, it's all about the proteins. The research at Baylor focused on a specific protein, deltaFosB. The research used mice that had been engineered to have an Alzheimer's like disorder. After the mice had seizures, the level of deltaFosB significantly increased in the hippocampus area of the mouse brain.This protein is already known to impact the brain in areas that are associated with neurological disorders. It's thought to be a factor in addiction as well as memory issues. It also has a much longer half-life than most proteins in the brain. While others last merely a few hours, the half-life of deltaFosB is eight days, making its impact much more powerful. In the brain, deltaFosB regulates other proteins and was found to have an inverse relationship with proteins involved in memory.
Dr. Chin explained, "These findings led us to predict that the increased deltaFosB levels might be responsible for suppressing the production of proteins that are necessary for learning and memory. In fact, we found that when the levels of deltaFosB increase, those of other proteins, such as calbindin, decrease. Calbindin also has been known for a long time to be involved in Alzheimer's disease and epilepsy, but its mechanism of regulation was not known." This same inverse relationship between calbindin and deltaFosB is also present in human patients who have Alzheimer's. Check out the video below to learn more.