The new research indicates that the build-up of beta-amyloid plaques, which are a probable factor for the development of Alzheimer’s disease, affect the brain in multiple ways. One factor is the role in causing seizures in patients with Alzheimer’s. With this is thought that the by-products of beta-amyloid trigger a “cortical excitability” in neurons, which leads to the neurons misfiring. The subsequent effect is to disrupt electrical activity in the brain, with the resultant excitability leading to the occurrence of seizures in some Alzheimer’s disease patients. This can also lead to memory loss.
The latest findings come from researchers at Baylor College of Medicine where the scientists have uncovered a mechanism for memory loss, via the use an animal model. The basis of this could lead to new treatments for addressing cognitive deficits and memory loss.
The researchers focused on a specific protein called deltaFosB. Using rodents engineered to have an Alzheimer’s like disorder, it was found, through digital image analysis that once the mice had seizures, the level of deltaFosB protein increased in the hippocampus area of the brain. This new research links with previous studies that have shown how this specific protein affects the brain in terms of other neurological disorders. The new study expands on this and shows how the deltaFosB protein regulates other proteins and affects other proteins involved in memory.
The research shows how significantly higher deltaFosB levels could suppress the production of proteins that are required for learning and memory. As the levels of deltaFosB rise, the levels of other proteins, such as calbindin, fall. Calbindin also has an association with Alzheimer’s disease and epilepsy. Focusing on this could be the basis of a treatment to help address memory loss associated with seizures.
Commenting on this further, Dr. Jeannie Chin, who was co-author on the study, told Laboratory Roots magazine: “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.”
The findings are published in the journal Nature Medicine. The research paper is titled “Epigenetic suppression of hippocampal calbindin-D28k by ΔFosB drives seizure-related cognitive deficits.”
