Preventing Abnormal Growth of New Neurons Reduces Epileptic Seizures and Memory Loss
Preventing Abnormal Growth of New Neurons Reduces Epileptic Seizures and Memory Loss
Using a mouse model, scientists have found that preventing the abnormal growth of new neurons reduces the severity of epileptic seizures and memory deficits caused by brain injury. The research was published March 26th in the journal Nature Communications.
When someone experiences a severe traumatic brain injury, they can develop epilepsy and cognitive deficits afterward, though sometimes not for several months or even years. Previous research has shown that in response to some brain injuries, a part of the brain called the hippocampus begins to grow new neurons, sometimes in an abnormal way. And while some studies have shown that stopping this process might reduce the occurrence of new seizures, others showed no benefit.
New research was performed by a team that included two-time (2002, 2004) NARSAD Young Investigator and 2010 NARSAD Independent Investigator grantee Amelia J. Eisch, Ph.D., of the University of Texas Southwestern Medical Center. Dr. Eisch, the team leader Jenny Hsieh, Ph.D., and colleagues found in a mouse model that suppressing the birth of new neurons in the hippocampus after a brain injury did reduce the frequency of chronic seizures. Although this did not prevent the development of symptoms like those seen in human epilepsy, the mice did not develop epilepsy-related memory deficits.
When a drug called ganciclovir was used to prevent the birth of new hippocampal neurons after brain injury, the mice had fewer and shorter seizures. The seizures continued to be fewer and shorter nearly a year later when the same mice were reexamined, suggesting the effects of preventing new neuron growth were permanent. These mice also performed better on a memory task, compared with mice in a control group.
The researchers conclude that stopping the abnormal growth of new neurons after a brain injury might help reduce the severity of epilepsy and related cognitive deficits in humans.