According to a new study conducted by researchers from Syracuse University, seizures can be suppressed in the brain by a protein called T-cell intracellular antigen-1 (TIA-1).
This study provided a new insight on epilepsy–a neurological disorder in which nerve activity in brain is affected leading to recurrent, unprovoked seizures.
James Hewett, associate professor of biology, said that TIA-1 helps in the regulation of gene expression during cellular stress. His research focusses on the suppression of severe electrical storms of brain which lead to seizures.
Hewett and Yifan Gong, a Ph.D. candidate in biology and neuroscience, thought that TIA-1 was included in seizure suppression but the study findings recommended something else.
The study authors observed the functions of an enzyme in the brain called cyclooxygenase-2 (COX-2). This enzyme produces prostaglandins; chemical compounds that support in the performance of general tasks, along with memory and learning.
The current study identified that seizure suppression was related with a raise in COX-2 expression in neurons.
Hewett explained: “Our findings raise the possibility that the level of neuronal COX-2 expression in the brain may be a determinant of the seizure threshold. This suggests that a better understanding of the regulation of COX-2 expression in the brain can provide new insights into molecular mechanisms that suppress seizure-induction.”
The researchers aimed to understand the relationship between TIA-1 and COX-2. They started their work by planning, conducting and analyzing experiments. Gong introduced the first TIA-1’s comprehensive expression profile in the normal brain.
Gong found that TIA-1 suppresses epileptogenesis – a slow process of normal brain to become epileptic. His research aimed to understand the molecular mechanisms behind epilepsy; particularly, the genes involved with seizure development and epileptogenesis.
Epilepsy can be acquired at any time during our lives, cures and preventive measures remain elusive, and the incidence of resistance to antiepileptic drugs is a clinical limitation. A better understanding of the function of neuromodulators, such as COX-2 and TIA-1, may help identify novel therapeutic targets for the treatment of epilepsy."
James Hewett, Associate Professor in Biology, Syracuse University