A new biological mechanism was found to damage a very specific type of memory, while at the same time provide resistance to epilepsy. The researchers came across this discovery while analyzing the underlying processes behind the creation and preservation of memories.

The study, published in the journal Cerebral Cortex, was conducted as part of a collaboration between scientists at the Sagol Department of Neurobiology at the University of Haifa and European colleagues.

Genetic Alteration In Epilepsy-Related Protein

Elham Taha, one of the authors of the study, noted that the relationship between the activities of nerve cells that are responsible for informational transfer and activities that delay it is crucial when it comes to understanding various brain diseases in healthy as well as affected brains.

Consequently, the purpose of the research was to isolate the molecular compounds that are employed in creating long-term memories, as any damage to the relationship between the informational transfer and its possible delay can be responsible for diseases such as epilepsy.

"We were surprised to find that the molecular change we created led to a minor change in this relationship in the hippocampus, but also created resistance to epileptic seizures. Thus the finding creates new possibilities for developing drugs for the treatment of epilepsy," noted Taha.

Preventing Epilepsy In Mice

As part of the research, the scientists analyzed the effects of genetic modifications that cause the total noexpression of the protein eEF2K in mice. Prior researches have suggested that the effects to this protein can also cause memory damage. The mice were subjected to behavioral tests, none of which managed to indicate the damage to memory consolidation, except for context memory.

The memory created regarding to context (usually related to space) is the only type of learning that was found to be affected by damage to the eEF2K protein in the hippocampus area of the brain. Consequently, the team examined whether a down regulation of this protein heightening the synapsin2b would impact the expression for this protein in mice.

Between a male mouse with no expression of the eEF2K protein and a female mouse with epilepsy, the offspring will almost always suffer from epilepsy at their turn, according to the study. As part of a second test, a substance that inhibited the expression of the proteins was administered to the mice who suffered from epilepsy, and the EEG tests showed that no seizure had taken place one week from the injection.

The study managed to create two distinct situations: one where mice born with epilepsy would not suffer from seizures, and one where the disease was prevented from affecting mice who should have been born with it. This opens a series of possibilities to be tested in the future, which could significantly shape the way epilepsy is currently being treated.

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