Epilepsy focus has wider implications

By REBECCA WALSH

Research into how the brain works in epileptics could result in a treatment to prevent the spread of damage to the brain, Auckland University scientists say.

Associate professors Louise Nicholson and Colin Green have just received a three-year Marsden Fund grant to research brain diseases and develop ways to block the damage spreading.

They will focus on temporal lobe epilepsy but they believe the work could have implications for other brain and central nervous system diseases.

In the past five years, researchers at the university have discovered that clusters of cells in the brain communicate with each other via gap junctions - direct cell-to-cell communication, almost as if a pipe links the cells together - as well as using chemical synapses.

Epileptics had huge numbers of gap junctions in some regions of the brain compared with other people.

"Our theory is that in diseases such as epilepsy, which increase in severity over time, these channels link cells together and spread the damage - increasing the area of degeneration and also forming a pathway for recirculating electrical activity," Dr Green said.

This was similar to what was known to happen after a heart attack, he said.

"For us, what's really exciting is, if you think about the last 30 years in brain research, people have been concentrating on the chemical synapses but that's only looking at half the story.

"We now know there's another whole side of communication which we know very little about."

Temporal lobe epilepsy produces disturbances in the normal electrical function of the brain, causing seizures.

It is a severe disease and cannot always be treated with medication. One treatment is surgery to remove part of the brain called the hippocampus.

If laboratory tests proved the hypothesis, then the researchers could test alternative and less invasive ways of preventing the damage from spreading.

A drug developed by Dr Green and colleagues in London has already been shown to reduce paralysis in spinal injuries and speed the healing of other wounds.

It could be injected into the damaged area of the brain.

"The gel would be administered with the treatment, which would then leak out and prevent the cells from making the protein which forms the communication channels," Dr Green said.

"This in effect would mean that the cells would no longer be able to 'talk' to each other and therefore would be unable to spread the lesion."

In the long term, that could mean stopping epileptic seizures from worsening over time, and could reduce their severity. Ultimately, it could avoid the need for surgery to remove the hippocampus.

The findings could be applied to other neurodegenerative diseases.

"We haven't even started to look at diseases like Huntington's or Parkinson's.

"We think these channels are quite important but have just been overlooked until now."

Dr Green said a team of five would be involved in the research, which would begin by next month.

Brain talk

* Brain cells communicate in one of two ways: through synapses, where a chemical is released by one cell and picked up by the receptor on the next cell; or via gap junctions, where cells "talk" directly to each other.

* Auckland University researchers have found epileptics have many more gap junctions in the part of the brain where epileptic events take place. They believe the gap junctions in epileptics link cells and create recirculating electrical signals, spreading damage.

* A drug to reduce the gap junctions, could stop seizures worsening.