Voices from the field
Donate Us
Forthcoming Events
Activities and Meetings
Home arrow News and Articles arrow In a First, Epilepsy Halted in Mice

In a First, Epilepsy Halted in Mice

Times of India
6 August 2009
Los Angeles, USA

Silencing A Gene Stops Disorder From Being Passed On To Offspring
Epilepsy sufferers have been given fresh hope after scientists at Leeds prevented the condition from being passed on to mice offspring.

In a First, Epilepsy Halted in Mice
The researchers were able to do so after identifying that a faulty version of a gene known as Atp1a3 is responsible for causing epileptic seizures in mice. The achievement may herald new therapies for people suffering from the condition.

“Atp1a3 makes an enzyme called a sodium–potassium pump that regulates levels of sodium and potassium in the nerve cells.”

“An imbalance of sodium and potassium levels has long been suspected to lead to epileptic seizures, but our study is the first to show beyond any doubt that a defect in this gene is responsible,” lead author Steve Clapcote, of the University of Leeds, said.

To prove the gene’s role, the research team studied a special strain of mouse, called Myshkin, after an epileptic character in Fyodor Dostoevsky’s ‘The Idiot’, which has an inherited form of epilepsy. The researchers found that these mice have a defective Atp1a3 gene, which led to them all having spontaneous seizures displaying the characteristic brain activity of epilepsy.

When the epileptic Myshkin strain was bred with a transgenic mouse strain that has an extra copy of the normal Atp1a3 gene, the additional normal gene counteracted the faulty gene – resulting in offspring, which were free from epilepsy. ANI

Disclaimer: The news story on this page is the copyright of the cited publication. This has been reproduced here for visitors to review, comment on and discuss. This is in keeping with the principle of ‘Fair dealing’ or ‘Fair use’. Visitors may click on the publication name, in the news story, to visit the original article as it appears on the publication’s website.