Faulty immune reaction implicated in epilepsy

November 24th, 2008 - 1:16 pm ICT by ANI  

London, November 24 (ANI): Studies in mice conducted by American and Italian researchers suggest that a faulty immune reaction may be responsible for the development of epilepsy.
The latest research looked at the behaviour of white blood cells, leukocytes, whose job is to defend the body from threats such as bacteria and viruses.
It has been found in mice that the initial seizure causes the release of a body chemical within the blood vessels, which increases the “adhesion” of leukocytes, keeping them in the brains blood vessels for longer.
The mice would normally move on to develop full epilepsy, but when the researchers blocked the “stickiness” chemical with the aid of antibodies or genetic therapy, the frequency of subsequent seizures was markedly reduced.
Further weight was added to the idea by an analysis of brain tissue from people with epilepsy, which showed a far greater abundance of leukocytes than in those without the condition.
Based on their observations, the researchers came to the conclusion that drugs targeting this “stickiness” might be a good way of preventing, or perhaps even treating, epilepsy in humans.
Professor Matthew Walker, a neuroscientist from University College London, and a member of Epilepsy Research UK’’s scientific advisory board, hailed the new findings as “interesting and exciting”.
“It provides a further piece of evidence for a breakdown in the blood brain barrier in the development of epilepsy,” the BBC quoted him as saying.
Though the researchers are still unsure whether the same mechanism leads to epilepsy in humans, they believe that their work may reveal a “whole new range” of drug targets.
“Importantly there are already drugs in use that may target this process, but which have not been tested in epilepsy and so this study could lead to trials of novel treatments for epilepsy in the near future,” they say.
A research article on the study has been published in the journal Nature Medicine. (ANI)

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