Page last updated at 18:05 GMT, Sunday, 23 November 2008

'Sticky cell' clues to epilepsy

Blood vessels in the brain
Harmful chemicals find it tough to pass from the blood to the brain

A faulty immune reaction may be responsible for the development of epilepsy, research suggests.

Studies in mice by US and Italian researchers linked seizures to brain changes which made immune cells stick inside its blood vessels.

This, in turn, the journal Nature Medicine reported, helped break down a vital filter which protects the brain from harmful chemicals.

"Unsticking" these cells helped prevent the development of epilepsy in mice.

This study could lead to trials of novel treatments for epilepsy in the near future
Professor Matthew Walker

Recent research has focused on problems with the "blood brain barrier" as a possible key to epilepsy, which, if poorly controlled, can mean regular and potentially damaging seizures.

Many molecules circulating in the bloodstream could cause damage if they reach the brain, and the role of the barrier is to keep them away.

The loss of the barrier is known to be connected to the "excitability" of neurons which may be the trigger for epileptic seizures, but the root cause of why the barrier could be breached remains mysterious.

The latest research may have found how an initial, non-epileptic, seizure could lead to a lifetime of epilepsy.

It looked at the behaviour of white blood cells - leukocytes - whose job it is to defend the body from threats such as bacteria and viruses.

The scientists found that, in mice at least, the initial seizure caused the release of a body chemical within the blood vessels which increased the "adhesion" of leukocytes, keeping them in the vessels for longer.

Normally, the mice would then go on to develop full epilepsy, but when this "stickiness" chemical was blocked using antibodies or by genetically changing the mice, the frequency of subsequent seizures was markedly reduced.

Analysis of brain tissue from people with epilepsy found a far greater abundance of leukocytes than in those without the condition, adding further weight to the idea.

The researchers suggested that drugs targeting this "stickiness" might be a good way of preventing, or perhaps even treating, epilepsy in humans.

Existing drugs

Professor Matthew Walker, a neuroscientist from University College London, and a member of Epilepsy Research UK's scientific advisory board, said the research was "interesting and exciting".

"It provides a further piece of evidence for a breakdown in the blood brain barrier in the development of epilepsy."

He said it was possible that the "stickiness" of immune cells contributed to the development of epilepsy in previously unaffected people who suffered brain injuries, strokes or prolonged seizures.

While it was not clear whether this same mechanism was at work in humans, it might 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."

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