Improving Clot-Busting Treatment | Action Medical Research | Children's Charity

Stroke: Improving clot-busting treatment

This research was completed on 30 April 2011

Published on 30 January 2009

Stroke is a major cause of death and disability worldwide. A drug called tPA is the only medicine licensed specifically to tackle blood clots in people experiencing a stroke. It can reduce long-term disability, but it is not suitable for all strokes, it must be given within a few hours of the stroke starting and in a few people it may cause harm. Researchers are investigating a possible way to improve the effectiveness of tPA, by stimulating the brain to produce a protective protein of its own.

What's the problem and who does it affect?

Death and disability

Each year in the UK, some 150,000 people have a stroke, often with devastating consequences.1 Stroke is the third most common cause of death in the UK, accounting for around 8% of deaths in men and 12% in women.2,3

Stroke is also a major cause of disability. This disability can affect all aspects of normal life, including walking, talking, eating, having sex and going to the toilet, meaning that survivors can find they are suddenly dependent on others for help.

A drug called tPA is the only medicine approved specifically to tackle blood clots in people who are experiencing a stroke. The benefits of treatment can be dramatic: tPA can reduce long-term disability, with people retaining a much better quality of life and higher level of independence.

However, tPA must ideally be given within three hours of a stroke starting, it cannot be given to everyone and in a minority of people it may actually prove harmful. In some people, for example, use of the drug is associated with bleeds in the brain. Improved treatment would have major healthcare benefits.

What is the project trying to achieve?

Helping the brain protect itself

The commonest form of stroke results from a blood clot in the blood vessels supplying the brain. This restricts blood flow to brain cells, injuring or killing some of the cells. Treatment with tPA works by dissolving blood clots, so blood flow can be restored.

Evidence suggests that sometimes the returning blood might somehow cause further damage to brain cells. The researchers think they may have identified a way to help prevent this damage. They have discovered a small molecule, provisionally called CI-6844, which seems to stimulate the brain to produce a protective protein of its own. The researchers think that giving people this molecule along with tPA might make treatment more successful.

They are investigating how well the molecule works in a laboratory model of stroke and finding out more about its influences on the brain’s own, protective protein. They are also studying the actions of this protein in more detail.

What are the researchers' credentials?

Project LeaderDr A H Hainsworth PhD
Project team
  • Dr James Murray PhD
  • Dr Rafael Yanez-Munoz PhD
LocationCentre for Clinical Neuroscience, Division of Cardiac & Vascular Sciences, St George’s University of London in conjunction with Centre for Cancer Research & Cell Biology, Queen's University Belfast and School of Biological Sciences, Royal Holloway-University of London
Other locations
  • Centre for Cancer Research and Cell Biology, Queen’s University, Belfast
  • School of Biological Sciences, Royal Holloway, University of London
DurationTwo years
Grant awarded30 October 2008
Start date30 March 2009
End date30 April 2011
Grant amount£126,632.00
Grant codeSP4394

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The project leader, Dr Atticus Hainsworth, is highly experienced in studying how drugs can protect brain cells from damage. He has focused on stroke for over ten years, investigating in detail the way candidate drugs work, evaluating their potential and planning how best to develop them as new treatments.

Dr Hainsworth is working with Dr James Murray, an expert in the brain’s own protective protein that seems to be stimulated by CI-6844, and Dr Rafael Yanez-Munoz, who is a specialist in using vehicles called ‘viral vectors’ to deliver drugs to injured brain cells. Together, the three members of the team have all the complementary skills needed to make this project a success.

Most of the research will be conducted at St George’s University of London, which has an international reputation in stroke research, providing an excellent environment for this project.

Who stands to benefit from this research and how?

Harnessing the brain’s own powers of protection

The researchers’ ultimate aim is to find a way to improve the treatment of stroke. In this project, they aim to find out whether combination treatment with CI-6844 and tPA seems feasible. They envisage that CI-6844 might work by harnessing the power of a naturally occurring protein within the brain, so encouraging the brain to protect itself.

More research would be needed before clinical trials could begin, but the researchers believe that combination treatment might help protect people from disability and save lives. Preliminary data suggest that CI-6844 is of low toxicity.

Currently, strokes kill over 60,000 people every year in the UK.2 and leave many others with devastating disabilities – more than 250,000 people in the UK are living with disabilities caused by a stroke.

Stroke is also costly. The direct cost to the NHS is estimated to be £2.8 billion per year.2 Stroke patients occupy about one in five short-term hospital beds and a quarter of long-term beds.2

It’s possible that this research may benefit other people as well. The results may prove useful to researchers who are searching for treatments for other brain diseases, such as Alzheimer’s disease, Huntington’s disease and multiple sclerosis.

References

  1. The Stroke Association. What is a stroke? June 2008
  2. The Stroke Association. Stroke statistics. Resources 11. October 2006 http://www.stroke.org.uk
  3. The British Heart Foundation Statistics Website: http://www.heartstats.org


Figure shows: A monolayer of brain neurones, one of which is expressing a novel gene carried by a viral vector reagent (green).

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