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Stroke and the pharmaceutical industry
Targets for medicines development in stroke
The account to the right of the biology of stroke points
towards several possible ways in which scientists can design
medicines to prevent or treat stroke. These fall into four
broad categories:
- Medicines that reduce fat and cholesterol – slowing plaque
formation
- Medicines that modify blood clotting
- Medicines that dissolve clots – the so-called ‘clot-busters’
- Medicines that limit the extent of brain cell death after
a stroke
Approaches to control plaque development include changing
lifestyle factors, but medicines can also help, including
a group that are designed to slow down the main step in the
production of cholesterol in the body. Cholesterol is an important
contributor to plaque formation.
- Approaches to the control of unwanted blood clotting include:
- stopping the formation of the chemicals that attract platelets
to each other
- blocking the expression or activity of the GPIIb/IIIa
receptors to reduce platelet stickiness
- preventing fibrin fibres binding the platelets and red
cells into a solid mass
Medicines that help dissolve existing clots include:
- enzymes from microbes and human tissues that break up
the clots (e.g. streptokinase, staphylokinase, and urokinase)
- substances able to activate plasminogen to dissolve the
blood clot naturally – e.g. tissue plasminogen activator
(t-PA) and recombinant t-PA (rt-PA)
Medicines that limit the extent of brain cell death include
agents that provide neuroprotection to brain nerve cells,
either by stabilising the cell membranes, reducing their over-excitability,
or by mopping up damaging chemicals found after stroke, and
compounds that have anti-inflammatory actions.
In recent years, all of these approaches have been explored
and medicines developed to assess their validity in treatment.
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