Stroke
is the third leading cause of death in the industrialized world, and
the first cause of invalidity. However, no effective treatment currently
exists. Results from the CNRS "Neuronal death, neuron protection,
and neural transmission" laboratory ("Mort neuronale, neuroprotection
et neurotransmission," CNRS-Université de Caen) could
bring new hope to patients.
This
team studies the molecular mechanisms underlying neuronal death, which
occur following a stroke. For the past few years, it has pursued two
objectives: to define the defense mechanisms mobilized by the brain
following a stroke, and to develop therapeutic strategies that take
advantage of the beneficial effects and limit the harmful consequences
of these physiological mechanisms.
When
an artery in the brain is occluded by a blood clot, neurons die through
lack of oxygen and glucose, leading to the release of large quantities
of a neurotransmitter, glutamate. At high concentrations, this molecule
is itself neurotoxic and induces the neuronal damage. Another molecule
which aggravates tissue damage following a stroke is tissue plasminogen
activator (t-PA), an inhibitor of blood clotting. In fact, t-PA, which
can also be released from damaged neurons, can exacerbate the toxicity
of glutamate by increasing the lethal role of the glutamate receptor
on the surface of neurons. In the US, t-PA is used clinically to remove
the clots responsible for stroke. However, these results question
the safety of t-PA treatment in humans and highlight the need for
new treatments for stroke.
