Université de Genève

Neuroscience center

Imprimer cette page
image

Group leader: Yvan Gasche

Group name: Ischemic Brain Injury

Affiliation: University Hospital

Research activities:

image The laboratory is interested in the molecular mechanisms involved in blood-brain barrier disruption and neuronal degeneration in ischemic brain injury. Brain edema and hemorrhagic transformation are the main cause of early mortality in ischemic stroke patients. Gelatinase B, an inducible matrix metalloproteinase overexpressed during cerebral ischemia, is associated to the proteolysis of the basal lamina resulting in blood-brain barrier disruption, brain edema and cerebral hemorrhage after stroke. We currently explore different therapeutic strategies focused on the role of gelatinase B to reduce the risk of hemorrhage and brain edema both in animal models of embolic stroke and in patients. We also investigate the mechanisms of ischemic brain injury in patients following cardiac arrest and in patients developing delayed ischemic injury due to vasospasm after subarachnoid hemorrhage.

Selected Publications:

  • Copin, J.C., Merlani, P., Sugawara, T., Chan, P.H., Gasche, Y., 2008. Delayed matrix metalloproteinase inhibition reduces intracerebral hemorrhage after embolic stroke in rats. Exp Neurol. 213, 196-201.
  • Copin, J.C., Gasche, Y., 2008. Effect of the duration of middle cerebral artery occlusion on the risk of hemorrhagic transformation after tissue plasminogen activator injection in rats. Brain Res. 1243, 161-6.
  • Copin J.C., Goodyear M.C., Gidday J.M., Shah A.R., Gascon E., Dayer A., Morel D.M. and Gasche Y. (2005) Role of matrix metalloproteinases in apoptosis after transient focal cerebral ischemia in rats and mice. European Journal of Neuroscience 22(7): 1597-608

Contact:
Département d'Anesthésiologie, Pharmacologie et Soins Intensifs
Geneva University Hospital
Email: Yvan (dot) Gasche (at) unige (dot) ch