The University of Geneva is offering this technology for licensing and for collaborations.
signature of a non-disclosure agreement.

Patent Status :
Application

Development Phase :
Research

Applications :
Stroke, but potentially also other diseases involving post-ischemic cell death: myocardial infarction, acute limb ischemia, complex surgical procedures involving vascular bypass, vascular dementia vascular bypass, multi-infarct and mixed dementia, etc.

Gene therapy, pharmaceutical and protein based therapies to enhance cellular production of the factor to block damaging effects of stroke.

Using any technique to enhance production of the target described above that protects against, blocks or treats the damaging effects of ischemia on living tissues such as the brain and heart.

Enhancement of this factor may be used in patients towards the prevention and/or treatment of disease processes that are a consequence of ischemic and/or post-ischemic tissue damage.

Contact :
Dr. Alexandra Richardson
tel: +41-22-705-7258
fax: +41-22-329-4290
Unitec
Office of Technology Transfer
University of Geneva
24 rue du General Dufour
Ch-1211 Geneva 4/Switzerland

e-mail: alexandra.richardson@unige.ch

A target for therapeutic intervention to prevent cell death in stroke patients.

Stroke is a major cause of death and disability. The problem occurs from a lack of blood flow (ischemia) and oxygen supply that quickly kills delicate brain tissue. Although the nerve cells of the ischemic core are destined to die by necrosis, cells in the area surrounding this core undergo delayed death by apoptosis.

Researchers at the University of Geneva have identified a factor that, when overexpressed, is effective in mediating resistance to apoptotic cell death in such a situation. In the study, mice were created that overexpress this protein, and stroke was induced by blocking the flow of an important blood vessel. The researchers observed that tissue damage and the number of apoptotic cells was greatly reduced in these mice compared to wild type mice or mice lacking this protein.

This discovery opens the path for novel stroke therapies involving therapeutic intervention that would have the potential to enhance cellular production of this factor that protects nerve cells from apoptotic death.