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Project

The role of insulin-like growth factor-I in protection and regeneration after transient focal brain ischemia (IWT439)

Stroke represents the principle cause of invalidity in adults. Brain damage as a result of cerebral ischemia is a consequence of necrosis and apoptosis of neurons and glial cells and leads to upregulation of IGF-I expression in the central nervous system. However, maximal IGF-I concentrations are reached only after 5 days or longer. The literature shows that administration of the neurotrophic growth factor IGF-I after induction of focal cerebral ischemia in rats reduces cell death and tissue damage. The purpose of the current project is to investigate the therapeutic potential of IGF-I. We will study:
1) the mechanism involved in the neuroprotective effects of IGF-I administration after induction of focal cerebral ischemia by application of endothelin-1 in rats.
2) the effects of IGF-I on inflammatory responses in the brain.
3) the role of local IGF-I production in neuroprotection and regeneration using cell-specific knock out mice.
4) the therapeutic potential of different ways of IGF-I administration in the endothelin-1 rat model for focal cerebral ischemia.
Date:1 Jan 2009 →  31 Dec 2012
Keywords:Pituitary Tumors, Gene Regulation, IGF-1, Hypophyse, Prolactin, PRL-R signalling pathways, In Situ Hybridization, Lymphohemopoietic System, Dopamine, Endocrinology, PRL isoforms, PRL gene regulation, termination of signalling, CIS and SOCS molecules, PRL-R pathways, PRL, Growth Hormone
Disciplines:Basic sciences, Biological sciences