Control mechanisms of degeneration and immune cell regulation after injury of peripheral nerves or spinal cord

• Antragstellerin: Professorin Dr. Antje Kroner-Milsch
• Fachliche Zuordnung: Molekulare und zelluläre Neurologie und Neuropathologie
• Förderung: Förderung von 2009 bis 2011
• Projektkennung: Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 156632509

Axons of the central nervous system (CNS) and peripheral nervous system (PNS) are wrapped by a lipid rich membrane, the myelin, which insulates the nerve fiber, and is essential for rapid electrical conductivity. In the CNS, the myelin sheath is formed by oligodendrocytes, while in the PNS it is formed by Schwann cells. In cases of injury, both the nerve and myelin sheath degenerate. As myelin contains molecules that inhibit axon regeneration, it is important that myelin is cleared by macrophages to allow for regeneration. A number of different factors have been shown to influence breakdown and phagocytosis of myelin after nerve injury. Recent work has shown that lipolytic enzymes are important in triggering breakdown and clearance of myelin after peripheral nerve injury (Lopez-Vales et al., 2008). However, it is currently not known how levels and activation of these enzymes are regulated. The aim of this proposal is to study the role of cytokines that are released by the injured nerve and of molecules that form pore-like channels (connexin 29 or connexin 32 channels) that regulate the passage of ions, which could allow calcium to reach certain parts of the myelin sheath and trigger the activation of the lipolytic enzymes. These studies could reveal new targets that can be studied to promote rapid myelin clearance after spinal cord injury to enhance regeneration, as myelin clearance is extremely slow in the central nervous system. They could also have important implications for clinical disorders of peripheral nerves.

• DFG-Verfahren: Forschungsstipendien
• Internationaler Bezug: Kanada
• Gastgeber: Professor Samuel David