Several molecules inhibit axonal growth cones and may account for the failure of central
nervous system regeneration, including myelin proteins and various chondroitan sulfate …

In injured adult neurons, the process of axonal regrowth and reestablishment of the
neuronal function have to be activated. We assessed in this study whether RhoA, a key …

Myelin-associated inhibitors limit axonal regeneration in the injured brain and spinal cord. A
common target of many neurite outgrowth inhibitors is the Rho family of small GTPases …

Abstract The small GTPase RhoA and its down-stream effector Rho-kinase (ROCK) are
important effector molecules of the neuronal cytoskeleton. Modulation of the RhoA/ROCK …

Axonal regeneration in the central nervous system is blocked by many different growth
inhibitory factors. Some of these inhibitors act on neurons by activating RhoA and Rho …

Inhibitory molecules derived from CNS myelin and glial scar tissue are major causes for
insufficient functional regeneration in the mammalian CNS. A multitude of these molecules …

The regeneration of adult peripheral neurons after transection is slow, incomplete and
encumbered by severe barriers to proper regrowth. The role of RHOA GTPase has not been …

Chondroitin sulfate proteoglycans (CSPGs) are a major component of the glial scar that
contributes to the limited regeneration of the CNS after axonal injury. However, the …

Axon regeneration is arrested in the injured central nervous system (CNS) by axon growth‐
inhibitory ligands expressed in oligodendrocytes/myelin, NG2‐glia, and reactive astrocytes …

Limited axonal plasticity within the central nervous system (CNS) is a major restriction for
functional recovery after CNS injury. The small GTPase RhoA is a key molecule of the …