CRMP2 binding compound accelerates functional recovery from central nervous system damage.

Brain injury causes temporary or permanent impairment of brain function due to an accident or circulation disorders. Even after rehabilitation training, there are often persistent functional impairments. Recent advances in our understanding of the repair mechanisms of neural circuits after brain injury have led to the possibility that these mechanisms may offer potential therapeutic targets for drugs that promote functional recovery after brain injury. Neuroplasticity is believed to be important for the recovery process after brain injury in the brain regions associated with injured region for compensation. The effectiveness of drugs for restoring brain function after stroke investigated in a variety of animal models and clinical trials has been focused on drugs that act on the monoamine system to modulate neuroplasticity, as well as other targets such as NMDA receptors and CCR5. Recently, we focused on novel small compound, edonerpic maleate, as a drug which facilitates experience-dependent synaptic delivery of AMPA receptor. We found that edonerpic maleate binds to Collapsin-response mediator protein 2, a downstream molecule of Semaphorin and enhance synaptic plasticity by facilitating synaptic delivery of AMPA receptors, thereby promoting functional recovery in a rehabilitation-dependent manner after brain injury in rodents and non-human primates. Further investigations is needed to seek more appropriate drug targets from both preclinical animal studies and clinical trials, and to translate preclinical results into successful clinical trials. [ABSTRACT FROM AUTHOR]