Optic nerve regeneration

Abstract

In the adult central nervous system (CNS), axon regeneration of damaged neurons is very difficult as the intrinsic regeneration capacity of neurons is suppressed by environmental conditions after birth. Like other mammalian CNS neurons, retinal ganglion cells (RGCs) are unable to regenerate after optic nerve injury and thus, once they are damaged it can cause irreversible visual loss. There are a number of reasons for the failure of axon regeneration. One such reason is the presence of myelin-associated axon growth inhibitors such as Nogo, myelin-associated glycoprotein (MAG), and oligodendrocyte myelin glycoprotein (OMgp). These molecules create an environment that restricts axon regeneration. On the other hand, there are molecules that promote axon regeneration, such as trophic factors and inflammation-related factors. Recent studies revealed that CNS neurons, including RGCs, can regenerate if the environment surrounding the damaged neurons is suitable for regrowth. This condition may be achieved by application of mixed trophic factors and proinflammatory molecules that promote axon regeneration and/or by suppression of axon growth-inhibition signaling, such as RhoA/ROCK signaling. In this review, recent discoveries on molecular mechanisms underlying optic nerve regeneration are discussed.