title: Optic nerve regeneration.
abstract: Retinal ganglion cells are usually not able to regenerate their axons after optic nerve injury or degenerative disorders, resulting in lifelong visual loss. This situation can be partially reversed by activating the intrinsic growth state of retinal ganglion cells, maintaining their viability, and counteracting inhibitory signals in the extracellular environment. Advances during the past few years continue to extend the amount of regeneration that can be achieved in animal models. These findings give hope that clinically meaningful regeneration may become a reality within a few years if regenerating axons can be guided to their appropriate destinations.
authors.affiliation: F.M. Kirby Neurobiology Center, Children's Hospital Boston, Department of Surgery, Harvard Medical School, Massachusetts, USA. larry.benowitz@childrens.harvard.edu
authors.forename: Larry I
authors.initials: LI
authors.lastname: Benowitz
authors.forename: Yuqin
authors.initials: Y
authors.lastname: Yin
mesh_terms: D000818:Animals; D001369:Axons / Q000502:physiology*; D002135:Calcium-Binding Proteins / Q000494:pharmacology; D000242:Cyclic AMP / Q000502:physiology; D006801:Humans; D008358:Mannose / Q000494:pharmacology; D009416:Nerve Regeneration / Q000187:drug effects / Q000502:physiology*; D009900:Optic Nerve / Q000502:physiology*; D020221:Optic Nerve Injuries / Q000378:metabolism; D012165:Retinal Ganglion Cells / Q000502:physiology*
chemical_list: D002135:Calcium-Binding Proteins; C034733:oncomodulin; D000242:Cyclic AMP; D008358:Mannose