Reprint

Optic Neuropathies: Current and Future Strategies for Optic Nerve Protection and Repair

Edited by
May 2023
322 pages
  • ISBN978-3-0365-7505-6 (Hardback)
  • ISBN978-3-0365-7504-9 (PDF)

This book is a reprint of the Special Issue Optic Neuropathies: Current and Future Strategies for Optic Nerve Protection and Repair that was published in

Biology & Life Sciences
Chemistry & Materials Science
Medicine & Pharmacology
Summary

Optic neuropathies are conditions in which there is damage to the optic nerve (ON) caused by a variety of causes, including glaucoma, inflammation, gene abnormalities, ischemia, trauma, and toxicity. ON damage triggers a process of axon degeneration, inflammatory cytokine upregulation, breakdown of the blood–optic nerve barrier, and, eventually, the induction of apoptosis of retinal ganglion cells (RGCs), resulting in optic atrophy. To date, there is no effective treatment for most optic neuropathies; however, because the damage initially is axogenic, there may exist a window of therapeutic opportunity before the death of RGCs. Thus, the search for effective treatments for various optic neuropathies before there is permanent damage to prevent or limit visual dysfunction and the development of methods to stimulate axon and/or RGC regeneration to restore vision after damage has occurred is pivotal.This reprint collected 19 articles published in this Special Issue of IJMS which covers the molecular mechanisms to protect RGCs and/or axonal damage, translational research, gene therapy, regenerative medicine, and neuroprotection for glaucoma.

Format
  • Hardback
License
© by the authors
Keywords
neuroprotection; retinal ganglion cells; optic neuropathy; glaucoma; pattern electroretinogram; NMO; astrocytes; apoptosis; BID; inflammation; neuroimmunology; erythropoietin; neuroprotection; retinal ganglion cell; optic neuropathy; optic nerve protection; neuromyelitis optica spectrum disease; aquaporin-4; myelin oligodendrocyte glycoprotein; ocular coherence tomography; complement; microcystic macular degeneration; Müller cell; astrocyte; oligodendrocyte; microglia; glaucoma; optic nerve head; lamina cribrosa; lamina cribrosa cells; scleral fibroblasts; glial cells; intraocular pressure; rat anterior ischemic optic neuropathy model; retinal ganglion cell death; TBP associated factor 9; TP53 regulated inhibitor of apoptosis 1; transcriptome; optic nerve; epigenetics; myelin; regeneration; oligodendrocytes; atypical optic neuritis treatment; typical optic neuritis; MOG; NMO; MS prevention; retina; inflammation; transcription; CNS repair; optic nerve; oncomodulin; myeloid cells; regeneration; glaucoma; glaucomatous optic neuropathy; fibrosis; miR-29; extracellular matrix; optic nerve crush; neuroprotection; azithromycin; NAION; neural injury; neural ischemia; neural inflammation; Leber’s hereditary optic neuropathy; LHON; whole exome sequencing; nuclear modifier genes; leber’s hereditary optic neuropathy; optic neuropathy; mitochondrial disorder; mitochondrial optic neuropathy; hereditary optic neuropathy; neuro-ophthalmology; idebenone; nonarteritic anterior ischemic optic neuropathy; retinal ganglion cells; optic nerve; neuroprotection; rodents; gene expression; models; diabetes; ischemic optic neuropathy; pioglitazone; HSF1; Klf4; Oct4; Sox2; Yamanaka factors; retina; optic nerve regeneration; zebrafish; oligodendrocyte precursor cells; secondary degeneration; oxidative stress; DNA damage; proliferation; blood-brain barrier; CNS injury; optic nerve injury; synaptamide; A8; axonal degeneration; retinal ganglion cells; neuronal survival; optic nerve crush; visual evoked potential; n/a