The optic nerve conveys information about the outside world from the retina to multiple subcortical relay centers. Until recently, the optic nerve was widely believed to be incapable of re-growing if injured, with dire consequences for victims of traumatic, ischemic, or neurodegenerative diseases of this pathway. Over the past 10-20 years, research from our lab and others has made considerable progress in defining factors that normally suppress axon regeneration and the ability of retinal ganglion cells, the projection neurons of the retina, to survive after nerve injury. Here we describe research from our lab on the role of inflammation-derived growth factors, suppression of inter-cellular signals among diverse retinal cell types, and combinatorial therapies, along with related studies from other labs, that enable animals with optic nerve injury to regenerate damaged retinal axons back to the brain. These studies raise the possibility that vision might one day be restored to people with optic nerve damage.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8789219PMC
http://dx.doi.org/10.3233/RNN-190960DOI Listing

Publication Analysis

Top Keywords

optic nerve
20
nerve injury
8
optic
5
nerve
5
nerve regeneration
4
regeneration long
4
long view
4
view optic
4
nerve conveys
4
conveys retina
4

Similar Publications

Meta-regression of optic nerve imaging and visual outcome in myelin oligodendrocyte glycoprotein antibody optic neuritis.

J Neurol Sci

December 2024

Toronto Eye Specialists and Surgeons, Toronto, Ontario, Canada; Department of Ophthalmology & Vision Science, University of Toronto, Toronto, Ontario, Canada; Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada; Division of Neurology, Department of Medicine, University of Toronto, Canada. Electronic address:

Background: Few predictors of visual outcome after myelin oligodendrocyte glycoprotein (MOG) auto-antibody disease optic neuritis (ON) have been reliably elucidated. We evaluate whether between-study differences in ON neuroimaging regional enhancement features may underlie heterogeneity in reported visual prognosis.

Methods: PROSPERO (CRD42024580123).

View Article and Find Full Text PDF

The optic nerve contains retinal ganglion cell (RGC) axons and functions to transmit visual stimuli to the brain. Injury to the optic nerve from ischemia, trauma, or disease leads to retrograde axonal degeneration and subsequent RGC dysfunction and death, causing irreversible vision loss. Inflammatory responses to neurological damage and axonal injuries in the central nervous system (CNS) are typically harmful to neurons and prevent recovery.

View Article and Find Full Text PDF

DLK-dependent axonal mitochondrial fission drives degeneration after axotomy.

Nat Commun

December 2024

Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.

Currently there are no effective treatments for an array of neurodegenerative disorders to a large part because cell-based models fail to recapitulate disease. Here we develop a reproducible human iPSC-based model where laser axotomy causes retrograde axon degeneration leading to neuronal cell death. Time-lapse confocal imaging revealed that damage triggers an apoptotic wave of mitochondrial fission proceeding from the site of injury to the soma.

View Article and Find Full Text PDF

Purpose: To observe the changes in peripapillary retinal nerve fiber layer (RNFL) thickness and peripapillary vessel densities (VD) in patients with rhegmatogenous retinal detachment (RRD) after scleral buckling (SB) by OCTA.

Methods: A total of 40 patients (40 eyes) with monocular RRD who underwent SB were included in the study, with the operated eyes (40 eyes) as the study group and the contralateral healthy eyes (40 eyes) as the control to analyse the changes in peripapillary RNFL thickness and VD before and after surgery. Data were analysed by paired samples -test or Wilcoxon signed rank sum test.

View Article and Find Full Text PDF

Tppp3 is a novel molecule for retinal ganglion cell identification and optic nerve regeneration.

Acta Neuropathol Commun

December 2024

Department of Ophthalmology, UPMC Vision Institute, University of Pittsburgh School of Medicine, 1622 Locust Street, Pittsburgh, PA, 15219, USA.

Mammalian central nervous system (CNS) axons cannot spontaneously regenerate after injury, creating an unmet need to identify molecular regulators to promote axon regeneration and reduce the lasting impact of CNS injuries. While tubulin polymerization promoting protein family member 3 (Tppp3) is known to promote axon outgrowth in amphibians, its role in mammalian axon regeneration remains unknown. Here we investigated Tppp3 in retinal ganglion cells (RGCs) neuroprotection and axonal regeneration using an optic nerve crush (ONC) model in the rodent.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!