Neurotrophin signaling and glaucoma

Research output: Contribution to journalArticle

Abstract

Purpose. To review the literature and recent experimental data suggesting that neurotrophic signaling is necessary for retinal ganglion cell (RGC) development and maintenance, and that perturbation of such signaling may he at least partially responsible for the apoptotic cell death associated with glaucoma, Summary. Nearly 100 years ago it was suggested that neurons require exogenous factors (now called neurotrophins) for survival. In many situations, withdrawal of such factors leads to cell death by apoptosis. Increasing evidence is accumulating that RGCs die by apoptosis in both animal models and human glaucoma. Transgenic experiments indicate that mice that overexpress the "anti-apoptosis" gene Bcl-2 in their RGCs demonstrate greater survival of RGCs during development, presumably due to reduced programmed cell death, and also demonstrate relative resistance to optic nerve transection. Since axonal transport is often blockexl in glaucoma, it is reasonable to speculate that in glaucoma there may be interruption of neurotrophic signaling from target cells to the RGC cell body. Recent evidence suggests that localization of some neurotrophin receptors is altered in glaucoma. Conclusions. If perturbation of neurotrophic signaling is responsible for RGC death in glaucoma, development of methods to restore normal signaling or to provide exogenous neurotrophic agents, either pharmacologically or by gene therapy, may lead to new neuroprotective approaches for the treatment of glaucoma.

Original languageEnglish (US)
JournalInvestigative Ophthalmology and Visual Science
Volume38
Issue number4
StatePublished - 1997

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Nerve Growth Factors
Glaucoma
Retinal Ganglion Cells
Cell Death
Apoptosis
Optic Nerve Injuries
Nerve Growth Factor Receptors
bcl-2 Genes
Axonal Transport
Survival
Genetic Therapy
Animal Models
Maintenance
Neurons

ASJC Scopus subject areas

  • Ophthalmology

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Neurotrophin signaling and glaucoma. / Zack, Donald J.

In: Investigative Ophthalmology and Visual Science, Vol. 38, No. 4, 1997.

Research output: Contribution to journalArticle

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