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Optic nerve and neuroprotection strategies
N N Osborne1, G Chidlow, C J Layton
1Nuffield Laboratory of Ophthalmology, Oxford University, Oxford, UK. neville.osborne@eye.ox.ac.uk
Background:
Experimental studies have yielded a wealth of information related to the mechanism of ganglion cell death following injury either to the myelinated ganglion cell axon or to the ganglion cell body. However, no suitable animal models exist where injury can be directed to the optic nerve head region, particularly the unmyelinated ganglion cell axons. The process of relating the data from the various animal models to many different types of optic neuropathies in man must, therefore, be cautious.
Results:
Extensive studies on the isolated optic nerve have yielded valuable information on the way white matter is affected by ischaemia and how certain types of compounds can attenuate the process. Moreover, there are now persuasive data on how ganglion cell survival is affected when the ocular blood flow is reduced in various animal models. As a consequence, the molecular mechanisms involved in ganglion cell death are fairly well understood and various pharmacological agents have been shown to blunt the process when delivered before or shortly after the insult.
Conclusions:
A battery of agents now exist that can blunt animal ganglion cell death irrespective of whether the insult was to the ganglion cell body or the myelinated axon. Whether this information can be applied for use in patients remains a matter of debate, and major obstacles need to be overcome before the laboratory studies may be applied clinically. These include the delivery of the pharmacological agents to the site of ganglion cell injury and side effects to the patients. Moreover, it is necessary to establish whether effective neuroprotection is only possible when the drug is administered at a defined time after injury to the ganglion cells. This information is essential in order to pursue the idea that a neuroprotective strategy can be applied to a disease like glaucoma, where ganglion cell death appears to occur at different times during the lifetime of the patient.
Insights
Researchers explored ganglion cell death mechanisms in animal models. While drugs can prevent cell death in animals, clinical application for optic neuropathies like glaucoma faces delivery and timing challenges.
Area of Science:
- Neuroscience
- Ophthalmology
- Pharmacology
Background:
- Extensive research exists on ganglion cell death mechanisms following injury to axons or cell bodies.
- Current animal models lack the ability to target optic nerve head injuries, specifically unmyelinated axons.
- Caution is advised when extrapolating findings from animal models to human optic neuropathies.
Purpose of the Study:
- To review the understanding of ganglion cell death mechanisms.
- To assess the potential clinical applicability of neuroprotective agents for optic neuropathies.
Main Methods:
- Review of experimental studies on isolated optic nerves and animal models of reduced ocular blood flow.
- Analysis of data on the effects of ischemia and pharmacological agents on white matter and ganglion cell survival.
Main Results:
- Molecular mechanisms of ganglion cell death are well-understood.
- Various pharmacological agents have demonstrated efficacy in blunting cell death in animal models.
- Studies on isolated optic nerves provide insights into ischemia's effects and potential treatments.
Conclusions:
- Existing agents can prevent animal ganglion cell death from various insults.
- Clinical application in humans is debated due to challenges in drug delivery and potential side effects.
- Determining optimal drug administration timing is crucial for neuroprotection strategies in diseases like glaucoma.
