Research Applications for Striatech Products

Retinal Ganglion Cell Pathology: Death, Dysfunction, and Functional Readouts Across Preclinical Models

Death and dysfunction of the projection neurons linking eye to brain. RGC-targeted assays detect functional loss before histological cell death, expanding the therapeutic window across glaucoma, axon injury, and neurodegeneration.
Introduction

What is Retinal Ganglion Cell Pathology?

This page covers retinal ganglion cell (RGC) pathology as a unifying mechanism, encompassing both RGC death (somal and axonal loss) and RGC dysfunction (synaptic and signalling impairment that precedes or accompanies death).

RGCs are the output neurons of the retina, transmitting visual information through their axons in the optic nerve to subcortical and cortical visual brain areas. Their irreplaceable position at the retina-brain interface means that RGC pathology – whether progressive degeneration, acute injury, inflammatory attack, or ischaemic damage – produces measurable visual dysfunction that can be quantified non-invasively using the optomotor reflex. Critically, RGC dysfunction can be detected before frank cell death, offering a functional window for early intervention assessment that structural histology alone cannot provide.

RGC pathology is not confined to any single disease: it is a shared downstream mechanism across glaucoma, multiple sclerosis and optic neuritis, traumatic brain injury, hereditary retinal dystrophies, aging-associated neurodegeneration, and metabolic retinopathy. This cross-disease scope is reflected in the following application areas: Glaucoma and Optic Nerve Neurodegeneration, Neuroinflammation and Autoimmune CNS Disease, Trauma and Acute Injury, Retinal Degeneration and Inherited Retinal Disease, Neurodegenerative Disease, Ocular Inflammation and Immune-Mediated Eye Disease, Systemic Aging and CNS Decline, Rare and Inherited CNS and Eye Disorders, Ocular and CNS Toxicity Models, Myopia, Refractive Development and Eye Growth, Vascular and Metabolic Disease, and Maintaining and Restoring Vision.

Animal Models

Common Animal Models for RGC Pathology Research

  • Optic nerve crush (ONC) in mice and rats: A standardised surgical model in which the optic nerve is mechanically crushed, inducing a wave of axon degeneration and secondary somal apoptosis over days to weeks. RGC death is well-characterised and tightly timed, making ONC the canonical model for studying Wallerian-like axon degeneration, neuroprotection, and axon regeneration. OptoDrum detects functional visual loss within the first post-injury week. (Liu et al., 2023, Neural Regen Res. | Varadarajan et al., 2023, Cell Rep. | Baya Mdzomba et al., 2020, Cell Death Dis.)
  • Retinal ischemia-reperfusion injury (IRI): Acute elevation of intraocular pressure to ischaemic levels followed by reperfusion, producing a mixed apoptotic and necroptotic RGC death consistent with vascular occlusion and acute glaucoma. Complement activation and neuroinflammation contribute to secondary RGC loss. (Kim et al., 2024, Cell Death Differ. | Zhao et al., 2025, Adv Sci (Weinh))
  • Intraocular pressure (IOP) elevation models (microbead occlusion, episcleral vein cauterisation, laser photocoagulation): Experimental glaucoma paradigms inducing chronic, sustained or intermittent IOP elevation and progressive RGC death. These models allow longitudinal correlation of structural RGC loss with functional visual acuity decline. (Mickevičius et al., 2025, Exp Eye Res. | Zeng et al., 2024, Acta Neuropathol Commun.| Zeng et al., 2022, Biomolecules)
  • DBA/2J mice (hereditary pigmentary glaucoma): A spontaneous genetic glaucoma model in which progressive anterior segment obstruction produces chronic IOP elevation, axon degeneration, and RGC death beginning at around 6 months of age. Useful for longitudinal studies. (Zeng et al., 2022, Biomolecules | Kuchtey et al., 2024, Am J Ophthalmol.)
  • Soluble guanylate cyclase (sGC)-deficient mice: A genetic model of progressive, age-dependent RGC degeneration relevant to glaucoma-like neurodegeneration, with OptoDrum-detectable functional visual decline preceding complete cell loss. (Bossardet et al., 2026, Sci Rep.)
  • Experimental autoimmune encephalomyelitis (EAE) / optic neuritis models: Active immunisation with myelin antigens (MOG35-55, CNS homogenate) or passive transfer of myelin-specific T cells produces inflammatory demyelination of the optic nerve (optic neuritis) and secondary RGC death, modelling the visual pathway damage of multiple sclerosis and related disorders. (Anders et al., 2023, Front Immunol. | Capper et al., 2025, Front Immunol. | Joly et al., 2022, J. Neuroinflammation | Groh et al., 2025, Nat Neurosci.)
  • NMDA-induced excitotoxicity: Intravitreal injection of N-methyl-D-aspartate (NMDA) produces rapid, synchronous excitotoxic RGC death via glutamate receptor overactivation. A well-controlled model for studying somal apoptosis mechanisms and neuroprotection time windows. (Eghbali et al., 2023, Cell J. | Li et al., 2025, Neurosci Bull.)
  • Blast injury / traumatic brain injury (TBI) models: Closed-head blast overpressure injury induces RGC dysfunction via mechanical shockwave transmission to the retina and optic nerve. Dose-dependent grading of blast exposures allows controlled characterisation of graded RGC functional deficits. (Harper et al., 2024, Exp Eye Res.)
  • Genetic and inherited retinal degeneration models (rd10, VPS35cKO, sGC-/-, AKT-dystrophy): Models in which inherited photoreceptor degeneration or primary genetic defects secondarily affect RGC function or viability, often via neuroinflammatory or metabolic crosstalk. (Fu et al., 2024, Nat Commun. | Brunet et al., 2026, Biomedicines. | Bossardet et al., 2026, Sci Rep.)
  • Alzheimer's disease / amyloid-beta accumulation models: Retinal amyloid-beta deposition in Alzheimer's disease mouse models produces RGC dysfunction measurable by OptoDrum, positioning the retina as a window for monitoring neurodegenerative CNS pathology. (Sheng et al., 2026, Invest Ophthalmol Vis Sci.)
Research Questions

How Can Striatech Tools support Your Study?

Select a question that matches your research objective to see which instruments are relevant, what challenge they address, and what the published evidence shows.
01
Can the Optomotor Reflex Detect RGC Dysfunction Before Cell Death Occurs, and How Does This Change the Therapeutic Window Assessment?
Audience A - Vision-focused

Quick Answer

Yes. Optomotor testing with OptoDrum can detect RGC dysfunction – measurable visual acuity and contrast sensitivity loss – before histological evidence of complete RGC death. This pre-death functional window is demonstrable in IOP-elevation glaucoma models and age-dependent genetic degeneration models, and it expands the therapeutic window beyond what structural endpoints alone can reveal.

The challenge

Histological methods that count surviving RGC soma or measure retinal nerve fibre layer (RNFL) thickness require terminal tissue collection and cannot be repeated longitudinally in the same animal. By the time structural loss is detectable at a statistically meaningful threshold, a substantial proportion of RGC soma and axons are already gone. This creates a systematic bias towards underestimating the therapeutic window: interventions tested when structural loss is first histologically apparent may already be past the point of maximal neuroprotective efficacy.

Electrophysiological methods such as pattern ERG (PERG) can detect early RGC dysfunction, but require electrode placement or contact with the anaesthetised animal and are not compatible with longitudinal, repeated, low-stress assessment of the same cohort. The optomotor reflex offers a fully non-invasive, anaesthesia-free, repeatable functional endpoint that can be sampled at any time point throughout a longitudinal study without terminal cost.

Two recent studies illustrate this directly. In a comprehensively characterised glaucoma model, Mickevičius et al. (2025, Exp Eye Res.) correlated structural RGC loss with optomotor-measurable visual acuity decline over an extended time course, revealing a dissociation: optomotor dysfunction was detectable on a timeline that informs optimal intervention scheduling. In the sGC-deficiency genetic model, Bossardet et al. (2026, Sci Rep.) demonstrated that OptoDrum resolves the visual acuity timeline of progressive RGC degeneration, establishing functional milestones that complement structural histopathology.

How Striatech products help

OptoDrum
Measures spatial visual acuity (cycles per degree) and contrast sensitivity via the subcortical optomotor reflex in awake, freely moving rodents. Fully non-invasive and repeatable; enables longitudinal functional tracking from early dysfunction through terminal degeneration in the same cohort without anaesthesia or electrode contact.
ScotopicKit
Extends OptoDrum to scotopic (dark-adapted) conditions, enabling separate assessment of rod-pathway contributions to visual loss. In models where RGC dysfunction precedes photoreceptor loss, scotopic OMR can discriminate inner retinal from outer retinal functional contributions.
DarkAdapt
Provides a controlled, light-tight environment for dark-adapting cohorts prior to scotopic testing with the ScotopicKit, ensuring reproducible baseline scotopic state across animals and time points.
Non-aversive Animal Platform
Minimises handling stress during repeated longitudinal testing sessions, reducing cortisol-mediated confounds in cohorts undergoing extended monitoring. Particularly valuable for aged or post-surgical animals.

Evidence from the Literature

  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.
    Feature →
  • Mickevičius et al (2025) Exp Eye Res.
    Using OptoDrum, this study directly correlated the time course of structural RGC loss (cell counts, RNFL, optic nerve pathology) with longitudinal optomotor-measured visual acuity decline, characterising the onset and progression of the functional-structural dissociation.
  • Bossardet et al (2026) Sci Rep.
    Progressive visual acuity decline measured by OptoDrum in sGC-deficient mice paralleled age-dependent RGC degeneration, establishing an OptoDrum-based functional timeline for a genetic glaucoma-like model and demonstrating that functional milestones can be resolved before terminal collection points.
02
How Do Apoptotic, Necroptotic, and Wallerian-Like RGC Death Pathways Differ, and Does the Specific Pathway Alter the Optomotor-Measurable Functional Outcome?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

RGC death proceeds via mechanistically distinct programmes – classical caspase-dependent apoptosis, RIPK1/RIPK3/MLKL-driven necroptosis, and SARM1-dependent Wallerian axon degeneration – each with different time courses and therapeutic vulnerabilities. OptoDrum detects the functional visual consequences of each pathway, making it a pathway-agnostic functional endpoint for evaluating pathway-specific neuroprotective interventions.

The challenge

Most neuroprotection studies in the RGC field have historically focused on caspase-dependent apoptosis as the primary death mechanism. However, accumulating evidence indicates that non-apoptotic death programmes are quantitatively significant contributors to RGC loss in multiple disease contexts. SARM1-dependent Wallerian axon degeneration operates in the optic nerve axon compartment independently of somal apoptosis – meaning that blocking somal caspase activation without addressing axon degeneration leaves a significant component of functional loss unaddressed. Similarly, necroptosis (regulated necrosis via the RIPK1-RIPK3-MLKL axis) is a major contributor to RGC death after acute ischaemic injury, proceeding in the absence of classical apoptotic markers.

Distinguishing these pathways requires molecular characterisation (TUNEL, caspase activation, phospho-MLKL immunostaining, SARM1 pathway intermediates) alongside functional endpoints. The functional dimension – whether the specific pathway produces detectably different optomotor-measurable visual loss – is critical for translational endpoint validation: if OptoDrum is sensitive to the functional consequences of all three death programmes, it serves as a universal functional correlate regardless of the mechanistic intervention target.

Also see: Trauma and Acute Injury and Glaucoma and Optic Nerve Neurodegeneration

How Striatech products help

OptoDrum
Provides a pathway-agnostic functional endpoint: measures visual acuity and contrast sensitivity loss regardless of which molecular death programme (apoptosis, necroptosis, Wallerian) is operative. Enables direct comparison of functional outcomes across pathway-specific intervention studies without changing the behavioural assay.
Non-aversive Animal Platform
Reduces stress-mediated confounding in acutely injured or post-surgical animals, maintaining data quality in time-course studies that sample across the acute phase of pathway activation.

Evidence from the Literature

  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.
    Feature →
  • Zeng et al (2024) Acta Neuropathol Commun.
    Genetic deletion of SARM1 – the executioner NADase of the Wallerian axon degeneration programme – protected both RGC axons and soma and preserved optomotor-measured visual acuity in a glaucoma model. Demonstrates that Wallerian-like axon degeneration is a quantitatively significant, functionally impactful RGC death mechanism in pressure-dependent glaucoma.
  • Kim et al (2024) Cell Death Differ.
    Journal Club →
    Feature →
    RIPK1 kinase inhibition blocked necroptotic RGC death in retinal ischemia-reperfusion injury and preserved visual function on OptoDrum, demonstrating that the non-apoptotic RIPK1/RIPK3/MLKL necroptosis pathway produces functional visual loss independently measurable by optomotor testing.
  • Liu et al (2023) Neural Regen Res.
    ZnT3 deletion reduced vesicular zinc-dependent axon degeneration and improved functional visual recovery measured by OptoDrum after optic nerve crush, characterising a zinc-mediated Wallerian-like death mechanism in the axon compartment.
  • Varadarajan et al (2023) Cell Rep.
    Journal Club →
    Enhancing postsynaptic activity in visual brain targets promoted RGC axon regeneration after crush-induced axon degeneration and translated to functionally measurable visual recovery on OptoDrum, establishing that structural axon regeneration from RGC axonal injury produces a behaviourally detectable functional gain.
  • Harper et al (2024) Exp Eye Res.
    Dose-dependent blast injury produced graded RGC dysfunction and visual acuity loss on OptoDrum in a murine TBI model, demonstrating that mechanical shockwave-mediated injury produces a distinct, quantifiable RGC functional deficit pattern.
03
How Does Neuroinflammation Drive RGC Death and Dysfunction Across Glaucoma, EAE, and Retinopathy Models, and Can a Single Functional Endpoint Capture All These Contexts?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Neuroinflammatory pathways – including TNF-α signalling, complement activation, microglial CX3CR1-dependent demyelination, and HIF-1-mediated hypoxia signalling – drive RGC death across glaucoma, EAE/optic neuritis, and inflammatory retinopathy models. OptoDrum detects the functional visual consequences of all these pathways with a single, non-invasive optomotor assay, enabling direct cross-study comparison of neuroinflammatory RGC pathology..

The challenge

Neuroinflammation is a convergent driver of RGC death that operates across mechanistically distinct disease contexts. In glaucoma, reactive gliosis and microglial activation promote RGC death via TNF-α and other pro-inflammatory cytokines even when IOP is controlled. In EAE and optic neuritis, T cell and B cell-mediated demyelination of the optic nerve produces secondary RGC death via inflammatory mediators and loss of trophic support. In aging, CX3CR1-dependent microglial activation drives progressive optic nerve demyelination and RGC death independent of glaucomatous IOP changes. Each context involves different upstream triggers but converges on a shared set of pro-death inflammatory signals in the RGC microenvironment.

This mechanistic convergence creates a challenge for study design: choosing endpoints that are sensitive and relevant across all these contexts is non-trivial. Pattern ERG and VEP are sensitive but require technical expertise, anaesthesia, and contact with the animal. RGC survival histology requires terminal collection. Optomotor testing provides a single non-invasive functional endpoint applicable across all these models, enabling direct functional comparison between neuroinflammatory contexts.

Complement-driven neuroinflammation in ischaemia adds a further dimension: the innate immune cascade activates independently of adaptive immunity, producing RGC dysfunction via a mechanistically distinct pathway that nonetheless converges on the same optomotor-detectable functional deficit.

How Striatech products help

OptoDrum
Provides a single, standardised functional endpoint applicable across glaucoma, EAE, optic neuritis, aging, and inflammatory retinopathy models, enabling cross-study comparison of neuroinflammatory RGC death without changing the assay. Measures visual acuity and contrast sensitivity via the subcortical optomotor reflex in awake, freely moving rodents.
Non-aversive Animal Platform
Reduces handling stress in EAE animals, which may exhibit motor and autonomic deficits that complicate restraint-based testing. Ensures data quality in immunised cohorts throughout the disease course.
AcuiSee
Where neuroinflammation-driven optic nerve damage extends to cortical visual processing, AcuiSee provides a cortical operant visual discrimination endpoint complementing the subcortical optomotor reflex measured by OptoDrum. Appropriate for studies addressing suprathreshold visual perception or cortical relay function.

Evidence from the Literature

  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.
    Feature →
  • Li et al (2025) Neurosci Bull.
    TNF-α-driven neuroinflammation caused quantifiable RGC death and visual acuity and contrast sensitivity loss measured by OptoDrum in a glaucoma model, directly linking the TNF-α cytokine pathway to a behaviourally measurable functional deficit.
  • Groh et al (2025) Nat Neurosci.
    Journal Club →
    Feature →
    Age-related microglial CX3CR1-dependent activation drove optic nerve demyelination and secondary RGC death with optomotor-measurable visual consequences, demonstrating neuroinflammatory RGC death in an aging context independent of glaucomatous IOP changes.
  • Zhao et al (2025) Invest Ophthalmol Vis Sci.
    Complement C3/C3aR-driven innate neuroinflammation caused RGC dysfunction measurable by OptoDrum after ischemia-reperfusion, and C3aR inhibition preserved visual function, demonstrating complement as a distinct neuroinflammatory target in the ischaemic RGC death context.
  • Anders et al (2023) Front Immunol.
    HIF-1 inhibition reduced EAE-associated optic neuritis, RGC death, and visual function loss measured by OptoDrum, implicating hypoxia-inducible transcription as a mediator of inflammatory RGC death in the EAE optic nerve context.
  • Capper et al (2025) Front Immunol.
    Dietary lipid composition modulated the severity of EAE-associated RGC death and visual function loss on OptoDrum, demonstrating that metabolic-neuroinflammatory interactions quantitatively affect optomotor-measurable RGC pathology.
  • Joly et al (2022) J. Neuroinflammation
    B cell-dependent EAE with MOG antibody responses produced RGC death and functional visual deficits measurable by OptoDrum, demonstrating that adaptive immune effector heterogeneity (B cell vs. T cell) produces distinct but optomotor-detectable RGC pathology profiles.
  • Zeng et al (2022) Biomolecules
    PPAR-γ agonist pioglitazone reduced microglial and macrophage neuroinflammation, preserved RGC survival, and maintained visual acuity on OptoDrum in glaucoma models, confirming that anti-neuroinflammatory treatment is functionally impactful as measured by optomotor testing.
04
Do Neuroprotective and Regenerative Interventions Rescue RGC Function, and How Is Recovery Confirmed at the Functional Level?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Multiple intervention strategies – pharmacological neuroprotection (erythropoietin, PPAR-γ agonists), gene therapy (OSK epigenetic reprogramming, RNA-targeting CRISPR, AKT activation), biological agents (anti-Nogo-A antibodies), and optogenetic restoration – have demonstrated functionally confirmed RGC rescue or restoration using OptoDrum as the primary or key secondary endpoint..

The challenge

Demonstrating that a neuroprotective intervention preserves or rescues RGC function – rather than merely slowing histological degeneration – requires a non-invasive, repeatable behavioural endpoint that is sensitive to graded functional change. Structural endpoints (RGC counts, RNFL thickness, optic nerve cross-sectional area) confirm cell survival but do not confirm that surviving cells are functionally competent: an RGC that has retracted its dendritic arbour and lost synaptic connectivity may survive as a cell body while contributing nothing to visual function. The distinction between "surviving but dysfunctional" and "surviving and functional" RGCs is essential for therapeutic evaluation.

OptoDrum resolves this distinction directly: it measures the integrated functional output of the RGC population through the subcortical optomotor reflex, providing a readout that depends on both RGC survival and functional connectivity. A neuroprotective intervention that preserves cell counts but does not restore function will produce no OptoDrum signal improvement; conversely, a regenerative intervention that reconnects surviving RGCs to their visual targets will produce a detectable functional gain even before full histological recovery.

For regenerative interventions specifically, the functional endpoint question is even more critical: anatomical axon regeneration after optic nerve injury does not necessarily translate to functional circuit restoration. OptoDrum provides the behavioural confirmation that regenerated axons have made functionally competent synaptic connections.

How Striatech products help

OptoDrum
Provides the primary non-invasive behavioural endpoint for neuroprotection and regeneration studies: measures visual acuity and contrast sensitivity, confirming whether surviving or regenerated RGCs contribute to functional visual output via the subcortical optomotor reflex.
ScotopicKit
In neuroprotection studies targeting both RGC and photoreceptor compartments (e.g. AKT pathway activation in dystrophies), the ScotopicKit extends OptoDrum to scotopic conditions, separately confirming rod-pathway and inner retinal functional contributions to the treatment response.
DarkAdapt
Ensures standardised dark adaptation prior to scotopic OMR testing, critical for reproducible scotopic endpoints in longitudinal neuroprotection studies.
Non-aversive Animal Platform
Reduces handling stress in post-surgical, gene-therapy-treated, or aged animals, maintaining data quality across prolonged follow-up periods in long-duration gene therapy efficacy studies.

Evidence from the Literature

  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.
    Feature →
  • Karg et al (2023) Cell Reprogram.
    Journal Club →
    AAV-mediated OSK epigenetic reprogramming of RGCs produced sustained, behaviourally measurable visual acuity recovery months after treatment in aged and glaucomatous mice, as confirmed by OptoDrum as the primary long-term efficacy endpoint.
  • Eghbali et al (2023) Cell J.
    EPO treatment reduced RGC apoptosis and preserved optomotor-measured visual acuity after acute optic nerve injury, demonstrating pharmacological neuroprotection with a direct functional endpoint.
  • Baya Mdzomba et al (2020) Cell Death Dis.
    Journal Club →
    Anti-Nogo-A antibody therapy reduced RGC death and produced behaviourally measurable visual recovery on OptoDrum after neuroinflammatory and toxic optic nerve injury, validating an axon growth inhibitor-targeting biological as a neuroprotective and pro-regenerative strategy.
  • Zhao et al (2025) Adv Sci (Weinh).
    RNA-targeting CRISPR editing suppressed pathogenic gene expression, reduced RGC death, and preserved visual acuity on OptoDrum in a glaucoma model, demonstrating that precision gene-editing neuroprotection translates to a measurable functional benefit.
  • Brunet et al (2026) Biomedicines.
    AKT pathway activation via SC79 preserved both photoreceptor and RGC function in an inherited retinal dystrophy model; the OptoDrum/ScotopicKit combination separately confirmed photopic (RGC/cone-driven) and scotopic (rod-driven) functional components of the neuroprotective response.
  • Lu et al (2024) Gene Ther
    Feature →
    Dose-dependent AAV-mediated optogenetic restoration of RGC light sensitivity produced measurable visual function recovery on OptoDrum in a photoreceptor-degenerate model, establishing dose-response parameters for optogenetic therapy efficacy.
Product Fit

Summary: Striatech Products supporting your research questions

Research Question OptoDrum ScotopicKit AcuiSee Photorefractor Keratometer DarkAdapt Non-aversive platform
Pre-death dysfunction window Yes Yes Yes Yes
Apoptotic / necroptotic / Wallerian pathways Yes Yes
Neuroinflammation-driven RGC death Yes Yes Yes
Neuroprotective and regenerative rescue Yes Yes Yes Yes
Cross-model comparison Yes Yes Yes
Measurement Modalities

Measuring Functional Visual Outcomes in Retinal Ganglion Cell Pathology: How Do Available Methods Compare?

The following table compares functional and structural methods commonly used alongside OptoDrum in RGC pathology research. OptoDrum is complementary to, not a replacement for, electrophysiological and histological endpoints.
Method What It Measures Invasiveness Repeatable? Anaesthesia? RGC-specific? Automation
OptoDrum (OMR) Visual acuity and contrast sensitivity (subcortical reflex; retina-to-pretectum) Non-invasive Yes – unlimited repeats No Moderate (driven by RGCs; also requires functional retinal output) Fully automated
AcuiSee (operant) Visual acuity (cortical operant; requires cortical processing) Non-invasive Yes No Low (full pathway from retina to cortex) Automated paradigm
Pattern ERG (PERG) RGC mass response (retinal electrical signal to patterned stimuli) Contact electrodes or corneal electrodes Yes (requires repeated anaesthesia) Yes High (predominantly inner retinal / RGC) Semi-automated
Visual evoked potential (VEP) Cortical response to visual stimulation; optic nerve conduction Cortical electrode implant (terminal or chronic) Limited (terminal or chronic implant required) Yes Moderate (pathway integrity from retina to cortex) Semi-automated
RGC count / RNFL histology RGC density; retinal nerve fibre layer thickness Terminal (tissue collection) No – single time point per animal Terminal High (direct RGC structural count) Semi-automated (image analysis)
Optical coherence tomography (OCT) RNFL and retinal layer thickness in vivo Minimally invasive (pupil dilation, immobilisation) Yes Typically yes Moderate (structural proxy for RGC axon loss) Semi-automated
OptoDrum's primary advantage in RGC pathology research is the combination of complete non-invasiveness, no anaesthesia requirement, unlimited longitudinal repeatability, and full automation – enabling dense time-course sampling across a disease progression study without the logistical or welfare cost of repeated anaesthetic procedures. PERG provides higher RGC-specificity and is the gold-standard electrophysiological complement to OMR testing; the two methods together provide structural-functional correlation at the RGC level.
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Publications on Retinal Ganglion Cell Pathology

Great Research, Interactive

Journal Clubs related to Retinal Ganglion Cell Pathology

Featured image for “Journal Club: RIP1 Inhibition Protects Retinal Ganglion Cells in Preclinical Glaucoma Models”
Q&A available
Watch now
Wednesday, 18 Jun 2025

Journal Club: RIP1 Inhibition Protects Retinal Ganglion Cells in Preclinical Glaucoma Models

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Bo Kyoung Kim, Ph.D. - Roche Pharma Research & Early Development, Roche Innovation Center Basel, F. Hoffmann-La Roche Ltd.
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This Journal Club features innovative research by Kim et al., who revealed that inhibiting RIP1 kinase protects retinal ganglion cells in preclinical glaucoma models. Their work demonstrates that targeting necroptosis and inflammation can prevent cell loss and functional decline, directly linking genetic risk to inflammatory degeneration and highlighting RIP1 as a promising therapeutic target for neuroprotection in glaucoma.
Featured image for “Journal Club: Aging and Injured Retinal Ganglion Cells Can Be Rejuvenated by Epigenetic Reprogramming”
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Thursday, 27 Feb 2025

Journal Club: Aging and Injured Retinal Ganglion Cells Can Be Rejuvenated by Epigenetic Reprogramming

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Bruce R. Ksander, Ph.D. - Schepens Eye Institute of Mass Eye & Ear, Harvard Medical School, Department of Ophthalmology
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This Journal Club highlights groundbreaking work by Harvard Medical School scientist Bruce R. Ksander and his team. They were able to reverse aging in retinal ganglion cells, improving visual function after injury or in disease.
Keep exploring

Related application areas, neighbouring research chapters, and the questions researchers ask most.

Application Area

Retinal Ganglion Cell Pathology

Death and dysfunction of the projection neurons linking eye to brain. RGC-targeted assays detect functional loss before histological cell death, expanding the therapeutic window across glaucoma, axon injury, and neurodegeneration.

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Research Chapters
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FAQs answered
Main Field where Retinal Ganglion Cell Pathology is studied
The Optic Nerve, its Neurons and Diseases
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Last updated: 15 July 2026