Research Applications for Striatech Products

Ocular Inflammation and Immune-Mediated Eye Disease

Inflammatory and immune-mediated disorders affecting the retina, optic nerve, and visual pathway, including uveitis, optic neuritis, demyelinating diseases such as multiple sclerosis (MS), MOGAD, and NMOSD, related preclinical models such as EAE, and selected rare inflammatory disorders. Across these areas, researchers examine how inflammation, demyelination, and immune-mediated tissue damage affect visual function. Longitudinal noninvasive measurements can provide functional readouts in preclinical studies.

Introduction

Animal Models

Research Questions

Measurement Modalities

Publications

Journal Clubs

Research Chapter Ocular Inflammation and Immune-Mediated Eye Disease

Application Areas

FAQs answered

Part of Eye & Retinal Disease

Main Application Areas

Optic Neuritis

Additional Topics

Autoimmune Demyelinating Diseases

Axon Degeneration

Experimental Autoimmune Encephalomyelitis (EAE)

Glial Suppression

MOG Antibody-Associated Disorder

Multiple Sclerosis

Optic Nerve Damage

Optic Nerve Regeneration

PLP defects

Rare Disease

Retinal Dystrophy

Introduction

What Is Ocular Inflammation and Immune-Mediated Eye Disease?

Ocular inflammation and immune-mediated eye disease encompass a heterogeneous group of conditions in which innate and adaptive immune mechanisms affect the eye and visual pathway. This includes uveitis, optic neuritis, immune-mediated retinal disease, and ocular involvement in systemic autoimmune, autoinflammatory, demyelinating, and rare genetic disorders.

Uveitis is the most familiar clinical category within this broader field and affects the uveal tract—the iris, ciliary body, and choroid. It remains an important cause of visual loss in developed countries and a significant therapeutic challenge, particularly because long-term corticosteroid treatment can be limited by systemic and ocular adverse effects.

Other disease contexts relevant to this chapter include optic neuritis associated with multiple sclerosis (MS), MOG antibody-associated disease (MOGAD), and neuromyelitis optica spectrum disorder (NMOSD); experimental autoimmune encephalomyelitis (EAE) and related demyelinating models; experimental uveitis; rare inflammatory disorders such as ROSAH syndrome; inherited leukodystrophies with inflammatory components; and post-traumatic ocular and visual-pathway inflammation following blast injury or traumatic brain injury.

Although these conditions differ in cause and anatomical distribution, they can converge on overlapping pathological mechanisms. Depending on the model and disease context, these may include immune-cell infiltration, cytokine and chemokine signaling, microglial activation, antibody-associated inflammatory injury, demyelination, axonal degeneration, and retinal ganglion cell loss.

In demyelinating disease in particular, the optic nerve is especially informative because it is a central nervous system white-matter tract. It can therefore participate directly in inflammatory lesion biology, making optic neuritis and related visual-system pathology valuable endpoints in models of CNS autoimmunity and neuroinflammation.

Vision: A Window into the Brain

Why Does Ocular Inflammation Matter to Researchers Beyond the Eye – and Why Do Visual Endpoints Matter to Systemic Autoimmune Disease Research?

For vision-focused researchers, the relevance is direct: uveitis, optic neuritis, immune-mediated retinal vasculitis, and the ocular complications of rare autoinflammatory disorders all produce retinal and optic nerve damage that can be quantified longitudinally using the OptoDrum's optomotor reflex assay. Visual acuity and contrast sensitivity thresholds provide a continuous, functional, circuit-level output that correlates with and complements structural endpoints such as OCT-measured retinal nerve fibre layer thickness and confocal RGC counting.

For systemic autoimmune and neurological disease researchers, the argument is somewhat different. EAE – the most widely used preclinical model of MS – reliably produces optic neuritis as one of its characteristic lesions, and the visual pathway provides an anatomically and functionally distinct readout of demyelinating disease severity that is largely independent of spinal cord motor impairment. This matters because conventional EAE scoring uses motor disability scales (tail paralysis, hind limb paresis) that reflect spinal cord disease but miss optic nerve and retinal involvement entirely. OptoDrum-based visual function testing provides a parallel, independent functional dimension: it captures optic nerve and RGC circuit integrity in the same animal that is being scored for motor disability, without anaesthesia, surgical access, or sacrifice. For researchers working on MOGAD, NMOSD, or rare inflammatory leukodystrophies in which optic nerve involvement is a defining feature, the visual endpoint is not merely complementary – it is often the primary functional correlate of the lesion of interest. If you are studying an autoinflammatory condition that affects the CNS and you are not measuring visual function, you may be overlooking one of the most informative noninvasive functional readouts available.

Animal Models

Common Animal Models for Ocular Inflammation and Immune-Mediated Eye Disease Research

Autoimmune demyelinating and optic neuritis models

Experimental autoimmune encephalomyelitis (EAE) is an induced inflammatory demyelinating disease model used primarily to study mechanisms relevant to multiple sclerosis and related disorders. In rodents, EAE is commonly initiated by immunization with myelin-derived antigens or, in some protocols, by the transfer of activated immune cells; the resulting CNS inflammation can produce motor deficits, optic neuritis, demyelination, and neurodegeneration, depending on the strain and induction paradigm.

Experimental autoimmune encephalomyelitis (EAE) – C57BL/6 MOG_35-55, SJL/J PLP_139-151, and related variants: One of the most widely used models of MS and autoimmune optic neuritis. MOG_35-55 immunization in C57BL/6 mice typically induces a chronic monophasic disease course with spinal cord and optic nerve demyelination, retinal ganglion cell loss, and measurable visual dysfunction, whereas PLP139-151 immunization in SJL mice is commonly used to model relapsing-remitting disease. (Stromnes et al., 2006, Nat Protoc.).
B cell-dependent EAE and MOGAD models: Immunization protocols incorporating anti-MOG antibodies or B cell-stimulating adjuvants produce a humoral immune component relevant to MOG antibody-associated disease (MOGAD), with antibody-associated demyelination and optic neuritis phenotypes. (Joly et al., 2022, J. Neuroinflammation)

Uveitis and ocular immune response models

Endotoxin-induced uveitis (EIU) and experimental autoimmune uveitis (EAU): Systemic lipopolysaccharide (LPS) administration induces an acute innate immune model of uveitis, whereas IRBP immunization induces experimental autoimmune uveitis, a T cell-driven model commonly used to study posterior segment inflammation and treatment responses. In B10.RIII mice, intravitreal anti-IL-6 treatment has been reported to attenuate EAU both clinically and functionally. (Hösel et al., 2024, J Ophthalmic Inflamm Infect.)

Rare genetic and inherited inflammatory models

PLP1-defect models (Pelizaeus-Merzbacher disease / jimpy mice): Mice carrying pathogenic PLP1 mutations or related PLP1 defects develop leukodystrophy with hypomyelination or dysmyelination, microglial activation, axon degeneration, and optic nerve involvement. Multiple publications use PLP-defect models to study inflammatory and immune-associated mechanisms in rare inherited demyelinating disease.
ALPK1 gain-of-function / ROSAH syndrome models: Knock-in mice carrying ALPK1 gain-of-function mutations that cause ROSAH syndrome develop retinal inflammation, optic disc edema, and RGC dysfunction. This model enables preclinical evaluation of ALPK1 inhibitors as precision immunotherapies for this rare autoinflammatory ocular disease. (Fan et al., 2025, Nat. Commun.)

Traumatic injury models

Blast injury and TBI models: Controlled-blast or weight-drop traumatic brain injury models in rodents produce post-traumatic ocular immune responses including retinal inflammation and retinal ganglion cell vulnerability. These models are relevant to immune-mediated mechanisms contributing to visual impairment after blast exposure or traumatic injury. (Harper et al., 2022, Exp. Eye Res.)

Aging-related neuroinflammation models

Aging-associated neuroinflammation models: Aged mice (typically 18-24 months) show progressive accumulation of cytotoxic CD8+ T cells and microglial activation in CNS white matter, including the optic nerve, with associated axon degeneration and functional decline. These models are useful for studying how age-related neuroinflammatory states may influence vulnerability of the visual pathway and can be paired conceptually or experimentally with demyelinating disease models such as EAE. (Groh et al., 2021, Nat. Aging)

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.

How Can I Measure Visual Dysfunction in Optic Neuritis, EAE, and Multiple Sclerosis Models?

Audience A - Vision-focused

Audience B - CNS/Systemic

Quick Answer

The OptoDrum provides a non-invasive, automated functional endpoint for visual dysfunction in EAE and optic neuritis models. It measures optomotor-based visual acuity and contrast sensitivity in awake, unrestrained rodents, providing a repeatable longitudinal readout that complements conventional EAE motor scoring and structural assessments of the retina and optic nerve.

The challenge

EAE is one of the most widely used preclinical models of multiple sclerosis (MS) and experimental optic neuritis, but its standard outcome measure - the EAE clinical score based on tail and limb paresis - primarily reflects spinal cord motor impairment rather than visual-pathway involvement. Optic neuritis occurs in up to 50% of people with MS and can be the presenting manifestation in approximately 20% of cases. In EAE, optic nerve inflammation, retinal ganglion cell (RGC) loss, and visual dysfunction are well documented, but visual function is not routinely included as a primary outcome in many experimental study designs.

As a result, interventions may be evaluated principally through motor disability measures, potentially overlooking effects on optic nerve, retinal, and visual function. Adding a visual endpoint can therefore provide complementary evidence of treatment effects within the visual system alongside conventional clinical scoring.

Visual evoked potentials (VEPs) provide an electrophysiological measure of the integrity and timing of visual-pathway responses and are widely used in clinical MS and optic neuritis assessment. In rodents, VEP recording commonly requires anesthesia and cortical electrodes or other invasive recording approaches, which can limit measurement frequency and introduce procedural considerations in longitudinal studies. OptoDrum does not replace VEP when a cortical or electrophysiological endpoint is required. It provides a powerful complementary functional endpoint for longitudinal EAE studies: an automated, noninvasive measure of visual acuity and contrast sensitivity that can be collected repeatedly in awake, unrestrained animals alongside conventional motor scoring.

OptoDrum measures visual acuity and contrast sensitivity through the subcortical optomotor reflex in awake, freely moving mice. This retina-to-brainstem circuit depends on retinal input transmitted through the optic nerve and can be affected by visual-system pathology, including optic nerve inflammation and RGC injury. Measurements can be repeated longitudinally in the same animals alongside EAE motor scoring, without anesthesia, surgical access, or animal training.

Scope note for EAE researchers: OptoDrum measures a subcortical reflex pathway, not cortically processed visual perception. It is therefore not designed to assess visual cortex lesions or cortical visual-processing deficits. VEPs, or AcuiSee when an operant, learned visual-discrimination endpoint is appropriate, are better suited to studies focused on cortical visual-pathway function.

Also see: Neuroinflammation & Autoimmune CNS Disease, Optic Neuritis, Autoimmune Demyelinating Diseases. Experimental Autoimmune Encephalomyelitis and Multiple-Sclerosis.

How Striatech products help

OptoDrum

Measures spatial visual acuity (cycles per degree) and contrast sensitivity threshold through the subcortical optomotor reflex in awake, unrestrained mice and rats. Provides a repeatable, functional readout of visual-system changes relevant to optic nerve and RGC pathology in EAE models, complementary to motor disability scores and structural assessments. No anesthesia, electrode placement, or animal training is required. Measurements can be repeated at multiple time points throughout the disease course.

AcuiSee

Measures visual acuity through an operant, cortically mediated visual-discrimination paradigm. It can be used in EAE and MS models when a learned, cortically processed visual endpoint is needed – for example, to assess whether improvements in visual-pathway physiology are accompanied by improved learned visual discrimination. This cortical dimension is not measured by OptoDrum’s subcortical reflex endpoint.

Evidence from the Literature

Mayer et al (2026) Nature
Identified intracellular neuronal complement factor H (CFH) as a protective factor during CNS inflammation. In EAE, neuron-specific Cfh deficiency worsened EAE disease severity and increased visual impairment, including reduced visual acuity and contrast sensitivity measured with OptoDrum. The study illustrates how longitudinal visual-function testing can capture functionally meaningful effects of inflammatory neurodegeneration in EAE.
Anders et al (2023) Front Immunol.
Reported that acriflavine, an HIF-1 inhibitor, reduced EAE severity and preserved visual function measured with OptoDrum. The findings support HIF-1-associated inflammatory signaling as a potential therapeutic target in EAE-related optic neuritis and retinal ganglion cell pathology.
Joly et al (2022) J. Neuroinflammation
Characterized visual deficits in a B cell-dependent EAE model with humoral contributions to demyelination. OptoDrum-based assessment identified visual dysfunction alongside optic neuritis and retinal ganglion cell pathology, supporting the model as a translational platform for investigating humoral mechanisms and evaluating B cell-targeted approaches relevant to MOG antibody-associated disease.
Morin et al (2021) J. Immunol.
Feature →
Used conditional cell-specific deletion of histidine decarboxylase (Hdc) to test whether histamine synthesis from distinct cellular sources modifies EAE. Although histamine deficiency produced expected effects in anaphylaxis and circadian activity, ubiquitous and cell-specific Hdc deletions did not alter the EAE course. Consistent with these findings, OptoDrum showed a comparable decline in visual acuity in EAE Hdc-knockout and wild-type animals, indicating that loss of histamine synthesis did not materially modify EAE-associated visual dysfunction in this model.

What Are the Visual Consequences of MOG Antibody-Associated Disorder and Neuromyelitis Optica Spectrum Disorder, and How Can I Model Them Preclinically?

Audience A - Vision-focused

Audience B - CNS/Systemic

Quick Answer

MOGAD and NMOSD are inflammatory demyelinating diseases distinct from classical MS, and optic neuritis is a major manifestation of both. In MOG-IgG- and AQP4-IgG-associated EAE models, longitudinal OptoDrum testing has detected reduced visual acuity, providing a noninvasive functional endpoint alongside measures of retinal and optic nerve injury.

The challenge

MOG antibody-associated disease (MOGAD) and aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder (AQP4-IgG-positive NMOSD) are now recognized as disease entities distinct from classical multiple sclerosis (MS). Both can cause severe optic neuritis, but their immunopathology differs: MOGAD is associated with MOG-IgG and inflammatory demyelination, whereas AQP4-IgG-positive NMOSD is an astrocytopathy in which antibody-mediated, often complement-associated injury contributes to lesion development.

These differences create a need for preclinical models that capture selected disease-relevant mechanisms and enable longitudinal measurement of visual function. MOG-IgG- and AQP4-IgG-associated EAE models can be used to examine retinal and optic nerve injury, including visual-acuity changes, alongside histological and structural measures. However, no individual model reproduces the full complexity of either human disease, and functional endpoints should be interpreted within the specific induction protocol and pathological context.

Repeated visual testing with OptoDrum can complement model characterization and therapeutic studies by providing a noninvasive functional outcome alongside assessments of optic nerve inflammation, retinal pathology, demyelination, and axonal injury. This is relevant when investigating candidate interventions that affect antibody-mediated inflammation, complement activity, B-cell biology, or other disease-associated pathways.

Also see: MOG-Antibody Associated Disorder and Optic Neuritis.

How Striatech products help

OptoDrum

Provides a noninvasive, automated functional endpoint for longitudinal studies of MOGAD- and NMOSD-relevant models. By measuring optomotor-based visual acuity and contrast sensitivity in awake, unrestrained animals, it complements structural and histological assessments of optic nerve inflammation, demyelination, axonal injury, and retinal ganglion cell pathology.

AcuiSee

Provides an operant, cortically mediated visual-acuity endpoint for studies requiring a learned visual-discrimination measure. It can complement OptoDrum where researchers wish to determine whether disease-associated visual-system injury, or an intervention, affects cortically processed visual performance in addition to subcortical optomotor function.

Evidence from the Literature

Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.
Feature →
Characterized longitudinal visual-system outcomes in MOG-IgG- and AQP4-IgG-associated EAE models. OptoDrum detected reduced visual acuity, complementing their assessments of retinal injury and optic nerve involvement. Provides an example for repeated functional visual testing in MOGAD- and NMOSD-relevant preclinical studies.
Jarius et al (2010) Nat Rev Neurol.
Foundational review of the pathogenic and diagnostic significance of aquaporin-4 antibodies in NMOSD, establishing clinical context for antibody-associated optic nerve and CNS injury. The review helps frame the translational relevance of preclinical visual-system endpoints in AQP4-IgG-associated disease models.
Reindl et al (2019) Nat Rev Neurol.
Comprehensive review of the immunopathology and clinical spectrum of MOG antibody-associated disease, including the prominent role of optic neuritis. This review provides translational context for interpreting visual outcomes in MOGAD-relevant preclinical models.

Does Metabolic and Dietary Status Modulate Immune-Mediated Visual Pathway Damage?

Audience A - Vision-focused

Audience B - CNS/Systemic

Quick Answer

Yes. Dietary composition and metabolic interventions can modify neuroinflammatory outcomes in EAE, but their effects depend on the specific intervention, timing, and disease model. Capper et al. (2025, Front Immunol.) found that a ketogenic diet high in long-chain saturated fatty acids did not improve visual outcomes in EAE; when initiated before disease manifestation, it modestly worsened motor-sensory deficits and visual-acuity loss measured with OptoDrum.

The challenge

The relationship between diet, systemic metabolism, and neuroinflammation in MS and related autoimmune demyelinating disease is an active area of research. Dietary composition can influence immune signaling, T-cell polarization, and microbiome-dependent inflammatory tone, all of which may modify EAE severity and visual-system involvement. However, the biological effects of dietary intervention depend strongly on the specific diet composition, timing, and disease model.

Capper et al. (2025, Front Immunol.) addressed this question directly using a ketogenic diet enriched in saturated, long-chain fatty acids in MOG_{35-55_{EAE. Rather than showing neuroprotection, this diet did not improve visual outcomes and, when initiated before disease manifestation, modestly worsened motor-sensory deficits and visual-acuity loss measured with OptoDrum. Importantly, these functional changes were not accompanied by significant differences in optic nerve axonal damage or retinal ganglion cell loss, indicating that dietary effects may be detectable functionally even when structural endpoints are unchanged at the measured time point.}}

This is where longitudinal visual testing becomes especially informative. Standard EAE motor scoring can detect changes in general neurological disability, but it does not quantify visual dysfunction directly. OptoDrum adds a repeatable, noninvasive functional endpoint that can reveal how dietary or metabolic interventions influence visual-system performance alongside motor outcomes and structural measures. This makes it well suited for studies evaluating ketogenic diets, microbiome-targeted interventions, fasting paradigms, or other metabolic strategies in autoimmune demyelinating disease.

Also see: Neuroinflammation & Autoimmune CNS Disease and Experimental Autoimmune Encephalomyelitis.

How Striatech products help

OptoDrum

Provides a repeatable, noninvasive functional visual endpoint for studies of dietary and metabolic modulation in EAE. By measuring optomotor-based visual acuity and contrast sensitivity in awake, unrestrained animals, it complements motor scoring and structural assessments to track how an intervention affects visual-system performance over time.

AcuiSee

Provides an operant, cortically mediated visual-acuity endpoint for studies in which a learned visual-discrimination measure is required. It can complement OptoDrum when researchers wish to assess whether dietary or metabolic interventions influence cortically processed visual performance in addition to subcortical optomotor function.

Evidence from the Literature

Capper et al (2025) Front Immunol.
Evaluated a ketogenic diet enriched in saturated, long-chain fatty acids in the MOG_{35-55_{EAE model. The diet did not improve EAE-associated motor or visual outcomes and, when initiated before disease manifestation, modestly worsened motor-sensory deficits and visual-acuity loss measured with OptoDrum. The study found no significant differences in optic nerve axonal damage or retinal ganglion cell loss at the assessed endpoint, highlighting the importance of diet composition and timing in preclinical metabolic-intervention studies.}}
Cignarella et al (2018) Cell Metab.
Showed that intermittent fasting reduced EAE severity and altered gut microbiome-associated immune responses, supporting the broader principle that dietary interventions can modify neuroinflammation. Although the study did not assess OptoDrum-based visual function, it provides mechanistic context for incorporating longitudinal visual endpoints when evaluating dietary, metabolic, or microbiome-targeted interventions in EAE.

How Do Neuroinflammatory Mechanisms Such as Microglia, T Cells, and Epigenetic Regulators Contribute to Visual Pathway Damage in Immune-Mediated Eye Disease?

Audience A - Vision-focused

Audience B - CNS/Systemic

Quick Answer

When investigating microglial activity, T cell-mediated injury, inflammatory gene regulation, or neuroprotective and regenerative interventions, OptoDrum provides a repeatable, noninvasive functional endpoint for assessing their effects on visual-system function.

The challenge

Neuroinflammatory damage to the visual pathway can arise through multiple interacting mechanisms. Microglia, the resident immune cells of the CNS and retina, can adopt context-dependent states that either contribute to tissue injury or support repair processes such as myelin-debris clearance. In aging white matter, dysregulated microglial activation can promote CXCL10-CXCR3-dependent recruitment of cytotoxic CD8+ T cells, linking glial dysfunction to axonal injury and visual-system decline. Cytotoxic CD8+ T cells can also contribute to axonal injury in inflammatory and inherited demyelinating conditions, while inflammatory transcriptional regulators, including BET bromodomain proteins, may influence gene-expression programs associated with retinal inflammation and degeneration.

These mechanisms are studied across diverse experimental contexts, including autoimmune demyelination, PLP1-defect leukodystrophy models, aging-associated white-matter degeneration, retinal injury, and light-induced retinal degeneration. Findings from one model should therefore be interpreted within its specific pathological context rather than generalized automatically to every immune-mediated disorder affecting the eye or visual pathway.

The practical challenge is to determine whether molecular, cellular, or structural changes have meaningful functional consequences. OptoDrum provides a repeatable, noninvasive measure of optomotor-based visual acuity and contrast sensitivity that can complement molecular, cellular, structural, and histological assessments. Used longitudinally, it can help determine whether interventions targeting microglia, T cells, inflammatory gene regulation, or regenerative pathways are associated with preserved or improved visual-system function.

Baya Mdzomba et al. (2020, Cell Death & Disease) provide an example of this translational approach: Nogo-A antibody treatment in a retinal-injury model was associated with improved visual function and reduced neuroinflammatory changes, illustrating how functional endpoints can complement evaluation of neuroprotective and regenerative strategies.

Also see: Axon Degeneration, Glial Suppression, Optic Nerve Damage, Optic Nerve Regeneration, PLP Defects, and Retinal Degeneration and Inherited Retinal Disease.

How Striatech products help

OptoDrum

a repeatable, noninvasive functional endpoint for neuroinflammatory mechanism studies. By measuring optomotor-based visual acuity and contrast sensitivity, it can assess the downstream functional effects of interventions targeting microglia, T cells, inflammatory gene regulation, or regenerative pathways. Longitudinal testing in awake, unrestrained animals complements molecular, cellular, structural, and histological measurements throughout the disease course.

AcuiSee

Provides an operant, cortically mediated visual-acuity endpoint for studies requiring a learned visual-discrimination measure. It can complement OptoDrum when researchers wish to evaluate whether an intervention is associated with changes in cortically processed visual performance as well as subcortical optomotor function.

Evidence from the Literature

Groh et al (2025) Nat Neurosci.
Journal Club →
Feature →
Investigated how dysregulated microglial activation promotes age-related white-matter degeneration in the optic nerve. In aged mice, PLX5622 treatment or Cx3cr1 deficiency increased reactive microglial states, myelin abnormalities, axonal damage, retinal thinning, and retinal ganglion cell loss, together with reduced visual acuity measured using OptoDrum. The study further identified CXCL10-CXCR3 signaling as a mechanism recruiting pathogenic CD8+ T cells; genetic interruption of this axis reduced CD8+ T cell accumulation and protected visual function.
Groh et al (2023) Nat Commun.
Feature →
Examined PLP-defect mouse models of inherited demyelinating disease and showed that microglia-mediated demyelination can protect axons from CD8+ T cell-driven degeneration. OptoDrum provided a longitudinal functional correlate of the genotype- and age-associated visual-pathway phenotype. The findings emphasize that microglial responses are context dependent: impaired handling of defective myelin can contribute to degeneration, whereas controlled microglia-mediated removal of defective myelin can limit axonal injury.
Abdelwahab et al (2023) iScience
Demonstrated that cytotoxic CNS-associated T cells can drive axon degeneration by targeting perturbed oligodendrocytes in PLP1-mutant mice. The findings support the use of functional assays such as OptoDrum to determine whether immune-mediated axonal injury in related models translates into measurable visual dysfunction.
Zhu et al (2023) J. Neuroinflammation
Reported that dBET6, a PROTAC designed to degrade BET bromodomain proteins, reduced cGAS-STING-associated inflammatory signaling and protected against retinal degeneration in a light-damage model. The study supports the value of functional readouts such as OptoDrum when testing anti-inflammatory interventions in suitable retinal models.
Baya Mdzomba et al (2020) Cell Death Dis.
Journal Club →
Reported that Nogo-A-targeting antibody treatment improved visual function and reduced neuroinflammatory changes after retinal injury. OptoDrum provided functional evidence that the neuroprotective and regenerative intervention was associated with measurable visual recovery.

Can OptoDrum Track Visual Function in Uveitis and Acute Ocular Immune Responses?

Audience A - Vision-focused

Audience B - CNS/Systemic

Quick Answer

Yes. In experimental autoimmune uveitis, OptoDrum-based testing has detected functional visual changes and has been used to assess the effects of intravitreal anti-IL-6 treatment. In an adoptive-transfer blast-TBI model, OptoDrum detected significant long-term visual dysfunction alongside immune-mediated retinal ganglion cell pathology, supporting its use as a functional endpoint in post-traumatic ocular immune-response studies.

The challenge

Uveitis encompasses a clinically heterogeneous group of intraocular inflammatory conditions that can impair visual function through multiple mechanisms, including inflammatory injury to retinal tissue, cystoid macular edema, vitreous haze, and posterior-segment complications such as epiretinal membrane formation. In rodent models, investigators commonly assess inflammation through slit-lamp examination, histology, inflammatory-cell quantification, and cytokine analysis. These endpoints are essential for characterizing disease activity, but they do not directly quantify the animal's visual performance.

OptoDrum addresses this gap by measuring spatial visual acuity and contrast sensitivity before, during, and after uveitis. Used alongside inflammatory, structural, and histological measures, it provides a repeatable, noninvasive functional endpoint for determining whether intraocular inflammation is associated with visual dysfunction and whether treatment is associated with functional preservation or improvement. In experimental autoimmune uveitis, OptoDrum has been used to assess the functional effects of intravitreal anti-IL-6 treatment.

Blast-mediated traumatic brain injury represents a distinct but related context in which mechanical injury and post-traumatic immune responses can contribute to retinal pathology. In the adoptive-transfer blast-TBI model studied by Harper et al. (2022), immune activation contributed to retinal ganglion cell dysfunction and death, while OptoDrum detected reduced optomotor performance at 5 and 6 months after injury. This illustrates how longitudinal functional testing can complement assessment of persistent post-traumatic retinal and visual-system consequences.

Also see: Trauma & Acute Injury and Optic Nerve Damage.

How Striatech products help

OptoDrum

Provides a non-invasive, repeatable functional endpoint for uveitis and post-traumatic ocular immune-response studies. It measures optomotor-based visual acuity and contrast sensitivity longitudinally in awake, unrestrained animals, allowing researchers to assess visual function longitudinally (before disease onset, during inflammation, and following intravitreal or systemic treatment) without anesthesia, manipulation of the inflamed eye, or sacrifice at each time point.

AcuiSee

Provides an operant, cortically mediated visual-acuity endpoint for uveitis and post-traumatic ocular injury studies when a learned visual-discrimination measure is required. It can assess whether intraocular inflammation or retinal injury affects cortically processed visual performance and is particularly useful when a study requires a trained, suprathreshold visual task rather than a reflex-based endpoint.

Evidence from the Literature

Hösel et al (2024) J Ophthalmic Inflamm Infect.
Feature →
Evaluated intravitreal anti-IL-6 treatment in experimental autoimmune uveitis. OptoDrum detected functional visual impairment associated with intraocular inflammation and showed that treatment was associated with improved visual function alongside reduced clinical disease activity.
Harper et al (2022) Exp. Eye. Res.
Characterized immune responses following blast-mediated traumatic brain injury and showed that post-traumatic immune activation contributes to retinal ganglion cell dysfunction and death. OptoDrum detected significantly reduced visual function at 5 and 6 months after injury, providing a direct functional endpoint for persistent post-traumatic retinal pathology.

How Do Rare Genetic Variants and Systemic Autoimmune Conditions Cause Immune-Mediated Visual Pathway Damage?

Audience A - Vision-focused

Audience B - CNS/Systemic

Quick Answer

Rare genetic and systemic autoimmune disorders can affect the retina, optic nerve, and visual pathway through distinct mechanisms, including primary genetic defects, autoinflammatory signaling, demyelination, vascular inflammation, and secondary immune activation. OptoDrum provides a repeatable, noninvasive functional endpoint for determining whether these disease processes, and candidate interventions, are associated with measurable changes in visual-system performance.

The challenge

Rare genetic, autoinflammatory, and systemic autoimmune disorders with ocular involvement present distinct challenges for preclinical research. Patient populations may be small, disease mechanisms can vary substantially, and relevant animal models are often newly developed or incompletely characterized. A central task is therefore to establish whether a genetic or immune perturbation produces a measurable visual phenotype and whether a candidate intervention is associated with functional preservation or improvement.

These conditions can affect the retina, optic nerve, or visual pathway through different mechanisms, including primary genetic defects, autoinflammatory signaling, dysmyelination, and secondary immune activation. Relevant preclinical examples include ALPK1-associated ROSAH syndrome, PLP1-related myelin disorders, neuronal ceroid lipofuscinosis, and SPG11-associated hereditary spastic paraplegia. Their common feature is not one uniform pathology, but the need to relate molecular, cellular, and structural findings to functional visual outcomes in the relevant model.

OptoDrum provides a repeatable, noninvasive measure of optomotor-based visual acuity and contrast sensitivity in awake, unrestrained animals. Used alongside disease-specific genetic, inflammatory, structural, and histological assessments, it can help determine whether a model produces measurable visual dysfunction and whether an intervention is associated with preserved or improved visual performance. This is particularly valuable when rare models limit animal numbers and when longitudinal measurements are needed before terminal tissue analysis.

Also see: Rare & Inherited CNS and Eye Disorders, Rare Disease, Retinal Dystrophy, and Systemic Aging & CNS Decline.

How Striatech products help

OptoDrum

Provides a repeatable, noninvasive functional endpoint for rare genetic, autoinflammatory, and systemic immune-mediated disease models with retinal, optic nerve, or visual-pathway involvement. By measuring optomotor-based visual acuity and contrast sensitivity in awake, unrestrained animals, it supports longitudinal phenotyping when animal numbers are limited and terminal tissue analyses must be reserved for genetic, immunological, structural, or histological assessment.

AcuiSee

Provides an operant, cortically mediated visual-acuity endpoint for studies in which a learned visual-discrimination measure is required. It can be used to assess whether rare genetic, autoinflammatory, or systemic immune-mediated disease models affect cortically processed visual performance, including suprathreshold visual discrimination and visual acuity.

Evidence from the Literature

Fan et al (2025) Nat Commun.
Identified a selective ALPK1 inhibitor in a mouse model of ALPK1-associated ROSAH syndrome, a rare autoinflammatory disease with ocular involvement. OptoDrum provided a functional visual endpoint alongside retinal and inflammatory assessments, supporting evaluation of whether ALPK1 inhibition was associated with preserved visual performance.
Kozycki et al (2022) Ann. Rheum. Dis.
Characterized ROSAH syndrome as an ALPK1-associated autoinflammatory disease through patient phenotyping, genetic analysis, and development of a mouse model. OptoDrum testing showed no measurable visual deficit in the newly generated mice, consistent with the absence of retinal degeneration and illustrating that the model reproduced only part of the human phenotype. This functional characterization helped define the model’s scope for subsequent mechanistic and therapeutic studies.
Groh et al (2021) Nat. Aging
Journal Club →
Showed that cytotoxic CD8+ T-cell accumulation in the aging CNS contributes to axonal degeneration and functional decline. OptoDrum detected visual dysfunction in aged mice, providing a functional endpoint for studying age-associated immune mechanisms that affect the visual pathway.
Berve et al (2020) J. Neuroinflammation
Feature →
Investigated sex- and region-dependent microglial and macrophage depletion in a CLN1 disease mouse model. OptoDrum captured visual functional outcomes, supporting longitudinal assessment of how microglia-directed interventions influence visual performance in rare neuroinflammatory disease models.
Hörner et al (2024) Thesis
Examined the contribution of inflammation to SPG11-associated hereditary spastic paraplegia, a rare progressive neurological disorder. OptoDrum was used to assess visual function, providing a longitudinal endpoint for evaluating whether inflammatory processes and candidate interventions are associated with visual-pathway dysfunction.

Product Fit

Summary: Striatech Products supporting your research questions

Research Question	OptoDrum	ScotopicKit	AcuiSee	Photorefractor	Keratometer	DarkAdapt	Non-aversive Platform
EAE / optic neuritis	Yes	–	Yes	–	–	–	–
MOGAD / NMOSD	Yes	–	Yes	–	–	–	–
Dietary / metabolic modulation	Yes	–	Yes	–	–	–	–
Neuroinflammatory mechanisms	Yes	–	Yes	–	–	–	–
Uveitis / acute ocular immune responses	Yes	–	Yes	–	–	–	–
Rare genetic / systemic autoimmune	Yes	–	Yes	–	–	–	Yes

Measurement Modalities

Measuring Functional Visual Outcomes in Ocular Inflammation and Immune-Mediated Eye Disease: How Do Available Methods Compare?

Modality	Invasiveness	Repeatability	Training Required	Automation	3Rs Considerations	Notes for Ocular Inflammation Research
OptoDrum (OMR)	Noninvasive; awake, unrestrained animal	High; suitable for repeated longitudinal measurements	None for the animal; operator familiarisation required	Automated stimulus presentation and threshold assessment	Supports longitudinal functional assessment without anaesthesia, restraint, or terminal tissue collection at each time point	Measures optomotor performance mediated primarily by subcortical visual circuits. It provides a functional readout that may be affected by retinal, optic-nerve, and downstream visual-pathway pathology, depending on the model. It does not measure cortical visual processing or optic-nerve conduction velocity.
EAE clinical score (motor disability scale)	Minimal; observer-based, with handling where required	High; commonly assessed repeatedly through the disease course	Inter-rater training and predefined scoring criteria required	Generally observer-dependent	Nonterminal, but does not replace terminal pathological assessment	Captures motor manifestations of spinal-cord disease but does not directly measure visual function, retinal pathology, or optic-nerve involvement. It can be paired with OptoDrum to add a visual functional endpoint in the same animals.
Visual evoked potentials (VEP)	Acute recordings commonly require anaesthesia and electrode placement; chronic recordings require surgical implantation	Moderate; depends on acute versus chronic recording design	Electrophysiology and, for chronic approaches, surgical expertise required	Stimulus delivery may be automated; recording setup and interpretation require expertise	Acute approaches may limit repeat sampling; chronic recordings can support repeated measurements but add surgical burden	Measures visually evoked cortical responses and can assess visual-pathway conduction-related changes. It can complement OptoDrum by providing electrophysiological information that is not captured by an optomotor behavioural readout.
Pattern ERG (PERG)	Moderately invasive; commonly uses corneal electrodes and anaesthesia, although alert protocols are available	Moderate; protocol and recording conditions influence longitudinal use	Electrophysiology expertise required	Partially automated acquisition and analysis	Nonterminal, but requires animal preparation and specialised recording procedures	Provides an electrophysiological measure of inner-retinal, including retinal-ganglion-cell-associated, function. It can help localise retinal contributions to visual dysfunction observed with OptoDrum.
OCT (retinal nerve fibre layer thickness)	Low to moderate; pupil dilation and topical agents or anaesthesia may be used depending on protocol	High; suitable for longitudinal imaging	Imaging, quality-control, and segmentation expertise required	Acquisition and segmentation can be partly automated	Nonterminal and repeatable, with preparation requirements that should be considered in study design	Provides structural measures such as retinal nerve fibre layer thickness that can serve as correlates of retinal-ganglion-cell axon pathology in optic neuritis and EAE. Pairing OCT with functional testing can help relate structural changes to visual performance.
AcuiSee (operant visual acuity)	Noninvasive; awake animal	High after acquisition of the task; session-based	Animal training required; time to criterion depends on protocol, strain, and study design	Automated	Nonterminal, although training and motivation requirements extend study time	Measures learned visual discrimination, including cortically mediated visual-acuity and contrast-sensitivity performance. It is appropriate when the study question requires an operant visual endpoint and the disease timeline permits training.
Histology / IHC (RGC count, optic-nerve axon density)	Terminal; requires tissue collection and processing	Single time point per animal	Tissue-processing, microscopy, and quantitative-analysis expertise required	Image analysis can be partly automated	Terminal by design; use at selected endpoints to complement longitudinal in-life measures	Provides structural and cellular validation, including retinal ganglion cell counts, inflammatory-cell markers, and optic-nerve axon measurements. It can be used at study end to interpret longitudinal functional findings.

Supported by Striatech Products

Publications on Ocular Inflammation and Immune-Mediated Eye Disease

Nature (Sep 02, 2026) Intracellular complement factor H protects neurons during CNS inflammation

Mayer C, Woo MS, Sonner JK, Binkle-Ladisch L, Fischbach F, Sekol P, Smith MD, Lucas-Ruiz F, Manteufel D, Mattern KM, Pfeffer LK, Guo Y, Siebels B, Miguela A, Vieira V, Meurs N, Bauer S, Schwarz S, Wulf S, Mühlig AK, Engler JB, Conrad M, Bareyre FM, Wiech T, Krasemann S, Glatzel M, Zipfel PF, Freiwald T, Calabresi PA, Schirmer L, Friese MA.

Ocular Inflammation and Immune-Mediated Eye Disease

What Is Ocular Inflammation and Immune-Mediated Eye Disease?

Why Does Ocular Inflammation Matter to Researchers Beyond the Eye – and Why Do Visual Endpoints Matter to Systemic Autoimmune Disease Research?

Common Animal Models for Ocular Inflammation and Immune-Mediated Eye Disease Research

How Can Striatech Tools Support Your Study?

The challenge

How Striatech products help

Evidence from the Literature

The challenge

How Striatech products help

Evidence from the Literature

The challenge

How Striatech products help

Evidence from the Literature

The challenge

How Striatech products help

Evidence from the Literature

The challenge

How Striatech products help

Evidence from the Literature

The challenge

How Striatech products help

Evidence from the Literature

Summary: Striatech Products supporting your research questions

Measuring Functional Visual Outcomes in Ocular Inflammation and Immune-Mediated Eye Disease: How Do Available Methods Compare?

Publications on Ocular Inflammation and Immune-Mediated Eye Disease

Journal Clubs related to Ocular Inflammation and Immune-Mediated Eye Disease

Journal Club: Seeing White Matter Aging Through the Visual System

Journal Club: In Vivo Modeling of Immune-mediated Optic Neuropathies

Journal Club: Anti-FcRn Treatment in Antibody-Associated Experimental Autoimmune Encephalomyelitis

Journal Club: Assessing Neuroinflammation-related Neural Damage by Monitoring the Retinotectal System

Journal Club: The role of Nogo-A in visual deficits induced by retinal injury.

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