Research Applications for Striatech Products

Ocular Inflammation and Immune-Mediated Eye Disease

Uveitis, optic neuritis, and the ocular manifestations of systemic and rare inflammatory disorders. Research targets the immune mechanisms behind a major share of preventable blindness in high-income countries.
Introduction

What is Ocular Inflammation and Immune-Mediated Eye Disease?

Ocular inflammation encompasses a heterogeneous group of conditions in which immune-mediated mechanisms – innate or adaptive, local or systemic – damage the structures of the eye and visual pathway. The uveal tract (iris, ciliary body, and choroid) is the most frequently involved site, giving rise to the clinical category of uveitis, which is responsible for approximately 10-15% of blindness in high-income countries and represents a significant unmet therapeutic need given the limitations of long-term corticosteroid use (Tsirouki et al., 2018, Ophthalmology). Beyond classical uveitis, immune-mediated mechanisms drive disease across a much wider spectrum of ocular conditions: optic neuritis in multiple sclerosis (MS), MOG-antibody-associated disorder (MOGAD), and neuromyelitis optica spectrum disorder (NMOSD); ocular manifestations of systemic rheumatic diseases including rheumatoid arthritis, Behcet's disease, and lupus; rare inherited autoinflammatory disorders such as ROSAH syndrome (caused by ALPK1 gain-of-function mutations) and inflammatory rare leukodystrophies; and post-traumatic ocular immune responses following blast injury or traumatic brain injury. What unifies these conditions is the convergence of immune cell infiltration, cytokine release, complement activation, and downstream structural damage on the visual pathway – the retina, optic nerve, and their central projections. At the cellular level, the key effector mechanisms include microglial activation and transition to pro-inflammatory states, CD4+ T cell-mediated delayed-type hypersensitivity, cytotoxic CD8+ T cell-mediated axon damage, B cell and antibody-mediated demyelination (particularly in MOGAD and NMOSD), complement cascade activation, and epigenetic reprogramming of inflammatory gene expression through BET bromodomain proteins and related regulators. These mechanisms rarely operate in isolation: in EAE, the canonical MS model, CD4+ T cells initiate lesion formation, B cells amplify humoral demyelination, microglia modulate lesion propagation, and the resulting neuroinflammatory milieu drives RGC death and optic nerve axon degeneration through both direct cytotoxic and indirect excitotoxic and ischaemic mechanisms (Compston and Coles, 2008, Lancet). The visual pathway is a primary target of this inflammatory cascade because the optic nerve is CNS white matter traversed by the same oligodendrocytes, microglia, and immune surveillance mechanisms affected in the brain and spinal cord. The Striatech OptoDrum is uniquely well suited to this application area because it measures the functional output of the entire retinofugal visual circuit – from photoreceptors through RGCs, along the optic nerve, to the accessory optic system and nucleus of the optic tract – in a single automated, non-invasive test. Since immune-mediated damage in this field predominantly targets the RGC-optic nerve axis, the optomotor reflex is precisely the circuit element most sensitive to the pathological changes under study.
Vision: A Window into the brain 

Why Are Visual Endpoints Relevant in Ocular Inflammation and Immune-Mediated Eye Disease Research?

Although this application page is focused on diseases of the eye, a substantial portion of its publication corpus originates from researchers whose primary subject is multiple sclerosis, autoimmune demyelinating disease, rare inherited neurological conditions, or systemic autoinflammatory disorders. The logic connecting these CNS and rheumatological programmes to visual function measurement deserves explicit treatment. For Audience A – 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 Audience B – 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 (Villoslada et al., 2015, Brain). 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 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 missing the most sensitive non-invasive functional readout available.
Animal Models

What Are Common Animal Models For Ocular Inflammation and Immune-Mediated Eye Disease?

  • Experimental autoimmune encephalomyelitis (EAE) – C57BL/6 MOG35-55, SJL/J PLP139-151, and related variants: The most widely used model of MS and autoimmune optic neuritis. MOG35-55 immunisation in C57BL/6 mice produces a monophasic or relapsing-remitting disease characterised by spinal cord and optic nerve demyelination, RGC death, and measurable visual dysfunction detectable by OptoDrum. Multiple publications on this pillar use this model or close variants. (Lassmann et al., 2018, Nat. Protocols)
  • B cell-dependent EAE and MOGAD models: Immunisation protocols incorporating anti-MOG antibodies or B cell-stimulating adjuvants produce a humoral immune component that more closely replicates MOGAD pathology, with complement-mediated demyelination and a distinct optic neuritis profile. (Joly et al., 2022, J. Neuroinflammation)
  • PLP1-defect models (Pelizaeus-Merzbacher disease / jimpy mice): Mice carrying hypomorphic or null mutations in the proteolipid protein 1 (PLP1) gene develop leukodystrophy with hypomyelination, microglial activation, axon degeneration, and optic nerve involvement. Multiple publications on this pillar (Groh 2023, Abdelwahab 2023, Berve 2020) use PLP-defect models to study immune-mediated mechanisms in rare inherited demyelinating disease.
  • Endotoxin-induced uveitis (EIU) and experimental autoimmune uveitis (EAU): Systemic lipopolysaccharide (LPS) injection or interphotoreceptor retinoid binding protein (IRBP) immunisation produce anterior and posterior uveitis models respectively. EIU produces rapid-onset intraocular inflammation accessible to intravitreal treatment evaluation (Hosel et al., 2024).
  • 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 oedema, 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.)
  • Blast injury and TBI models: Controlled-blast or weight-drop TBI models in rodents produce post-traumatic ocular immune responses including retinal inflammation and RGC vulnerability. These models are relevant to the immune-mediated component of combat- and accident-related visual impairment. (Harper et al., 2022, Exp. Eye Res.)
  • Aging + neuroinflammation models: Aged mice (typically 18-24 months) show progressive accumulation of cytotoxic T cells and microglial activation in the CNS and optic nerve. Used alongside EAE to study how aging modifies the severity and visual functional consequences of immune-mediated demyelinating disease. (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.
01
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 pathway damage in EAE and optic neuritis models, capturing the integrated retinal and optic nerve circuit integrity that conventional EAE motor scoring misses entirely. Three Striatech publications on this pillar demonstrate OptoDrum-measured visual acuity and contrast sensitivity as the primary functional endpoint for evaluating distinct immunological mechanisms in EAE: HIF-1 inhibition (Anders 2023), B cell-mediated humoral immune responses (Joly 2022), and histaminergic immune regulation (Morin 2021). Together they establish that OptoDrum-based visual functional assessment adds a reproducible, independent, and biologically informative dimension to EAE study designs that conventional scoring alone cannot provide.

The challenge

EAE is the most widely used preclinical model of MS and autoimmune optic neuritis, but its standard outcome measurement – the EAE clinical score based on tail and limb paresis – reflects spinal cord disease rather than optic nerve or retinal involvement. Optic neuritis occurs in approximately 50% of MS patients and is the presenting symptom in 25% of cases; in EAE, demyelinating lesions in the optic nerve and corresponding RGC death are well-documented but rarely quantified functionally in the context of individual experimental studies. The result is that immunological interventions are routinely evaluated by motor disability alone, potentially overlooking optic nerve-specific treatment benefits or optic nerve-specific treatment failures.

Visual evoked potentials (VEPs) provide a direct electrophysiological readout of optic nerve conduction velocity and are widely used in clinical MS diagnosis. In rodents, however, VEP recording requires anaesthesia and cortical electrode placement, limiting the frequency of measurement and adding procedural confounds in longitudinal studies. The OptoDrum resolves these limitations: it measures visual acuity and contrast sensitivity via the subcortical optomotor reflex (a retina-to-brainstem pathway that traverses the optic nerve and is therefore sensitive to optic nerve demyelination and RGC loss) in awake, freely moving mice without anaesthesia, surgical access, or specialist electrophysiology infrastructure. Results are obtained in approximately four minutes per animal and can be collected at any time point throughout the EAE disease course in the same animals being scored for motor disability, providing a parallel and independent functional dimension at no additional welfare cost.

Important scope note for EAE researchers: the OptoDrum measures a subcortical reflex pathway (retina through nucleus of the optic tract), not a cortically processed visual response. Cortical visual pathway involvement in EAE models – including visual cortex lesions and cortical visual processing deficits – is not captured by OptoDrum; VEPs or AcuiSee (Striatech’s operant conditioning-based visual acuity system, which requires cortical processing) are more appropriate instruments for those endpoints. For a comprehensive overview of the neuroinflammation literature spanning over 20 Striatech publications across EAE, MS, MOGAD, and related conditions, see the Neuroinflammation & Autoimmune CNS Disease application page. For the optic neuritis cluster specifically, see https://stria.tech/application/optic-neuritis. For autoimmune demyelinating disease, see https://stria.tech/application/autoimmune-demyelinating-diseases. For the EAE model cluster, see https://stria.tech/application/experimental-autoimmune-encephalomyelitis. For MS specifically, see https://stria.tech/application/multiple-sclerosis.

How Striatech products help

OptoDrum

Measures spatial visual acuity (cycles per degree) and contrast sensitivity threshold via the subcortical optomotor reflex in awake, freely moving mice and rats. Provides an independent functional readout of optic nerve and RGC circuit integrity in EAE models, complementing motor disability scores and structural assessments. No anaesthesia, no electrode placement, no animal training. Repeatable at any time point throughout the disease course.

AcuiSee

Measures visual acuity via an operant, cortically mediated paradigm. Assesses cortical visual processing in EAE and MS models – for example, confirming that optic nerve conduction recovery translates to improved learned visual discrimination. This cortical dimension cannot be assessed by the OptoDrum’s subcortical reflex endpoint.

Evidence from the Literature

  • Kinuthia et al (2025) JCI Insight.
  • Anders et al (2023) Front Immunol.

    Demonstrated that acriflavine, a HIF-1 inhibitor, reduces EAE severity and preserves visual function as measured by OptoDrum, confirming that HIF-1-driven pro-inflammatory transcription is a therapeutically targetable mechanism in EAE-related optic neuritis and RGC death.

  • Joly et al (2022) J. Neuroinflammation

    Developed a B cell-dependent EAE model with humoral immune contributions to demyelination, characterising its optic neuritis and RGC death profile by OptoDrum-based visual function assessment. Establishes a translational platform for evaluating B cell-targeting therapies for optic neuritis and provides the functional visual phenotype of this MOGAD-relevant model.

  • Morin et al (2021) J. Immunol.
    Feature →

    Used conditional cell-specific deletions of histidine decarboxylase (Hdc) to confirm that the histaminergic system modulates EAE severity and visual pathway outcomes. OptoDrum provided the functional visual endpoint for assessing how histaminergic immune regulation influences EAE-related optic nerve and retinal disease. Demonstrates OptoDrum’s utility for mechanistic EAE studies using conditional immune gene knockouts.

02
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 increasingly recognised as clinically and pathologically distinct from classical MS, with optic neuritis as a cardinal feature of both conditions. Remlinger et al. (2023) developed EAE-based rodent models for these disease entities and used OptoDrum to establish the functional visual phenotype of each, demonstrating that disease-specific pathological differences (axon degeneration patterns, demyelination severity, MOG-antibody involvement) translate to measurable differences in visual functional outcomes accessible via the optomotor reflex.

The challenge

For much of the past two decades, MOGAD and NMOSD were classified as variants of MS and studied primarily in conventional MOG35-55 or MBP-based EAE models. The recognition that MOGAD is driven by pathogenic anti-MOG IgG antibodies while classical MS is predominantly T cell-mediated, and that NMOSD is driven by anti-aquaporin-4 (AQP4) antibodies with a distinct CNS lesion distribution, has created a need for disease-specific preclinical models that accurately replicate the immunopathology of each condition. This matters directly for visual research because MOGAD and NMOSD produce optic neuritis with different histopathological profiles – MOGAD causes predominantly demyelinating optic neuritis with relative axon sparing in early disease, while NMOSD causes more destructive astrocyte-targeted lesions with secondary axon loss and more severe visual functional deficits – and these differences should be reflected in the pattern of visual function decline measurable by OptoDrum.

Developing these models and validating their functional visual phenotypes with OptoDrum serves two scientific purposes. First, it provides model validation: confirming that a new EAE protocol produces the intended disease-specific pattern of optic nerve and visual pathway damage. Second, it enables the parallel evaluation of disease-specific treatments – anti-CD20 therapies (rituximab, ocrelizumab) for MOGAD and anti-AQP4 therapies (inebilizumab, satralizumab) for NMOSD – against the visual functional endpoint most directly relevant to their therapeutic target. For the broader MOGAD cluster, see https://stria.tech/application/mog-antibody-associated-disorder. For the optic neuritis cluster, see https://stria.tech/application/optic-neuritis.

How Striatech products help

OptoDrum

Provides the non-invasive functional visual endpoint for characterising and distinguishing optic nerve damage profiles in MOGAD- and NMOSD-relevant EAE models. Captures the functional retinofugal circuit output that reflects the combined effect of demyelination, axon degeneration, and RGC loss – the three pathological processes that vary in relative severity between disease models.

AcuiSee

Provides a cortically mediated, operant visual acuity endpoint for MOGAD and NMOSD model characterisation. Assesses whether disease-specific optic nerve damage patterns impair learned visual discrimination and suprathreshold visual perception in addition to subcortical reflex function measured by OptoDrum.

Evidence from the Literature

  • Kinuthia et al (2025) JCI Insight.
  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.

    Developed and validated EAE-based rodent models for MOGAD and NMOSD, using OptoDrum to establish their functional visual phenotypes including patterns of optic neuritis and axon degeneration. Provides a direct model validation and functional characterisation reference for researchers entering the MOGAD or NMOSD preclinical space.

  • Jarius et al. (2010) Nat Rev Neurol.

    Foundational review establishing the pathogenetic and diagnostic significance of AQP4 antibodies in NMOSD, providing clinical context for the OptoDrum-based optic nerve functional profiling in NMOSD rodent models. Establishes the human disease biology against which preclinical functional visual endpoints are translated.

  • Reindl et al. (2019) Nat Rev Neurol.

    Comprehensive review of MOGAD pathophysiology and clinical spectrum, including the prominent role of optic neuritis in MOG-antibody-associated disease. Provides the translational framework for interpreting OptoDrum visual outcomes in MOGAD rodent models in the context of human disease visual prognosis.

03
Does Metabolic and Dietary Status Modulate Immune-Mediated Visual Pathway Damage?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Yes. Capper et al. (2025) demonstrated that a high-saturated, long-chain fatty acid diet worsens EAE-associated optic nerve damage, RGC loss, and visual function decline as measured by OptoDrum. This study places dietary fat composition among the modifiable variables that influence visual pathway vulnerability in autoimmune demyelinating disease, supporting the growing evidence base for dietary intervention as a component of MS disease management – and positions OptoDrum-based visual function testing as the functional endpoint for metabolic and nutritional modulation of immune-mediated eye disease in preclinical research.

The challenge

The relationship between diet, systemic metabolism, and neuroinflammation in MS and autoimmune demyelinating disease is an increasingly active research frontier. Saturated fatty acids activate Toll-like receptor 4 (TLR4) and NF-kappaB signalling in immune cells, promoting pro-inflammatory cytokine production and T cell skewing toward Th17 and Th1 phenotypes. This inflammatory priming is hypothesised to amplify the neuroinflammatory cascade in EAE lesions, including at the level of the optic nerve and retina. The gut microbiome, which is profoundly altered by dietary fat composition, provides an additional indirect route through which diet modulates CNS immune surveillance and neuroinflammatory severity.

What distinguishes Capper et al. (2025) methodologically is the use of OptoDrum to measure the specifically visual functional consequences of dietary fat-induced EAE exacerbation independently of motor disability. Motor scoring alone would capture the worsened spinal cord disease but would not specifically confirm optic nerve involvement or quantify the degree of visual circuit damage as a distinct pathological endpoint. OptoDrum provides this separation, enabling the optic nerve-specific consequences of dietary fat modulation to be quantified independently of limb motor deficits that may reflect spinal cord disease predominantly. This methodological design is directly applicable to any EAE study where dietary, metabolic, or microbiome-targeted interventions are evaluated for effects on optic nerve and visual pathway outcomes. For the broader EAE and MS experimental framework, see the FAQ above and the Neuroinflammation & Autoimmune CNS Disease application page. For the EAE cluster, see https://stria.tech/application/experimental-autoimmune-encephalomyelitis.

How Striatech products help

OptoDrum

Provides an independent, non-invasive functional readout of the optic nerve and visual circuit consequences of dietary and metabolic modulation in EAE. Enables researchers to dissect diet-driven visual pathway damage from motor disability, quantifying the optic neuritis-specific effects of dietary interventions as a distinct endpoint.

AcuiSee

Provides a cortically mediated, operant visual acuity endpoint for dietary and metabolic EAE modulation studies. Assesses whether diet-driven optic nerve and RGC damage impairs learned visual discrimination and suprathreshold visual perception, complementing the subcortical reflex readout from OptoDrum.

Evidence from the Literature

  • Kinuthia et al (2025) JCI Insight.
  • Capper et al (2025) Front Immunol.

    Demonstrated that a high-saturated long-chain fatty acid diet worsens EAE severity including optic nerve damage, RGC loss, and visual function decline measurable by OptoDrum.

  • Cignarella et al. (2018) Cell Metab.

    Demonstrated that intermittent fasting protects against EAE severity through gut microbiome- mediated immunomodulation, providing complementary evidence that dietary and metabolic interventions modulate neuroinflammation through mechanisms accessible to OptoDrum-based functional visual endpoint measurement. This study established the mechanistic principle that dietary factors alter the EAE neuroimmune response; Capper et al. (2025) extend this to dietary fat composition with explicit visual function measurement.

04
How Do Neuroinflammatory Mechanisms – Microglia, T Cells, and Epigenetic Regulators – Drive Visual Pathway Damage in Immune-Mediated Eye Disease?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Five Striatech publications directly address distinct neuroinflammatory mechanisms driving visual pathway damage, all using OptoDrum as the functional circuit-level endpoint: microglial CX3CR1 orchestration of optic nerve damage (Groh 2025), microglial neuroprotective demyelination in PLP-defect disease (Groh 2023), cytotoxic T cell-mediated axon degeneration (Abdelwahab 2023), BET PROTAC epigenetic anti-inflammatory strategy (Zhu 2023), and Nogo-A antibody-mediated axon protection and regeneration (Baya Mdzomba 2020). Together these publications demonstrate that OptoDrum provides a sensitive, circuit-level functional endpoint across the full mechanistic breadth of neuroinflammatory visual pathway damage – from innate microglial biology through adaptive T cell effectors to epigenetic reprogramming of inflammatory gene expression.

The challenge

Neuroinflammatory damage to the visual pathway in immune-mediated eye disease operates through multiple parallel and interacting mechanisms. Microglia, the resident innate immune cells of the CNS and retina, exist on a spectrum from homeostatic surveillance states to highly activated pro-inflammatory or disease-associated phenotypes; their functional outcome is context-dependent, with CX3CR1-signalling microglia capable of both amplifying optic nerve lesions (as in Groh 2025) and providing neuroprotective myelin debris clearance (as in Groh 2023). CD8+ cytotoxic T cells represent an adaptive immune effector mechanism that inflicts direct axonal damage through perforin and granzyme B-mediated mechanisms, contributing to progressive axon degeneration in PLP-defect diseases and potentially in secondary progressive MS (Abdelwahab 2023). At the epigenetic level, BET bromodomain proteins drive the transcriptional upregulation of entire pro-inflammatory gene programmes, and their PROTAC-mediated degradation suppresses neuroinflammation more completely than classical BET inhibition (Zhu 2023).

The challenge in this mechanistically diverse field is selecting the right endpoint to confirm that a given mechanism is functionally significant at the circuit level and that targeting it produces a measurable clinical benefit, not merely structural or molecular changes. OptoDrum addresses this challenge uniformly across all of these mechanisms: regardless of whether the intervention targets microglia, T cells, epigenetic regulators, or axon growth inhibitors, the functional output – visual acuity and contrast sensitivity via the optomotor reflex – captures the net impact on the retinofugal visual circuit that these mechanisms collectively affect. This circuit-level integration is particularly valuable in complex neuroinflammatory models where multiple mechanisms operate simultaneously, because it reports the aggregate functional consequence rather than any single pathway’s contribution in isolation.

Baya Mdzomba et al. (2020) add a translational dimension by demonstrating that Nogo-A antibody treatment – which both inhibits the Nogo-A-mediated axon growth block and attenuates neuroinflammation – can preserve and potentially restore visual function after inflammatory optic nerve damage, establishing OptoDrum as the functional endpoint for combined neuroprotective and regenerative strategies. For axon degeneration mechanisms across disease contexts, see https://stria.tech/application/axon-degeneration. For glial suppression and microglial modulation, see https://stria.tech/application/glial-suppression. For RGC death, see https://stria.tech/application/retinal-ganglion-cell-death. For optic nerve damage, see https://stria.tech/application/optic-nerve-damage. For optic nerve regeneration, see https://stria.tech/application/optic-nerve-regeneration. For PLP-defect models, see https://stria.tech/application/plp-defects. For retinal neuroinflammation intersecting with retinal degeneration, see the Retinal Degeneration & Inherited Retinal Disease application page.

How Striatech products help

OptoDrum

Provides the integrated circuit-level functional endpoint for all neuroinflammatory mechanism studies. Measures the net functional consequence – visual acuity and contrast sensitivity via the optomotor reflex – of microglia modulation, T cell targeting, epigenetic intervention, or axon regeneration strategies, confirming that structural or molecular protection translates to preserved or recovered visual circuit function. Non-invasive and repeatable, enabling temporal resolution of neuroinflammatory damage and therapeutic recovery across longitudinal disease courses.

AcuiSee

Provides an operant, cortically mediated visual acuity endpoint for neuroinflammatory mechanism studies. Confirms whether anti-inflammatory, neuroprotective, or axon regeneration interventions preserve learned visual discrimination and suprathreshold cortical visual processing, complementing the subcortical reflex readout from OptoDrum.

Evidence from the Literature

  • Kinuthia et al (2025) JCI Insight.
  • Groh et al (2025) Nat Neurosci.
    Journal Club →
    Feature →

    Demonstrated that microglial CX3CR1 activation orchestrates optic nerve damage, optic neuritis, and RGC death in an aging autoimmune demyelinating disease context. OptoDrum confirmed that CX3CR1-dependent microglial biology translates to a functionally measurable visual circuit deficit, establishing this pathway as a target for microglial modulation in immune-mediated optic nerve disease.

  • Groh et al (2023) Nat Commun.
    Feature →

    Demonstrated that microglia-mediated myelin debris clearance is neuroprotective in a PLP-defect rare inherited demyelinating disease, with OptoDrum confirming that protective microglial activity preserves visual circuit function.

  • Abdelwahab et al (2023) iScience

    Demonstrated that cytotoxic CNS-infiltrating T cells drive axon degeneration and visual dysfunction in a PLP-defect rare demyelinating disease, with OptoDrum capturing the functional circuit-level consequences of adaptive immune-mediated axon damage.

  • Zhu et al (2023) J. Neuroinflammation

    Demonstrated that PROTAC-mediated BET bromodomain protein degradation suppresses retinal neuroinflammation and preserves visual function, positioning epigenetic anti-inflammatory PROTACs as a novel therapeutic modality for immune-mediated retinal and optic nerve disease.

  • Baya Mdzomba et al (2020) Cell Death Dis.
    Journal Club →

    Demonstrated that Nogo-A-targeting antibodies preserve and potentially restore visual function after inflammatory optic nerve damage by combining axon growth inhibition relief with attenuation of neuroinflammation. OptoDrum confirmed functional visual benefit, establishing this strategy as a combined neuroprotective and regenerative approach with functional circuit-level efficacy.

05
Can OptoDrum Track Visual Function in Uveitis and Acute Ocular Immune Responses?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Yes. Hösel et al. (2024) demonstrated that OptoDrum-based visual function measurement captures the functional consequences of intraocular inflammation in a uveitis model and confirms the efficacy of intravitreal treatment in restoring visual circuit integrity. Harper et al. (2022) extended this to the post-traumatic immune response following blast injury, showing that OptoDrum measures the visual functional consequences of acute ocular immune activation following TBI. Together these publications establish the OptoDrum as a functional endpoint for the acute and sub-acute phases of intraocular immune activation across both autoimmune and trauma-induced contexts.

The challenge

Uveitis encompasses a clinically heterogeneous group of intraocular inflammatory conditions that produce visual dysfunction through multiple mechanisms: direct photoreceptor and RGC damage by inflammatory infiltrates, cystoid macular oedema, vitreous haze, and posterior segment complications including epiretinal membrane formation. Conventional assessment in rodent models relies on slit-lamp grading of anterior chamber inflammation, histological quantification of inflammatory cell infiltrates, and cytokine profiling from ocular fluid – all of which are either terminal or require technical expertise beyond standard laboratory capacity. None of these endpoints confirms whether the inflammatory episode has produced a functionally significant visual circuit deficit, which is the most clinically relevant outcome for any anti-inflammatory treatment evaluation.

OptoDrum resolves this gap: by measuring spatial visual acuity and contrast sensitivity before and during uveitis, and at defined intervals following treatment, researchers can directly assess whether the inflammatory episode has impaired the retinofugal visual circuit and whether intravitreal or systemic treatment has preserved or restored it. This functional readout is independent of structural or inflammatory grading and provides a circuit-level efficacy endpoint that bridges the preclinical and clinical research contexts in which visual acuity is the primary outcome measure for uveitis treatment trials.

Blast-related TBI represents a distinct but mechanistically relevant context: blast waves produce a combination of direct mechanical retinal damage and an intense post-traumatic immune response characterised by microglial activation, blood-retina barrier breakdown, and neutrophil infiltration that inflicts secondary retinal damage in the days to weeks following the primary injury. Harper et al. (2022) characterised this immune response and its visual functional consequences by OptoDrum, establishing the measurement paradigm for post-traumatic ocular immune response studies. For the trauma context of these findings, see the Trauma & Acute Injury application page. For optic nerve damage mechanisms, see https://stria.tech/application/optic-nerve-damage.

How Striatech products help

OptoDrum

Provides a non-invasive, repeatable functional endpoint for visual circuit integrity during intraocular inflammation. Enables longitudinal measurement of visual function before uveitis onset, at peak inflammation, during resolution, and following intravitreal or systemic treatment, without anaesthesia, manipulation of the inflamed eye, or sacrifice at each time point.

AcuiSee

Provides a cortically mediated, operant visual acuity endpoint for uveitis and acute ocular immune response studies. Assesses whether intraocular inflammation impairs learned visual discrimination and suprathreshold visual perception, adding a cortical processing dimension to the subcortical reflex readout from OptoDrum.

Evidence from the Literature

  • Kinuthia et al (2025) JCI Insight.
  • Hösel et al (2024) J Ophthalmic Inflamm Infect.
    Feature →

    Evaluated intravitreal treatment in a uveitis model, using OptoDrum to confirm that anti-inflammatory intervention attenuated the functional visual consequences of intraocular inflammation. Provides direct evidence for OptoDrum as the functional efficacy endpoint for intravitreal treatment in immune-mediated eye disease.

  • Harper et al (2022) Exp. Eye. Res.

    Characterised the ocular immune response following blast injury in a TBI model, demonstrating that post-traumatic immune activation produces a measurable visual functional deficit captured by OptoDrum. Establishes the measurement framework for evaluating immune-targeted treatments for post-traumatic visual impairment.

06
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

Four primary Striatech publications on this pillar address immune-mediated visual pathway damage driven by rare genetic variants and systemic autoinflammatory conditions: selective ALPK1 inhibition in ROSAH syndrome (Fan 2025), gain-of-function mutations in systemic autoinflammatory disease (Kozycki 2022), sex-biased immune depletion in a rare inherited neuroinflammatory disorder (Berve 2020), and cytotoxic T cell accumulation driving age-related immune-mediated visual loss (Groh 2021). Together these publications demonstrate that OptoDrum-based visual function testing provides a consistent functional endpoint across the full genetic and mechanistic heterogeneity of rare autoinflammatory and systemic immune-mediated eye disease.

The challenge

Rare inherited autoinflammatory disorders and systemic autoimmune conditions with ocular manifestations pose a distinct set of research challenges. Patient populations are small, genetic heterogeneity is substantial, and the relevant mouse models are often newly developed and incompletely characterised. Researchers entering these spaces face two sequential challenges: first, confirming that the genetic or immunological perturbation produces a quantifiable ocular phenotype; second, demonstrating that an experimental treatment reverses or attenuates that phenotype at the functional circuit level. OptoDrum addresses both challenges through the same automated, non-invasive measurement protocol.

The diseases addressed on this pillar span the spectrum from single-gene autoinflammatory disorders – ALPK1 gain-of-function (ROSAH syndrome) and other innate immune gene mutations – to polygenic and complex immune conditions including those driven by sex-biased immune cell depletion and age-related T cell accumulation. What unites them is that immune activation, in each case, damages the retinal ganglion cell layer and optic nerve in a way that is functionally measurable by the optomotor reflex. Fan et al. (2025) demonstrate this most precisely: selective ALPK1 inhibitor treatment restored or preserved RGC function in a ROSAH syndrome model, with OptoDrum providing the definitive functional confirmation.

Sex differences in immune-mediated ocular disease deserve particular attention, given that MS, MOGAD, and most other autoimmune conditions affecting vision show marked female predominance. Berve et al. (2020) demonstrated sex- and region-biased immune depletion with visual functional consequences in a rare neuroinflammatory disease model, establishing the methodological approach for sex-stratified immune-mediated visual function studies. For comprehensive coverage of rare inherited CNS and eye disorders, see the Rare & Inherited CNS and Eye Disorders application page (20 Striatech publications). For the rare-disease cluster, see https://stria.tech/application/rare-disease. For retinal dystrophy in immune-mediated context, see https://stria.tech/application/retinal-dystrophy. For aging-associated immune-mediated visual decline, see also the Systemic Aging & CNS Decline application page.

How Striatech products help

OptoDrum

Provides the standard non-invasive functional phenotyping endpoint for rare and genetically defined immune-mediated eye diseases. Its training-free, non-invasive design is particularly valuable when animal numbers are limited by model rarity, and when terminal endpoints must be reserved for high-value genetic, immunological, and histological characterisation.

AcuiSee

Provides a cortically mediated, operant visual acuity endpoint for rare autoinflammatory and systemic autoimmune disease models. Assesses whether immune-mediated visual pathway damage impairs learned visual discrimination and suprathreshold visual perception, complementing the subcortical reflex phenotyping provided by OptoDrum.

Evidence from the Literature

  • Kinuthia et al (2025) JCI Insight.
  • Fan et al (2025) Nat Commun.

    Discovered a selective ALPK1 inhibitor that reduces innate immune NF-kappaB activation in a ROSAH syndrome model. OptoDrum confirmed that ALPK1 inhibition preserved RGC-dependent visual circuit function.

  • Kozycki et al (2022) Ann. Rheum. Dis.

    Characterised gain-of-function mutations in an innate immune signalling gene producing a rare systemic autoinflammatory syndrome with retinal dystrophy and neuroinflammation. OptoDrum confirmed that mutation-driven systemic autoinflammation produces measurable visual circuit deficits, bridging rheumatological and ophthalmic research with a shared functional visual endpoint.

  • Groh et al (2021) Nat. Aging
    Journal Club →

    Demonstrated that cytotoxic T cell accumulation in the aging CNS drives axon degeneration and visual dysfunction, with OptoDrum confirming functional visual circuit deficits. Establishes age-related adaptive immune activation as a driver of visual pathway damage, connecting immunosenescence to clinically relevant visual loss in older animals.

  • Berve et al (2020) J. Neuroinflammation
    Feature →

    Characterised sex- and region-biased immune cell depletion in a rare inherited neuroinflammatory disease, with OptoDrum measuring visual functional consequences. Provides the methodological framework for sex-stratified immune-mediated visual pathway studies and highlights the importance of sex as a co-variable in rare autoinflammatory disease research.

  • Hörner et al (2024) Thesis

    Investigated the role of neuroinflammation in hereditary spastic paraplegia, a rare inherited progressive neurological disease, demonstrating that inflammatory amplification of axon degeneration has visual pathway consequences measurable by OptoDrum.

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 Impact Notes for Ocular Inflammation Research
OptoDrum (OMR) None; awake, freely moving animal Very high; daily measurement feasible without welfare cost None (animal); minimal (operator) Fully automated threshold determination Strong: supports Reduction (no sacrifice per time point) and Refinement (no restraint or anaesthesia) Measures subcortical retinofugal pathway (retina through nucleus of the optic tract). Sensitive to optic nerve demyelination, RGC loss, and inner retinal neuroinflammatory damage. Does not assess cortical visual processing or optic nerve conduction velocity directly.
EAE clinical score (motor disability scale) Minimal (observer-based; handling for scoring) High; scored daily throughout disease course Yes: inter-rater calibration required Not automated; observer-dependent Moderate: no surgical access but terminal sacrifice not avoided; handling required Captures spinal cord motor disease but provides no information on optic nerve or retinal involvement. Standard in EAE studies but misses the visual pathway dimension entirely. OptoDrum adds the optic nerve-specific functional dimension at no additional welfare cost, in the same animals being scored for motor disability.
Visual Evoked Potentials (VEP) High for chronic recordings (cortical electrode implantation surgery required); moderate for acute recordings (anaesthesia, skull thinning or needle electrodes) Low (acute, terminal) to moderate (chronic implant) Yes: surgical and electrophysiology expertise Minimal: stimulus delivery automated; recording setup manual Low (acute studies); moderate (chronic implant avoids terminal surgery) Measures cortical visual processing and optic nerve conduction velocity; the clinical gold standard for optic neuritis assessment in MS. In rodent EAE, VEP provides direct electrophysiological evidence of demyelination-related conduction slowing. Strongly complementary to OptoDrum: OptoDrum captures the retinal circuit output, VEP captures the cortical response. Not practical as a primary longitudinal endpoint in large EAE cohort studies.
Pattern ERG (PERG) Moderate; corneal electrodes, anaesthesia or training for alert recording Moderate Yes Semi-automated Moderate Specifically measures RGC-level inner retinal function (N2 component), providing electrophysiological confirmation of RGC dysfunction in immune-mediated eye disease. Complementary to OptoDrum: PERG localises dysfunction to the RGC layer while OptoDrum measures the retinofugal circuit output. Most useful as a mechanistic endpoint in studies requiring RGC-layer-specific confirmation alongside optomotor functional data.
OCT (retinal nerve fibre layer thickness) Low to moderate; topical anaesthesia and pupil dilation typically required High; suitable for longitudinal monitoring Yes: imaging and segmentation expertise Semi-automated (acquisition automated; segmentation requires software) Good; less invasive than ERG or VEP but requires drug administration steps absent from OptoDrum Provides retinal nerve fibre layer (RNFL) thickness as a structural correlate of RGC axon survival in optic neuritis and EAE. Standard clinical endpoint in MS optic neuritis trials; directly translatable to OptoDrum-based functional assessment. Structural-functional correlation studies pairing OCT with OptoDrum represent the most informative combination for optic neuritis research.
AcuiSee (operant visual acuity) None; mild food restriction during training period High once trained; session-based Yes: 10-14 days to criterion (animal) Partially automated Good; non-invasive; training period extends study duration Measures cortically processed visual acuity and contrast sensitivity. Appropriate for EAE or optic neuritis studies requiring evidence of cortical visual processing recovery, or for confirming that optic nerve conduction restoration detected by VEP translates to improved learned visual discrimination. Training requirement makes it impractical as a primary endpoint in rapidly progressing or acutely staged EAE models.
Histology / IHC (RGC count, optic nerve axon density) Terminal; requires sacrifice and tissue processing None; single time point per animal Yes: tissue processing, microscopy, cell counting Semi-automated (image analysis software) Low; terminal by definition; best reserved as endpoint confirmation Gold standard for structural validation of RGC survival and optic nerve axon density in immune-mediated disease models. Recommended as the terminal confirmation endpoint following OptoDrum longitudinal functional tracking, providing structural evidence for the circuit-level functional changes measured non-invasively throughout the study.
In immune-mediated eye disease research, OptoDrum is most powerful when used as the primary longitudinal non-invasive functional endpoint throughout a study, with VEP, PERG, and OCT deployed at selected time points to provide electrophysiological and structural mechanistic detail, and histology confirming the structural correlates of functional change at sacrifice. This multi-modal approach is more informative than any single endpoint and maintains the welfare advantages of non-invasive, repeated OptoDrum measurement throughout the full disease and treatment course.
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Publications on Ocular Inflammation and Immune-Mediated Eye Disease

Keep exploring

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

Research Chapter

Ocular Inflammation and Immune-Mediated Eye Disease

Uveitis, optic neuritis, and the ocular manifestations of systemic and rare inflammatory disorders. Research targets the immune mechanisms behind a major share of preventable blindness in high-income countries.

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Application Areas
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FAQs answered
Part of Eye & Retinal Disease

Main Application Areas

Optic Neuritis

Additional Topics

Autoimmune Demyelinating Diseases
Axon Degeneration
Experimental Autoimmune Encephalomyelitis
Glial Suppression
MOG Antibody-Associated Disorder
Multiple Sclerosis
Optic Nerve Damage
Optic Nerve Regeneration
PLP defects
Rare Disease
Retinal Dystrophy