Research Applications for Striatech Products

Neuroinflammation and Autoimmune CNS Disease

EAE, optic neuritis, MOGAD, and NMOSD models in which dysregulated immunity damages neurons, myelin, and axons. The optic nerve and retina provide the most quantifiable functional endpoints in the field.
Introduction

What is Neuroinflammation and Autoimmune CNS Disease?

Neuroinflammation and autoimmune CNS disease encompass a spectrum of conditions in which dysregulated immune activity – whether driven by adaptive autoimmunity, innate microglial activation, or both – produces damage to neurons, myelin, and axons in the brain, spinal cord, and visual pathway. In preclinical research, this application area is anchored by three major experimental paradigms: experimental autoimmune encephalomyelitis (EAE), the principal rodent model of multiple sclerosis, induced by immunisation with myelin antigens (MOG, MBP, PLP) and characterised by ascending paralysis, demyelination, and optic nerve inflammation; optic neuritis models, in which autoimmune or toxic injury targets the optic nerve specifically, producing rapid and quantifiable visual acuity loss relevant to the most common presenting symptom of MS; and antibody-mediated demyelinating disease models for MOG antibody-associated disorder (MOGAD) and neuromyelitis optica spectrum disorder (NMOSD), which are clinically distinct from MS but share the feature of severe, often bilateral optic neuritis as a defining manifestation (Remlinger et al, 2023, Neurology NI). Across all three paradigms, the retina and optic nerve occupy a central position in the research toolkit. The optic nerve is a CNS white matter tract in which demyelinating lesions identical to MS plaques can be reproducibly induced, monitored, and treated. The retina is the only CNS tissue directly accessible to non-invasive assessment in the living animal, meaning that retinal ganglion cell (RGC) loss and optic nerve dysfunction can be tracked longitudinally with functional and structural endpoints that would be inaccessible in spinal cord or brain white matter without terminal intervention. This anatomical accessibility is the defining experimental advantage of the visual pathway in neuroinflammation research, and Striatech's OptoDrum exploits it fully: by measuring visual acuity and contrast sensitivity via the optomotor reflex in awake, freely moving animals, it provides a non-invasive, repeatable, fully automated functional readout of optic nerve and RGC pathway integrity across the entire time course of EAE, optic neuritis, or chronic demyelinating disease (Capper et al, 2025, Front Immunol)(Groh et al, 2025, Nat Neurosci). The scientific scope of this application area has expanded significantly in recent years. Beyond the classical EAE and optic neuritis paradigms, research is increasingly addressing the neuroinflammatory contributions to rare inherited CNS diseases (neuronal ceroid lipofuscinoses, hereditary spastic paraplegia, PLP-deficient leukodystrophies), the role of immunosenescence and cytotoxic T cell accumulation in age-related CNS decline (Groh et al, 2021, Nat Aging), and the mechanistic overlap between neuroinflammation and metabolic or vascular CNS disease. Across all these contexts, OptoDrum-measured visual function serves as the longitudinal functional biomarker that connects cellular and molecular findings to a quantifiable and clinically interpretable visual outcome.
Vision: A Window into the brain 

Why Are Visual Endpoints Relevant in Neuroinflammation and Autoimmune CNS Disease Research?

Multiple sclerosis causes clinically significant visual impairment in more than 50% of patients over the course of their disease, with optic neuritis occurring as the presenting symptom in approximately 25% of cases. This clinical reality reflects the biological vulnerability of the visual pathway: the optic nerve is a CNS white matter tract that is preferentially targeted by autoimmune demyelinating disease, and the retina – as the proximal end of this pathway – undergoes secondary neurodegeneration measurable as progressive RGC layer thinning and visual acuity loss even in MS patients who have never experienced a clinical optic neuritis episode. Visual endpoints are therefore not peripheral to MS and autoimmune CNS disease research; they are among its most sensitive and translationally relevant functional readouts. For researchers whose primary interest is the brain, spinal cord, or systemic immune system rather than the eye, the following points establish why visual function monitoring is directly relevant to your experimental work. First, the retina and optic nerve are affected by the same inflammatory, demyelinating, and degenerative processes operating in the brain and spinal cord, and they respond to the same immunological interventions. Including OptoDrum visual acuity monitoring in your EAE or neuroinflammation protocol adds a quantitative, non-invasive, longitudinally repeatable functional endpoint at essentially zero additional experimental burden – approximately four minutes per animal, without anaesthesia, animal training, or ophthalmological specialist involvement. Second, because the retina is directly accessible to non-invasive assessment, it provides a window onto CNS inflammation dynamics in real time, in the same animals in which you are studying systemic immune parameters, motor scores, and histological endpoints. Third, visual function is increasingly expected as a primary or secondary endpoint in preclinical neuroinflammation studies by peer reviewers and ethics committees, who recognise it as a 3Rs-compliant replacement for multiple terminal assessments at separate time points. The OptoDrum measures the optomotor reflex (OMR), a subcortical reflex mediated by the accessory optic system that detects the retina-to-brainstem signal with no requirement for cortical visual processing. For researchers in the neuroinflammation field who want to specifically evaluate whether autoimmune injury has affected cortical visual processing – for example, in EAE models with cortical demyelination, or in progressive MS models where cortical atrophy contributes to visual disability – AcuiSee provides a complementary endpoint that requires cortical visual processing through its operant conditioning paradigm.
Animal Models

What Are Common Animal Models For Neuroinflammation and Autoimmune CNS Disease?

  • MOG35-55 EAE (C57BL/6 mouse): The most widely used EAE model. Immunisation with MOG peptide 35-55 in complete Freund's adjuvant produces a monophasic or relapsing-remitting ascending motor paralysis with spinal cord and optic nerve demyelination. Visual acuity loss is detectable by OptoDrum from the peak of paralysis through the chronic phase, with deficits reflecting both optic nerve demyelination and RGC degeneration (Capper et al, 2025)(Morin et al, 2021).
  • PLP139-151 EAE (SJL/J mouse): Produces a relapsing-remitting course more closely resembling the relapsing pattern of human MS. Optic nerve inflammation and RGC loss are consistent features, making it well suited for studies of visual function across relapse-remission cycles, where OptoDrum enables tracking of functional recovery between attacks.
  • B cell-dependent EAE with MOG antibody responses: Models that incorporate humoral immunity alongside T cell-driven demyelination, relevant to MOGAD and to the subset of MS patients with antibody-associated pathology (Joly et al, 2022). Visual function measurements by OptoDrum differentiate the visual impairment profile from classical T cell-driven EAE.
  • MOGAD and NMOSD models (MOG-IgG and AQP4-IgG passive transfer): Passive transfer of human MOG-IgG or AQP4-IgG into rodents with an adjuvant optic nerve inflammatory trigger produces a severe, rapidly evolving optic neuritis that is distinct from EAE in its severity and the poor visual recovery that follows (Remlinger et al, 2023)(Remlinger et al, 2022).
  • Proteolipid protein (PLP)-deficient models (Jimpy, Plp-null): Genetic models of dysmyelination with secondary neuroinflammation, relevant to Pelizaeus-Merzbacher disease and related leukodystrophies. The microglia-demyelination interaction in these models has been characterised with OptoDrum as the functional endpoint (Groh et al, 2023, Nat Commun).
  • Lysophosphatidylcholine (LPC) optic nerve demyelination: Focal chemical demyelination of the optic nerve producing a controlled, geographically defined lesion for studying the kinetics of demyelination, remyelination, and functional recovery without the systemic immune activation of EAE. OptoDrum tracks the visual function deficit and any recovery in the same animals across the full time course.
  • Aged mice and immunosenescence models: Natural aging in mice (18-24 months) produces progressive cytotoxic T cell accumulation in CNS white matter and age-related axon degeneration with measurable visual acuity loss, establishing a model for the inflammaging component of progressive neurological disease (Groh et al, 2021, Nat Aging).
  • Neuronal ceroid lipofuscinosis (CLN1/INCL) models: Genetic models of rare lysosomal storage diseases in which microglial neuroinflammation is a primary driver of CNS degeneration, enabling OptoDrum-based visual function monitoring as a non-invasive endpoint for disease progression and neuroinflammation-targeted treatment response (Groh et al, 2021, Brain Commun).
  • Hereditary spastic paraplegia (HSP) models: Axon degeneration disease models in which neuroinflammation has been identified as a contributory driver, providing a platform for studying the interaction between inherited axonopathy and secondary immune activation (Horner et al, 2024).
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 Longitudinally in EAE and Multiple Sclerosis Models?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

The OptoDrum automates visual acuity and contrast sensitivity measurement via the optomotor reflex in awake, freely moving rodents, providing a non-invasive, repeatable functional endpoint for longitudinal monitoring of optic nerve and RGC pathway integrity across the full EAE time course – from induction through peak paralysis, the chronic phase, and any relapse-remission cycles. Multiple published studies using Striatech OptoDrum in EAE models confirm its sensitivity to between-group differences driven by immunological manipulations, dietary factors, and pharmacological treatments (Capper et al, 2025) (Remlinger et al, 2022) (Morin et al, 2021). For studies where the research question specifically involves cortical visual processing – for example, in EAE models with cortical demyelination or in studies of MS-related visual cortex dysfunction – AcuiSee provides the cortical complement to the subcortical OMR.

The challenge

EAE is a dynamic, multi-phase disease: the acute inflammatory peak typically occurs at days 12-18 post-immunisation in MOG35-55 C57BL/6 models, followed by a chronic phase in which persistent demyelination and axon degeneration drive ongoing neurological deterioration. In relapsing-remitting models (PLP-SJL), this is followed by further attack-remission cycles. Measuring visual function at a single end-point time point captures only a snapshot of this dynamic process, and – because visual recovery can occur between relapses – end-point measurements may miss the functional disability accumulated over the full disease course. Longitudinal optical acuity tracking in the same animals provides a continuous functional record that correlates with EAE severity scores, optic nerve histology, and molecular neuroinflammatory markers across the full disease trajectory. Classical visual assessment methods – ERG and VEP – require anaesthesia and specialised electrophysiology equipment, and in the EAE context carry the additional confound that anaesthesia alters neuroinflammatory signalling, potentially blunting or exaggerating the measured response. The OptoDrum's anaesthesia-free, automated paradigm eliminates both problems, delivering a functional visual acuity measurement that can be repeated daily during peak EAE without any additional procedural burden. Remlinger et al (2022) demonstrated that this approach is sensitive enough to detect the differential visual outcomes produced by FcRn blockade in an antibody-driven EAE/MOG model (Remlinger et al, 2022), and Morin et al (2021) used OptoDrum to confirm histaminergic modulation of EAE as a functional visual endpoint (Morin et al, 2021). Capper et al (2025) showed that OptoDrum detects diet-driven differences in EAE visual outcomes, confirming its sensitivity across a range of effect sizes and intervention types (Capper et al, 2025). An important consideration for MS researchers is the distinction between subcortical and cortical visual pathway involvement. The OptoDrum measures the OMR, which is mediated by the subcortical accessory optic system and is therefore sensitive to retinal and optic nerve damage but not to selective cortical demyelination. In EAE models with significant cortical lesion burden, AcuiSee provides the complementary cortical endpoint: its operant forced-choice paradigm requires cortical visual processing and specifically detects deficits arising from demyelinating lesions in the optic radiation, lateral geniculate nucleus, or primary visual cortex. This distinction is particularly relevant for models of progressive MS in which cortical atrophy is a key pathological feature. For the full EAE/MS publication landscape, see also the Experimental Autoimmune Encephalomyelitis cluster page and the Multiple Sclerosis cluster page.

How Striatech products help

OptoDrum
Measures photopic visual acuity (cycles per degree) and contrast sensitivity via the optomotor reflex in awake, freely moving EAE rodents. Non-invasive, fully automated; no anaesthesia or training required; approximately 4 minutes per animal. Provides pre-immunisation baselines, tracks acuity loss during the acute phase, and monitors recovery in remission periods. Sensitive to between-group differences driven by immunological, dietary, and pharmacological variables in EAE.
AcuiSee
Measures visual acuity and contrast sensitivity via operant conditioning, requiring cortical visual processing. Directly applicable when the EAE or MS model produces significant cortical demyelinating lesions, or when the research question specifically concerns whether autoimmune injury has impaired cortical visual function. In these contexts, AcuiSee detects cortical visual deficits that the subcortical OMR cannot capture, providing a more complete picture of visual pathway involvement across subcortical and cortical compartments. Requires 10–14 day training phase.
Non-aversive Animal Platform
Minimises handling stress during OptoDrum testing in EAE animals, who may be debilitated, pain-sensitised by neurological deficit, or reluctant to move due to paralysis. The tunnel-lid design allows voluntary entry from the home cage, ensuring that between-group visual acuity differences reflect genuine functional status rather than differential stress-related suppression of the optomotor response.

Evidence from the Literature

02
How Does Neuroinflammation Drive Retinal Ganglion Cell Death and Visual Dysfunction?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

In neuroinflammatory CNS disease, RGC death and visual acuity loss are driven by a convergent set of molecular mechanisms – TNF-alpha-mediated cytotoxicity, complement C3/C3aR-dependent inflammatory amplification, microglial and macrophage activation, and glutamate excitotoxicity – each of which has been validated as a functional visual endpoint using OptoDrum in published studies. Li et al (2025) demonstrated that TNF-alpha directly drives RGC death and quantifiable visual acuity loss (Li et al, 2025), while Zhao et al (2025) showed that complement C3/C3aR signalling produces RGC dysfunction measurable by OMR (Zhao et al, 2025), and Zhu et al (2023) established that BET protein-dependent inflammatory gene expression programmes drive retinal degeneration with a functional visual consequence (Zhu et al, 2023). Together these studies establish OptoDrum as a functional decoder of the mechanistic pathways by which neuroinflammation impairs the visual pathway.

The challenge

Mechanistic neuroinflammation research produces a rich catalogue of molecular findings – elevated cytokine levels, complement deposition, microglial transcriptomic signatures, axon degeneration markers – but connecting these molecular events to a functionally meaningful visual outcome requires a behavioural endpoint that integrates the combined effect of all these processes on the retina-to-brainstem pathway. This integration is precisely what the OptoDrum provides. A single OptoDrum measurement captures the cumulative functional effect of everything happening between the photoreceptor and the brainstem: if TNF-alpha is killing RGCs, if complement is disrupting synaptic function, if axon degeneration is reducing optic nerve conduction fidelity – all of these processes will reduce the optomotor acuity threshold in a graded, dose-sensitive way. TNF-alpha is the most therapeutically targeted neuroinflammatory cytokine in both experimental and clinical autoimmune CNS disease. Its role in RGC death is well established: TNF receptor 1 (TNFR1) activation triggers both apoptotic and necrotic RGC death cascades, while TNF receptor 2 (TNFR2) may have neuroprotective functions in some contexts. Li et al (2025) used OptoDrum to demonstrate the functional magnitude of TNF-alpha-driven RGC degeneration, establishing the OMR as a sensitive endpoint for testing TNFR-selective therapeutic strategies (Li et al, 2025). Complement activation – a parallel amplification system engaged downstream of both antibody- mediated and innate immune triggers – was validated as a visual dysfunction driver by Zhao et al (2025), who demonstrated that C3/C3aR inhibition preserves OMR-measured visual acuity (Zhao et al, 2025). For the optic nerve damage and axon degeneration cluster pages, see Optic Nerve Damage, Retinal Ganglion Cell Death, and Retinal Ganglion Cell Dysfunction. For the broader retinal degeneration context, see the Retinal Degeneration and Inherited Retinal Disease application page and the Retinal Degeneration cluster page. The glaucoma connection is relevant here too – elevated IOP, neuroinflammation, and RGC loss share mechanisms – see the Glaucoma and Optic Nerve Neurodegeneration application page and the Glaucoma cluster page.

How Striatech products help

OptoDrum
Serves as the integrative functional endpoint that links molecular neuroinflammatory mechanisms to quantifiable visual outcome. Detects the cumulative functional effect of TNF-alpha-driven RGC death, complement-mediated dysfunction, and microglial activation on the optomotor reflex pathway. Graded threshold-seeking algorithm is sensitive to partial RGC pathway compromise well before complete visual loss, enabling early-window mechanistic comparisons.
AcuiSee
Provides a cortically mediated, operant visual acuity endpoint for neuroinflammation-driven RGC loss studies. Assesses whether neuroinflammatory damage impairs learned visual discrimination and suprathreshold visual perception, complementing the subcortical reflex readout from OptoDrum.

Evidence from the Literature

03
How Does Optic Neuritis Develop in Neuroinflammatory Models, and How Do I Track Its Progression?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Optic neuritis in EAE and related models produces rapid, quantifiable visual acuity loss driven by a cascade involving microglial activation, optic nerve demyelination, axon degeneration, and secondary RGC death. Groh et al (2025, Nat Neurosci) established that microglial CX3CR1-dependent activation orchestrates this demyelination process, producing functional visual deficits quantifiable by OptoDrum (Groh et al, 2025). Groh et al (2023, Nat Commun) provided an important counter-intuitive finding: that controlled microglia-mediated demyelination in PLP-deficient models can actually protect against secondary axon degeneration (Groh et al, 2023), and Godwin et al (2022) demonstrated that cholesterol homeostasis modulation alters optic neuritis severity with functional visual consequences measurable by OMR (Godwin et al, 2022).

The challenge

Optic neuritis in rodent EAE and related models follows a reproducible time course that mirrors the human clinical course in its broad features but compresses the time frame: acute demyelination and optic nerve inflammation typically peak between days 12 and 20 post- immunisation in MOG-EAE, producing rapid RGC loss and visual acuity decline; partial remyelination and some functional recovery may follow, but a proportion of RGCs are permanently lost due to secondary axon degeneration. Identifying the therapeutic window within which an intervention must be applied to prevent this secondary irreversible loss is one of the most clinically consequential questions in optic neuritis research. The mechanistic complexity of optic neuritis – involving T cell and B cell infiltration of the optic nerve, microglial activation, oligodendrocyte and myelin loss, axon degeneration driven by energy failure and calcium overload, and secondary RGC apoptosis via deprivation of retro-axonal trophic support – means that individual histological and molecular endpoints each capture only one component of the overall pathological process. OptoDrum provides the integrative functional endpoint that reflects the combined output of all these processes: the optomotor acuity threshold declines when enough optic nerve conduction fidelity has been lost to impair the visual signal reaching brainstem targets, regardless of which specific pathological mechanism drove that loss. The key insight from Groh et al (2025) is that microglial CX3CR1 signalling is a central orchestrator of optic nerve demyelination, providing a specific molecular target whose inhibition alters the functional visual trajectory in a way OptoDrum can detect longitudinally (Groh et al, 2025, Nat Neurosci). This type of longitudinal OptoDrum monitoring – with pre-immunisation baseline, repeated measurements through the acute phase, and tracking into the chronic or remission phase – is the design recommended for any study aiming to characterise the timing and kinetics of optic neuritis onset and recovery. For the dedicated cluster pages, see Optic Neuritis, Autoimmune Demyelinating Diseases, Axon Degeneration, and Glial Suppression. For the ocular inflammation context, see the Ocular Inflammation and Immune-Mediated Eye Disease application page.

How Striatech products help

OptoDrum
Tracks the temporal profile of visual acuity loss and recovery during optic neuritis, from pre-inflammatory baseline through acute demyelination, RGC death, and the recovery or chronic deterioration phase. The graded threshold-seeking algorithm is sensitive to partial recovery above the acute-phase floor, enabling detection of remyelination- associated functional improvement that would be missed by a fixed-frequency stimulus paradigm. Non-invasive; enables daily monitoring during the critical acute window without anaesthesia burden.
Non-aversive Animal Platform
Facilitates reliable OptoDrum testing during and after the acute EAE/optic neuritis phase when animals may be at their most debilitated, ensuring that measured visual acuity reflects the genuine neurological status of the optic nerve rather than handling-related stress suppression of the OMR.
AcuiSee
Provides a cortically mediated, operant visual acuity endpoint for tracking optic neuritis progression. Reveals whether demyelination-driven visual pathway damage impairs learned visual discrimination over time, complementing the subcortical reflex trajectory from OptoDrum.

Evidence from the Literature

04
Which Visual Endpoints Apply in MOGAD and NMOSD Models, and How Do These Differ from EAE?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

MOGAD (MOG antibody-associated disorder) and NMOSD (neuromyelitis optica spectrum disorder) are clinically distinct from MS and are characterised by more severe, often bilateral, optic neuritis with poor visual recovery. In rodent models, these differences are reflected in the profile of OptoDrum-measured visual dysfunction, with greater deficits and less spontaneous recovery than in classical EAE. Remlinger et al (2023) provided the first detailed OptoDrum-based characterisation of NMOSD/MOGAD visual impairment in a rodent model (Remlinger et al, 2023), and Joly et al (2022) characterised B cell-dependent EAE incorporating MOG antibody responses as a bridge model between classical EAE and MOGAD (Joly et al, 2022).

The challenge

MOGAD and NMOSD have been recognised as entities distinct from MS only in the last decade, and their preclinical modelling remains less standardised than EAE. The key pathological distinction is the effector mechanism: NMOSD is driven primarily by aquaporin-4 antibody (AQP4-IgG) attack on astrocytic endfeet, producing tissue-destructive lesions at the blood-CNS barrier; MOGAD is driven by MOG-IgG attack on oligodendrocyte cell surfaces and myelin. Both produce more severe optic neuritis than classical T cell-driven EAE, with less tendency for spontaneous remission, more extensive RGC loss, and greater functional visual deficits at equivalent disease duration. These clinical and pathological differences must be captured by the functional endpoint used in preclinical model development: an endpoint insensitive to the difference between EAE and MOGAD visual profiles cannot serve as a valid translational model characterisation tool. OptoDrum provides the necessary discriminating sensitivity. Its graded threshold-seeking algorithm detects visual acuity across the full range from near-normal to near-abolished, making it capable of documenting the more severe and sustained deficits characteristic of MOGAD/NMOSD models as well as the partial, fluctuating deficits of classical relapsing- remitting EAE. Remlinger et al (2023) exploited this range to characterise the distinct visual deficit profile of NMOSD/MOGAD in rodents, providing a functional benchmark against which therapeutic interventions in these models can be evaluated (Remlinger et al, 2023). For the dedicated MOG and autoimmune demyelinating disease cluster pages, see MOG Antibody-Associated Disorder, Autoimmune Demyelinating Diseases, Experimental Autoimmune Encephalomyelitis, and Multiple Sclerosis. For the ocular inflammation context of antibody-mediated optic nerve disease, see the Ocular Inflammation and Immune-Mediated Eye Disease application page.

How Striatech products help

OptoDrum
Characterises the functional visual deficit profile in MOGAD and NMOSD models, distinguishing the severity and recovery kinetics of antibody-mediated optic neuritis from classical T cell-driven EAE. Provides a quantitative, longitudinally repeatable visual acuity endpoint capable of documenting the more severe and sustained deficits characteristic of these conditions. Non-invasive and automated; no anaesthesia required, enabling frequent monitoring across the acute and recovery phases.
AcuiSee
In MOGAD and NMOSD models where the research question extends to cortical visual recovery (for example, assessing whether therapeutic intervention restores not just subcortical OMR function but cortically mediated visual acuity following optic nerve attack) AcuiSee provides the cortically validated functional endpoint. This is particularly relevant for therapeutic studies targeting remyelination and axon reconnection, where the translational question is whether the treated animal regains the ability to use visual information for learned behaviour, directly paralleling clinical vision recovery endpoints used in MOGAD/NMOSD trials.

Evidence from the Literature

  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.
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  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.
    Feature →
    A rodent NMOSD/MOGAD model was developed and characterised. OptoDrum was used to document the distinct pattern of visual dysfunction produced by antibody-mediated optic nerve attack.
  • Joly et al (2022) J. Neuroinflammation
    A B cell-dependent EAE model in which MOG antibody responses contribute to demyelination and visual pathway damage was characterised, using OptoDrum to document functional visual outcomes in this hybrid T cell/B cell model that bridges the classical EAE and MOGAD paradigms.
  • Wingerchuk et al. (2015) Neurology.
    The international consensus criteria for NMOSD, establishing the disease-defining role of severe bilateral optic neuritis and providing the clinical context within which preclinical NMOSD models must demonstrate pathological and functional fidelity. OptoDrum-measured visual dysfunction in NMOSD rodent models must be evaluated against the severe, bilateral clinical visual impairment documented under these criteria.
05
Does Neuroprotective or Immunomodulatory Treatment Preserve Visual Function in EAE and Optic Neuritis Models?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Yes – multiple neuroprotective and immunomodulatory treatment strategies produce OptoDrum-measurable improvements in visual function in EAE and optic neuritis models. Anders et al (2023) demonstrated that HIF-1 inhibition with acriflavine preserves optomotor visual acuity in EAE (Anders et al, 2023), and Zhu et al (2023) showed that BET PROTAC-mediated neuroinflammation suppression produces functional visual protection (Zhu et al, 2023). For studies evaluating whether treatment also restores cortical visual processing – a translational claim of increasing importance in MS neuroprotection research – AcuiSee provides the cortically validated complement to the subcortical OptoDrum endpoint.

The challenge

The preclinical MS and optic neuritis field has a well-documented translational gap: many interventions that reduce clinical EAE scores, decrease spinal cord lesion burden, or improve histological RGC counts fail to produce robust functional visual recovery as measured by behavioural endpoints. This gap exists because EAE clinical scoring (predominantly measuring hindlimb paralysis) does not capture optic nerve functional integrity, and because histological RGC counts confirm cell survival but not whether surviving cells are functionally contributing to the visual circuit. OptoDrum bridges this gap by providing the behavioural functional endpoint that confirms whether a neuroprotective or immunomodulatory treatment has actually preserved the retina-to-brainstem visual pathway sufficiently to support a tracking response. The EAE neuroprotection literature has moved beyond classical immunosuppression to target specific molecular pathways: HIF-1-driven hypoxia in demyelinating lesions (Anders et al, 2023), BET protein-dependent inflammatory transcription (Zhu et al, 2023), cholesterol metabolism (Godwin et al, 2022, covered in FAQ 3), and optic nerve regeneration through Nogo-A pathway inhibition (Baya Mdzomba et al, 2020). Each of these intervention strategies has been validated with OptoDrum as the functional visual endpoint, providing a set of published precedents for researchers designing new neuroprotection studies in this application area. For the optic nerve regeneration angle, see the Optic Nerve Regeneration cluster page. For the therapeutic vision restoration context, see the Gene Therapy, Optogenetics and Regeneration application page.

How Striatech products help

OptoDrum
Confirms that a neuroprotective or immunomodulatory treatment produces a behaviourally meaningful improvement in visual function in EAE or optic neuritis, validating molecular and cellular protection findings with a functional behavioural endpoint. Longitudinally repeatable; enables pre-treatment baseline, acute-phase treatment effect, and chronic-phase durability all to be tracked in the same animals. Approximately 4 minutes per animal; no anaesthesia or training required.
AcuiSee
In treatment studies where the claim includes restoration of cortical visual processing (for example, when a remyelination therapy is expected to restore signal conduction through the optic radiation, or when a neuroprotective intervention is tested in a model with significant cortical demyelination) AcuiSee provides the operant endpoint that confirms whether the treated animal has recovered the ability to use visual information for learned behaviour. This is the most clinically relevant endpoint for MS neuroprotection studies targeting higher-order visual function, and it directly parallels the contrast sensitivity and spatial acuity tests used in MS clinical trials.
Non-aversive Animal Platform
In long-duration treatment studies where animals undergo repeated procedures (injections, EAE monitoring, clinical scoring), the non-aversive platform reduces accumulated handling stress, ensuring that detected functional improvements reflect genuine treatment effects rather than differential stress responsiveness.

Evidence from the Literature

  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.
    Feature →
  • Anders et al (2023) Front Immunol.
    HIF-1 inhibition with acriflavine preserves optomotor-measured visual acuity in EAE by reducing hypoxia-driven neuroinflammation in optic nerve lesions, establishing HIF-1 as a neuroprotective target with a directly quantifiable visual functional readout.
  • Zhu et al (2023) J. Neuroinflammation
    Validation of BET PROTAC-mediated suppression of neuroinflammatory gene expression as a neuroprotective strategy that preserves OptoDrum-measured visual function, demonstrating that epigenetic anti-inflammatory intervention produces a behaviourally meaningful functional benefit.
  • Baya Mdzomba et al (2020) Cell Death Dis.
    Journal Club →
    Nogo-A antibody treatment promotes RGC survival and visual recovery after neuroinflammatory optic nerve injury, with OptoDrum confirming that Nogo-A inhibition produces a behaviourally meaningful gain in visual acuity.
  • Raftopoulos et al. (2016) Lancet Neurol.
    This randomised controlled trial of sodium channel blockade as neuroprotection in human optic neuritis provides the translational context for the preclinical neuroprotection studies above. OptoDrum-based visual acuity endpoint in rodent EAE models is directly analogous to the high- and low-contrast visual acuity endpoints used in this trial, demonstrating the translational fidelity of the preclinical endpoint.
06
Can Visual Function Serve as a Non-Invasive Biomarker for Systemic Neuroinflammatory CNS Disease Activity?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Yes – and this is the application most directly relevant to researchers whose primary subject is brain, spinal cord, or systemic inflammation rather than the eye. Published studies using Striatech OptoDrum demonstrate that visual acuity loss correlates with systemic neuroinflammatory disease activity across paradigms ranging from EAE to Alzheimer's disease to ischaemic demyelination and inflammatory retinopathy, with the retinal and optic nerve visual pathway serving as a non-invasive window into CNS inflammatory status in the same animals in which other systemic endpoints are being measured. For CNS researchers, OptoDrum adds a quantitative, four-minute, anaesthesia-free functional biomarker to any neuroinflammatory study protocol without additional animal procedures.

The challenge

CNS neuroinflammation research in areas outside ophthalmology – brain inflammation, spinal cord disease, meningitis, encephalitis, systemic autoimmunity – faces the fundamental problem that CNS functional endpoints are difficult to measure non-invasively in rodents. Motor scoring (rotarod, beam walk, EAE clinical scale), cognitive tests (Morris water maze, novel object recognition), and biopsy or imaging-dependent measures each capture one aspect of CNS function but require significant procedural resources, suffer from high variability and floor/ceiling effects, or are terminal. Visual acuity measured by OptoDrum provides a non-invasive, rapidly repeatable, quantitative CNS functional endpoint that can be incorporated into any neuroinflammatory research protocol at minimal additional cost, simultaneously with other behavioural and imaging assessments. The scientific basis for this biomarker argument is solid. Sheng et al (2026) demonstrated that neuroinflammatory amyloid accumulation in the retina – a hallmark of Alzheimer's disease pathology – produces OptoDrum-measurable visual acuity deficits, validating visual function as a biomarker of neuroinflammatory burden in a non-demyelinating neurodegenerative context (Sheng et al, 2026). Kinuthia et al (2025) demonstrated that OptoDrum tracks the functional visual benefit of immunomodulation in inflammatory retinopathy with metabolic overlap (Kinuthia et al, 2025), and Xue et al (2023) showed that alleviating ischaemic demyelination preserves OptoDrum- measured visual function, bridging vascular and neuroinflammatory mechanisms (Xue et al, 2023). For the Alzheimer's disease biomarker context, see the Alzheimer's Disease cluster page. For the retinal degeneration cluster cross-reference, see Retinal Degeneration. For the ischaemia and vascular disease angle, see the Vascular and Metabolic Disease application page, the Retinal Ischaemia-Reperfusion Injury cluster page, and the Blindness cluster page.

How Striatech products help

OptoDrum
Provides a non-invasive, automated, four-minute functional biomarker of CNS neuroinflammatory disease activity and treatment response, applicable across EAE, Alzheimer's disease, ischaemic demyelination, and inflammatory retinopathy paradigms. Can be incorporated into any neuroinflammatory study protocol without anaesthesia, additional animal procedures, or ophthalmological specialist involvement, providing an independent functional axis orthogonal to motor and cognitive assessments.
AcuiSee
For neuroinflammation researchers specifically studying whether CNS inflammation impairs cortical visual processing (such as in models of cortical encephalitis, limbic encephalitis, or anti-NMDAR antibody-mediated disease where visual cortex involvement is suspected) AcuiSee provides the cortically validated functional endpoint. As an operant discrimination task, it specifically tests whether inflammation-related cortical disruption impairs the animal's ability to use visual information for decision-making, a functional level that the subcortical OMR does not address.

Evidence from the Literature

  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.
    Feature →
  • Sheng et al (2026) Invest Ophthalmol Vis Sci.
    Neuroinflammatory amyloid accumulation in the retina produces OptoDrum-measurable visual acuity deficits, validating visual function as a biomarker of neuroinflammatory burden across disease paradigms that extend beyond classical autoimmune demyelination.
  • Kinuthia et al (2025) JCI Insight.
    OptoDrum tracks the functional visual benefit of immunomodulatory treatment in inflammatory retinopathy, providing evidence that OMR-based visual acuity is a sensitive functional biomarker of neuroinflammatory disease activity across the metabolic-vascular and autoimmune disease spectrum.
  • Xue et al (2023) Brain Pathol.
    Demyelination after ischaemia produces visual dysfunction measurable by OptoDrum. It's alleviation preserves visual function, bridging ischaemic and neuroinflammatory white matter injury mechanisms under a shared visual functional endpoint.
07
How Does Chronic Neuroinflammation Interact with Rare Inherited CNS Diseases and Aging to Drive Progressive Visual Loss?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Chronic neuroinflammation is now recognised as a primary driver of progressive visual loss in both aging and in a range of rare inherited CNS diseases where immune dysregulation amplifies the underlying genetic pathology. Groh et al (2021, Nat Aging) established that cytotoxic T cell accumulation in the aged CNS drives axon degeneration and measurable visual acuity loss. Groh et al (2021, Brain Commun) demonstrated OptoDrum-based monitoring of immune modulation efficacy in neuronal ceroid lipofuscinosisand, and Abdelwahab et al (2023) showed that cytotoxic T cells drive visual pathway degeneration through PLP-deficient axon segments. Together with Horner et al (2024) and Berve et al (2020), these studies establish OptoDrum as the practical longitudinal functional tool for tracking neuroinflammatory visual decline across the aging and rare disease landscape.

The challenge

Progressive CNS diseases – whether age-related, rare-inherited, or degenerative – typically evolve over months to years, demanding monitoring tools that are practical for long-duration studies in the same animals, non-invasive enough to avoid cumulative welfare burden, and sensitive enough to detect gradual functional changes that might be missed by infrequent end-point measurements. Rare inherited neuroinflammatory CNS diseases present the additional challenge that most are ultrarare, meaning that any given research laboratory works with a small number of animals and cannot afford to sacrifice animals at multiple time points for histological monitoring – each animal must provide repeated functional data points across the study. OptoDrum is ideally designed for this role. Its four-minute, anaesthesia-free paradigm is low enough burden to be applied weekly or even more frequently in long-duration natural history or treatment studies, generating a rich longitudinal dataset of visual function trajectories in the same animals across the full study period. In aging studies, this longitudinal sensitivity was demonstrated by Groh et al (2021, Nat Aging), who tracked progressive visual acuity loss as a readout of immunosenescence-driven CNS axon degeneration across the mouse lifespan (Groh et al, 2021, Nat Aging). In rare disease models, the same approach was validated in CLN1 disease by Groh et al (2021, Brain Commun) (Groh et al, 2021) and in HSP by Horner et al (2024) (Horner et al, 2024). The sex-dimorphic microglial dynamics documented by Berve et al (2020) add an important experimental design consideration: researchers studying microglial neuroinflammation in rare or aging models should include sex as a biological variable and track visual function separately in male and female cohorts (Berve et al, 2020). For the rare inherited disease context, see the Rare and Inherited CNS and Eye Disorders application page and the Rare Disease cluster page. For the aging and aging-neuroinflammation intersection, see the Systemic Aging and CNS Decline application page and the Aging cluster page. The axon degeneration cluster is directly relevant to all contexts in this FAQ: see the Axon Degeneration cluster page. For the Alzheimer's disease and neurodegeneration overlap, see the Alzheimer's Disease and Age-Related Macular Degeneration cluster pages.

How Striatech products help

OptoDrum
Provides the longitudinal functional monitoring tool for chronic neuroinflammatory visual decline in aging and rare disease models. The four-minute, anaesthesia-free paradigm is practical for weekly or biweekly long-duration study designs. The graded threshold-seeking algorithm detects gradual functional decline months before terminal histological assessment is planned, enabling dynamic tracking of disease progression and early detection of treatment benefit. Enables pre-disease baseline, progressive natural history, and treatment response all in the same animal cohort.
Non-aversive Animal Platform
Critical for long-duration studies in aged animals, which are often more handling- averse, more susceptible to stress-related physiological changes, and more variable in their response to standard restraint. The voluntary-entry tunnel-lid design allows aged animals to enter the OptoDrum platform at their own pace, minimising stress-related OMR suppression in the precise demographic where detecting genuine disease-related visual decline is most important.
AcuiSee
Provides a cortically mediated, operant visual acuity endpoint for studies of chronic neuroinflammation interacting with rare inherited CNS diseases and aging. Assesses whether compound pathology impairs learned visual discrimination and suprathreshold visual perception, complementing the subcortical reflex readout from OptoDrum.

Evidence from the Literature

  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.
    Feature →
  • Groh et al (2021) Nat. Aging
    Journal Club →
    Cytotoxic CD8+ T cell accumulation in the aged CNS drives progressive axon degeneration and visual acuity loss, with OptoDrum providing the longitudinal functional biomarker that documents this inflammaging process in the living animal.
  • Groh et al (2021) Brain Commun.
    Journal Club →
    Immune modulation attenuates disease progression in CLN1 disease and preserves visual function as monitored by OptoDrum, establishing OMR-based visual acuity as a practical endpoint for rare neuroinflammatory CNS disease research.
  • Abdelwahab et al (2023) iScience
    Cytotoxic T lymphocytes infiltrating the CNS drive visual pathway degeneration through PLP-deficient axon segments, with OptoDrum documenting the functional visual consequence of adaptive immune-driven axon injury in a rare demyelinating disease model.
  • Hörner et al (2024) Thesis
    The neuroinflammatory contribution to axon degeneration in hereditary spastic paraplegia was investigated, using OptoDrum to document visual functional consequences of the inflammatory component of this rare motor neuron disease.
  • Berve et al (2020) J. Neuroinflammation
    Feature →
    Sex- and region-specific patterns of retinal microglial depletion and their visual functional consequences were characterised using OptoDrum, highlighting that microglial neuroinflammatory dynamics have sex-dimorphic visual outcomes – a methodological consideration for neuroinflammation experimental design.
Product Fit

Summary: Striatech Products supporting your research questions

Research Question OptoDrum ScotopicKit AcuiSee Photorefractor Keratometer DarkAdapt Non-aversive Platform
Longitudinal EAE and MS measurement Yes Yes* Yes
Neuroinflammation and RGC mechanisms Yes Yes
Optic neuritis progression and tracking Yes Yes Yes
MOGAD and NMOSD models Yes Yes**
Neuroprotection and immunomodulation Yes Yes* Yes
Visual function as CNS neuroinflammation biomarker Yes Yes***
Aging, rare disease, and chronic neuroinflammation Yes Yes Yes
*AcuiSee for EAE/MS and neuroprotection: applicable specifically when the model produces significant cortical demyelinating lesions or when the treatment being evaluated is hypothesised to restore cortical visual processing (for example, remyelination therapies expected to restore conduction through the visual cortex). Not required for studies focused on subcortical optic nerve and RGC pathway monitoring, where OptoDrum is sufficient and AcuiSee would add procedural burden without additional scientific value. **AcuiSee for MOGAD and NMOSD: most directly applicable in treatment studies targeting optic nerve remyelination or axon reconnection in MOGAD/NMOSD, where the translational question is whether restored optic nerve conduction is sufficient to support cortically mediated visual function, the endpoint most directly relevant to clinical visual recovery outcomes in these conditions. ***AcuiSee as CNS neuroinflammation biomarker: specifically applicable for CNS researchers whose models involve cortical or limbic neuroinflammation rather than purely spinal cord or optic nerve disease, where cortical visual processing might be directly affected by the inflammatory process. In models where only optic nerve and subcortical visual pathway involvement is expected, OptoDrum is sufficient. ScotopicKit: The neuroinflammatory and autoimmune CNS disease models covered by this pillar primarily affect RGCs, optic nerve axons, and inner retinal neurons rather than rod photoreceptors, so photopic OMR testing with the OptoDrum captures the relevant functional deficit without requiring scotopic extension. ScotopicKit would become applicable in neuroinflammation models where secondary photoreceptor degeneration is a documented feature of the disease course.  
Measurement Modalities

Measuring Functional Visual Outcomes in Neuroinflammation and Autoimmune CNS Disease: How Do Available Methods Compare?

The table below compares Striatech functional assessment instruments with other modalities routinely used in EAE, optic neuritis, MOGAD, and neuroinflammation research. It is intended as an honest guide to where each method adds specific value and where Striatech tools complement rather than replace established approaches.
Modality What It Measures Pathway Assessed Invasiveness Anaesthesia Longitudinal Repeatability Automation 3Rs Impact Key Limitation in Neuroinflammation Studies
OptoDrum (OMR) Photopic visual acuity and contrast sensitivity; subcortical RGC-to-brainstem pathway integrity Retina → brainstem (subcortical) Non-invasive No Daily if required; no upper limit Fully automated Within-animal longitudinal design eliminates separate terminal cohorts at each time point; reduces total animal numbers Subcortical only; does not detect selective cortical visual pathway demyelination (see AcuiSee)
AcuiSee (operant) Visual acuity and contrast sensitivity requiring cortical processing; learned visual discrimination Retina → cortex (full pathway) Non-invasive No Yes, after training phase Moderate Food-reward design; training adds procedural overhead Requires 10–14 day training phase; not suitable for studies where severe motor or cognitive impairment prevents operant learning
EAE clinical scoring (Khoury scale) Motor and sensorimotor neurological deficit; hindlimb and tail paralysis Spinal cord / brainstem motor pathway Non-invasive No Daily Low (observer-dependent) Standard EAE outcome measure; low additional burden Does not capture optic nerve or visual pathway involvement; observer-dependent; floor effects in severe disease
Pattern ERG (PERG) RGC-specific electrophysiological response; inner retinal electrical function RGC layer (inner retina) Minimally invasive Yes (typically) Limited by anaesthesia; typically weekly Moderate Provides RGC-specific electrophysiological readout complementary to OMR Anaesthesia burden in long EAE studies; anaesthesia alters neuroinflammatory signalling
Visual evoked potential (VEP) Cortical visual response; optic nerve conduction and cortical signal Optic nerve conduction to V1 Invasive (cortical electrodes) Yes Low; surgical implantation required Low Direct measure of optic nerve conduction integrity – the primary deficit in optic neuritis and EAE Surgical burden; implanted electrodes may influence EAE progression; anaesthesia-dependent
OCT (optical coherence tomography) Retinal nerve fibre layer and RGCL thickness; structural degeneration Retinal structure (inner layers) Non-invasive (mydriasis typically required) Yes (typically) Weekly to monthly Semi-automated Structural readout complementing OMR functional data Structural endpoint only; does not confirm functional consequence; anaesthesia adds cumulative burden in EAE
Histological RGC counts and axon quantification RGC survival; optic nerve axon density; myelin thickness Retinal structure and optic nerve anatomy (terminal) Terminal Yes (terminal) None (terminal) Semi-automated Gold-standard for confirming structural endpoints Terminal; cannot provide functional evidence; separate cohorts required at each time point
MRI (small-animal MRI) Brain and spinal cord lesion volume; white matter tract integrity; structural atrophy CNS structure (brain, spinal cord, optic nerve) Non-invasive Yes Weekly to monthly Semi-automated (segmentation) Directly detects CNS lesions in EAE; high translational value for clinical MS endpoint mapping Resource-intensive; anaesthesia required; dedicated preclinical MRI facility needed
For neuroinflammation and autoimmune CNS disease research, the recommended endpoint combination couples OptoDrum (and AcuiSee where cortical visual function is specifically relevant) with at least one structural endpoint (OCT or histology) and – for EAE and optic neuritis studies where regulatory alignment is important – VEP or ERG as the electrophysiological standard. The Striatech instruments' specific value is the longitudinally repeatable, anaesthesia-free functional layer that can be sampled as frequently as daily across the full disease and treatment course, replacing the need for multiple terminal cohorts at different time points and enabling within-animal statistical designs that substantially reduce total animal numbers. For further information on Striatech instrument capabilities, see stria.tech.
Supported by Striatech Products

Publications on Neuroinflammation and Autoimmune CNS Disease

Great Research, Interactive

Journal Clubs related to Neuroinflammation and Autoimmune CNS Disease

Featured image for “Journal Club: Seeing White Matter Aging Through the Visual System”
Q&A available
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Thursday, 11 Jun 2026

Journal Club: Seeing White Matter Aging Through the Visual System

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Janos Groh, Ph.D. - Institute of Neuronal Cell Biology, Technical University of Munich
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This Journal Club by Janos Groh et al. covers white matter aging and neuro-immune interactions. Aging is associated with progressive white matter degeneration. Dysfunctional microglia drive the recruitment and retention of pathogenic CD8+ T cells through chemokine-mediated signaling, promoting neuroinflammation in aging white matter. Glial–immune interactions contribute to structural and functional decline, with microglia–immune crosstalk as a key driver of age-related neurodegeneration.
Featured image for “Journal Club: RIP1 Inhibition Protects Retinal Ganglion Cells in Preclinical Glaucoma Models”
Q&A available
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Wednesday, 18 Jun 2025

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

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Bo Kyoung Kim, Ph.D. - Roche Pharma Research & Early Development, Roche Innovation Center Basel, F. Hoffmann-La Roche Ltd.
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This Journal Club features innovative research by Kim et al., who revealed that inhibiting RIP1 kinase protects retinal ganglion cells in preclinical glaucoma models. Their work demonstrates that targeting necroptosis and inflammation can prevent cell loss and functional decline, directly linking genetic risk to inflammatory degeneration and highlighting RIP1 as a promising therapeutic target for neuroprotection in glaucoma.
Featured image for “Journal Club: In Vivo Modeling of Immune-mediated Optic Neuropathies”
Q&A available
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Wednesday, 09 Nov 2022

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

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Oliver W. Gramlich, Ph.D. - The University of Iowa
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This presentation will outline the pathobiology and visual phenotype of immune mediated optic neuropathies that include Multiple Sclerosis (MS), Neuromylitis optica spectrum disorders (NMOSD), and Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD).
Featured image for “Journal Club: Endothelial Caspase-9 Mediates Inflammatory and Vision Function Changes in Retinal Vascular Injury”
Q&A available
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Wednesday, 20 Jul 2022

Journal Club: Endothelial Caspase-9 Mediates Inflammatory and Vision Function Changes in Retinal Vascular Injury

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Crystal Colón Ortiz, Ph.D. - Columbia University Medical Center
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In retinal vein occlusion (RVO), non-apoptotic expression of endothelial caspase-9 (EC Casp9) induces pathology including retinal edema, capillary ischemia, and neurodegeneration. Crystal Colón Ortiz presents mechanistic insights into EC Casp9 action, and the behavioral consequences such as contrast sensitivity decline.
Featured image for “Journal Club: Anti-FcRn Treatment in Antibody-Associated Experimental Autoimmune Encephalomyelitis”
Q&A available
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Tuesday, 22 Mar 2022

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

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Jana Remlinger, MSc - Department of Neurology, Inselspital, Bern University Hospital and Department for BioMedical Research (DBMR)
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Jana Remlinger et al. showed preserved visual function and ameliorated course of disease after anti-FcRn treatment in an experimental model using a monoclonal MOG-IgG to mimic MOGAD.
Featured image for “Journal Club: Assessing Neuroinflammation-related Neural Damage by Monitoring the Retinotectal System”
Q&A available
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Thursday, 27 May 2021

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

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PD Dr. Janos Groh - Department of Neurology, Section of Developmental Neurobiology, University Hospital Würzburg
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Neuroinflammation amplifies neural damage caused by genetic disorders or aging. Groh et al show that neuroinflammation has deleterious consequences for the optic nerve, and disease progression can be monitored with the OptoDrum.
Featured image for “Journal Club: The role of Nogo-A in visual deficits induced by retinal injury.”
Q&A available
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Thursday, 28 Jan 2021

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

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Julius Baya Mdzomba, PhD - Université Laval
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Nogo-A, an inhibitor of neural growth, prevents regeneration after injury. Blocking of Nogo-A aides recovery, also in the visual system after retinal damage. Baya Mdzomba show with our OptoDrum that visual behavior benefits from Nogo-A neutralization after retinal damage typically found in diabetic retinopathy or glaucoma.
Featured image for “Journal Club: Measuring Visual Acuity and Contrast Sensitivity by Optomotor Reflex in Rodents”
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Thursday, 02 Apr 2020

Journal Club: Measuring Visual Acuity and Contrast Sensitivity by Optomotor Reflex in Rodents

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Dr. Thomas Münch - Striatech
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Dr. Kaushikaram Subramanian - Max Planck Institute of Molecular Cell Biology and Genetics
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Prof. Volker Enzmann - Department of Ophthalmology, University of Bern
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In vision research, observing the optomotor reflex (OMR) is an important and widely established method for assessing visual acuity and contrast sensitivity in rodents. In this event, we will hear about several applications of OMR measuremnts, ranging from quantification of retinal degeneration to characterization of night vision.
Keep exploring

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

Research Chapter

Neuroinflammation and Autoimmune CNS Disease

EAE, optic neuritis, MOGAD, and NMOSD models in which dysregulated immunity damages neurons, myelin, and axons. The optic nerve and retina provide the most quantifiable functional endpoints in the field.

20
Application Areas
7
FAQs answered
Part of CNS & Neurodegeneration

Main Application Areas

Autoimmune Demyelinating Diseases
Experimental Autoimmune Encephalomyelitis (EAE)
MOG Antibody-Associated Disorder
Multiple Sclerosis
Neuroinflammation

Additional Topics

Age-Related Macular Degeneration
Aging
Alzheimer's Disease
Axon Degeneration
Blindness
Glaucoma
Glial Suppression
Optic Nerve Damage
Optic Nerve Regeneration
Optic Neuritis
Parkinson's Disease
PLP defects
Rare Disease
Retinal Degeneration
Retinal Ischemia-Reperfusion Injury