Research Applications for Striatech Products

Neuroinflammation

A unifying pathological thread running through MS, glaucoma, diabetic retinopathy, age-related decline, stroke, and rare autoinflammatory disorders. Not a disease but a shared mechanism with cross-cutting therapeutic targets.
Introduction

What is Neuroinflammation?

Neuroinflammation – the activation of resident glial cells, infiltration of peripheral immune cells, and production of inflammatory mediators within the nervous system – is a unifying pathological mechanism shared across a remarkably broad range of CNS and ocular diseases. It does not define a single disease but rather a common biological thread that runs through conditions as diverse as multiple sclerosis and its optic neuritis manifestation, glaucomatous retinal ganglion cell (RGC) loss, diabetic retinopathy, inherited lysosomal storage disorders, age-related CNS decline, acute stroke, and rare autoinflammatory genetic syndromes. The following application areas each incorporate neuroinflammation as a significant mechanistic component: Neuroinflammation and Autoimmune CNS Disease, Glaucoma and Optic Nerve Neurodegeneration, Ocular Inflammation and Immune-Mediated Eye Disease, Retinal Degeneration and Inherited Retinal Disease, Rare and Inherited CNS and Eye Disorders, Systemic Aging and CNS Decline, Ocular and CNS Toxicity Models, Neurodegenerative Disease, Trauma and Acute Injury, and Vascular and Metabolic Disease. This page focuses on the specific experimental question of how neuroinflammatory mechanisms are measured and modulated using visual function endpoints.  
Vision: A Window into the brain 

Why Are Visual Endpoints Relevant in Neuroinflammation Research?

For researchers working in neuroimmunology, MS biology, stroke, metabolic disease, or rare inherited CNS disorders whose primary interest is not visual science, there are strong pragmatic reasons to incorporate retinal visual endpoints into your work. The retina and optic nerve are anatomically contiguous with the brain, share the same immune privilege mechanisms, host a resident microglial population that responds to systemic neuroinflammatory signals, and are accessible without craniotomy. Neuroinflammatory processes that unfold in white matter tracts, the hippocampus, or the spinal cord frequently produce parallel changes in the retinal ganglion cell layer and optic nerve, making them detectable by non-invasive optomotor testing. OptoDrum measurements require no anaesthesia, are completed in under five minutes per animal, and can be repeated across the full disease course, making them especially valuable as a longitudinal biomarker of CNS inflammatory activity in models where repeated CNS tissue sampling is not feasible. For researchers interested in therapeutic approaches to restoring and preserving vision in disease contexts with an inflammatory component, see also Neuroinflammation and Autoimmune CNS Disease.
Animal Models

What Are Common Animal Models For Neuroinflammation?

The following animal models appear specifically in the cluster of neuroinflammation studies covered here, each with documented OptoDrum or combined scotopic/photopic visual function data.
  • Experimental autoimmune encephalomyelitis (EAE). The most widely used rodent model of autoimmune demyelinating CNS disease, induced by MOG35-55, PLP139-151, or MBP peptides with complete Freund's adjuvant. EAE produces optic neuritis, RGC death, and measurable visual acuity decline detectable by OptoDrum.
  • B cell-dependent EAE with MOG antibody responses. A variant of EAE designed to model the humoral (B cell/antibody) arm of MS-like disease and MOG-antibody-associated disorder (MOGAD), producing additional myelin damage via anti-MOG immunoglobulins.
  • Retinal ischemia-reperfusion injury (IRI). Transient elevation of intraocular pressure to interrupt retinal perfusion followed by reperfusion, producing rapid RGC death with a strong complement-mediated and necroptotic neuroinflammatory component. Widely used to model acute glaucomatous injury and neurovascular insults.
  • Streptozotocin (STZ) diabetic retinopathy model. Systemic STZ injection produces hyperglycaemia and a slowly progressing diabetic retinopathy phenotype with inner blood-retinal barrier breakdown driven in part by innate immune STING/cGAMP activation, measurable longitudinally by OptoDrum.
  • PLP1-deficient and hypomyelinating demyelinating models (jimpy, PLP-null). Genetic models of Pelizaeus-Merzbacher disease (PMD) and related leukodystrophies in which CNS hypomyelination is accompanied by secondary neuroinflammation. OptoDrum detects the resulting visual pathway dysfunction.
  • Neuronal ceroid lipofuscinosis models (CLN1/INCL, PPT1-null mice). Models of rare lysosomal storage disorders in which neuroinflammation drives CNS and retinal degeneration. Immune modulation in these models preserves OptoDrum-measured visual function.
  • Wolfram syndrome (Wfs1-mutant) mice. Model of rare inherited optic neuropathy in which MCT1-dependent metabolic failure drives secondary neuroinflammation and optic nerve degeneration, tracked longitudinally by OptoDrum.
  • VPS35 rod-specific knockout mice. Model of Parkinson's disease-linked retromer dysfunction producing rod photoreceptor degeneration with neuroinflammatory features; assessed by both OptoDrum (photopic) and ScotopicKit (scotopic).
  • Hereditary spastic paraplegia (HSP) models. Rare inherited axon degeneration disorders with a neuroinflammatory component; OptoDrum detects visual pathway impairment.
  • Uveitis models (endotoxin-induced or experimental autoimmune uveitis). Intraocular inflammation affecting the uveal tract and retina, with OptoDrum confirming the functional consequence of intraocular neuroinflammation on retinal circuit function.
  • Stroke and neurovascular injury models. Middle cerebral artery occlusion or controlled retinal/CNS neurovascular injury in which OptoDrum visual function serves as a downstream non-invasive biomarker of CNS injury severity and neuroinflammatory sequelae.
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 Track Visual Dysfunction Longitudinally in EAE, Optic Neuritis, and Related Autoimmune Demyelinating Models?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

OptoDrum provides a non-invasive, repeatable visual acuity and contrast sensitivity readout at every time point from disease induction through peak and resolution phases, enabling detailed natural-history profiling and detection of between-group differences due to treatment, diet, or genetic background without requiring terminal procedures at each measurement point.

The challenge

EAE models exhibit highly variable clinical scores between animals and across disease phases, making it difficult to attribute between-group differences to a single variable. Optic neuritis – the inflammatory attack on the optic nerve that occurs in most EAE variants – produces functional visual deficits that correlate with RGC loss and axon injury, but these are often assessed histologically at a single terminal time point. Researchers need a robust functional endpoint that is sensitive enough to detect dietary or pharmacological modulation of disease severity, that does not require terminal procedures, and that can be repeated serially in the same animals. In MOGAD and related B cell-mediated variants, it is additionally important to confirm that the humoral arm of the immune response produces functional visual pathway damage comparable to the T cell-mediated EAE paradigm.

How Striatech products help

OptoDrum

Measures photopic spatial acuity (cycles per degree) and contrast sensitivity via the subcortical optomotor reflex at multiple time points from EAE induction to resolution; detects between-group differences driven by disease severity, treatment, or dietary modulation; requires no anaesthesia and no ophthalmic surgical access.

AcuiSee

Available as a cortical operant acuity complement for researchers who wish to add a higher-order visual discrimination endpoint alongside the subcortical optomotor readout; no peer-reviewed publications in EAE models to date.

Evidence from the Literature

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

    The dietary intervention study showed that a high-saturated, long-chain fatty acid diet significantly exacerbated EAE severity and worsened visual pathway outcomes compared with a control diet, with OptoDrum detecting the resulting between-group differences in functional visual acuity – validating OptoDrum as sensitive to environmentally driven modulation of EAE severity.

  • Anders et al (2023) Front Immunol.

    Acriflavine, a HIF-1 inhibitor, preserves visual function in EAE by targeting optic nerve hypoxia-driven neuroinflammation, with OptoDrum providing the primary quantitative functional endpoint.

  • Joly et al (2022) J. Neuroinflammation

    A B cell-dependent EAE model was characterised, in which MOG antibody responses drive demyelination and visual pathway damage. OptoDrum was used to document the functional visual consequence of this humoral immune attack.

  • Godwin et al (2022) Biomolecules
    Journal Club →

    Investigation whether targeting cholesterol homeostasis reduces neuroinflammation and preserves optic nerve function in an optic neuritis model, confirming by OptoDrum that cholesterol pathway modulation produces a statistically meaningful functional benefit.

  • Hösel et al (2024) J Ophthalmic Inflamm Infect.
    Feature →

    In the intraocular neuroinflammation setting, the researchers demonstrated that intravitreal anti-inflammatory treatment preserved OptoDrum-measurable visual function in a uveitis model, establishing that OptoDrum is sensitive to intraocular inflammation affecting the retina and its neural circuitry.

02
Which Cellular Mechanisms – T Cells, Microglia, and Complement – Drive Neuroinflammatory RGC Loss and Visual Pathway Damage?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Cytotoxic CD8+ T cell infiltration, context-dependent microglial activation and depletion, TNF-α cytokine signalling, and complement C3/C3aR cascades are independently validated drivers of RGC and visual pathway dysfunction in neuroinflammatory rodent models, with OptoDrum confirming that each mechanism produces measurable circuit-level visual impairment.

The challenge

Neuroinflammation is not a monolithic process: the cellular and molecular components that drive tissue damage differ markedly between adaptive immune disease (T cell or B cell-mediated), innate immune activation (microglial, complement), and cytokine-mediated bystander injury. A key challenge in preclinical neuroinflammation research is attributing functional visual deficits to a specific cellular mechanism rather than to a generic inflammatory state. This requires studies in which a defined immune cell type is genetically depleted, transferred, or pharmacologically modulated – and the functional consequence is measured. Sex differences in microglial biology add additional complexity, as male and female animals may show strikingly different functional phenotypes under identical genetic or inflammatory conditions.

How Striatech products help

OptoDrum

Provides the non-invasive functional endpoint that confirms whether a specific cellular manipulation (T cell depletion, microglial depletion, complement blockade, cytokine neutralisation) translates from histological protection to circuit-level visual preservation; enables between-sex comparisons within the same experiment.

Evidence from the Literature

  • Kinuthia et al (2025) JCI Insight.
  • Abdelwahab et al (2023) iScience

    For the adaptive immune arm, the researchers demonstrated that cytotoxic CD8+ T cells infiltrating the CNS drive visual pathway degeneration through PLP-deficient axon segments, with OptoDrum documenting functional visual consequences of T cell-driven axon injury.

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

    Controlled microglia-mediated demyelination protects against axon degeneration in a PLP-deficient model. OptoDrum was used to confirm that microglial activity preserved rather than damaged visual circuit function.

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

    Sex- and region-biased retinal microglial depletion produces differential functional visual consequences measured by OptoDrum, highlighting that sex must be included as a biological variable in neuroinflammation studies.

  • Li et al (2025) Neurosci Bull.

    At the cytokine level, TNF-α has been characterised as a direct driver of optic nerve RGC death in a glaucoma model, with OptoDrum confirming that TNF-α-dependent neuroinflammatory signalling produces measurable functional visual acuity decline.

  • Zhao et al (2025) Invest Ophthalmol Vis Sci.

    Complement pathway activation was examined and demonstrated that complement C3/C3aR signalling drives RGC dysfunction and functional visual acuity loss following retinal ischemia-reperfusion injury, establishing the complement cascade as a tractable anti-neuroinflammatory target with functional OptoDrum-validated endpoints.

03
Which Neuroprotective, Immunomodulatory, and Gene-Editing Strategies Preserve Visual Function in Neuroinflammatory Models, and How Is Efficacy Demonstrated?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

A wide range of interventions – antibody-based biologics, PROTAC protein degraders, RIP1 kinase inhibitors, PPAR-γ agonists, RNA-targeting gene editing, and cellular immunotherapy – all use OptoDrum as the primary or confirmatory functional endpoint, demonstrating that structural neuroprotection translates to behavioural visual circuit preservation in neuroinflammatory rodent models.

The challenge

A fundamental challenge in translational neuroprotection research is the disconnect between structural endpoints (RGC counts, axon density, myelin integrity) and circuit-level function. A drug may rescue RGC numbers by histological count while failing to produce functionally integrated synaptic connections capable of driving the downstream visual circuit. Conversely, modest structural protection may yield unexpectedly large functional gains if the surviving cells are the most functionally critical. This challenge is compounded when the intervention targets an inflammatory pathway with broad effects on multiple cell types: anti-neuroinflammatory treatment may protect RGCs via several parallel mechanisms, and a single structural endpoint cannot distinguish these contributions. Demonstrating that an intervention produces a behaviourally meaningful gain in visual performance is essential for establishing translational relevance, particularly for biologics and gene-editing approaches where the therapeutic window is narrow and the dose-response relationship is non-linear.

How Striatech products help

OptoDrum

Provides the primary behavioural visual function endpoint confirming that neuroprotective or immunomodulatory treatment produces a gain in subcortical optomotor performance, bridging structural histological outcomes to circuit-level function; can be used serially to define the therapeutic window and dose-response relationship.

AcuiSee

Provides cortical operant acuity as a higher-order complement to OptoDrum where researchers wish to confirm that functional preservation extends beyond the subcortical reflex to the learned visual discrimination level; no peer-reviewed publications in neuroinflammatory neuroprotection models to date.

Evidence from the Literature

  • Kinuthia et al (2025) JCI Insight.
  • Baya Mdzomba et al (2020) Cell Death Dis.
    Journal Club →

    Nogo-A inhibition – targeting a key inhibitor of axon regeneration expressed by oligodendrocytes – promotes visual recovery and RGC survival after neuroinflammatory optic nerve injury, with OptoDrum confirming the behaviourally meaningful functional gain.

  • Zhu et al (2023) J. Neuroinflammation

    Suppressing BET-regulated inflammatory gene expression reduces retinal degeneration and preserves OptoDrum-measured visual function.

  • Kim et al (2024) Cell Death Differ.
    Journal Club →
    Feature →

    Necroptotic RGC death was targeted using RIP1 kinase inhibition in a retinal ischemia-reperfusion model, with OptoDrum confirming that structural RGC protection translates to preserved visual circuit function.

  • Zeng et al (2022) Biomolecules

    In a glaucoma context, systemic PPAR-γ activation by pioglitazone was shown to suppress microglial and astrocyte activation in the optic nerve head and preserve OptoDrum- measured visual acuity.

  • Zhao et al (2025) Adv Sci (Weinh).

    A high-fidelity RNA-targeting CRISPR-Cas system silencing pathogenic gene expression in a glaucoma/neuroinflammation model produced measurable visual acuity preservation by OptoDrum alongside RGC survival data.

  • Kinuthia et al (2025) JCI Insight.

    Immunomodulatory treatment in inflammatory retinopathy with metabolic overlap was studied, confirming by OptoDrum that modulating the retinal immune environment preserves visual function across vascular and neuroinflammatory disease contexts.

  • Yu et al (2022) Biomaterials

    Neural stem cell therapy preconditioned with TNF-α was evaluated, showing by OptoDrum functional readouts that TNF-α-primed stem cells exhibit enhanced neuroprotective efficacy after ischemic retinal injury.

04
How Does Neuroinflammation Mediated by Innate Immune Pathways – STING, Complement, and NF-kappaB – Drive Visual Loss in Vascular, Metabolic, and Autoinflammatory Disease Contexts?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Innate immune pathways including the STING/cGAMP axis, complement cascades, and NF-kappaB-linked kinases (ALPK1) drive blood-retinal barrier breakdown, RGC loss, and functional visual decline in diabetic retinopathy, stroke, and rare autoinflammatory syndromes – all detectable by OptoDrum as a non-invasive functional biomarker.

The challenge

Innate immune neuroinflammation in vascular and metabolic disease contexts is often underappreciated relative to the adaptive immune mechanisms that dominate MS and optic neuritis research. Yet STING pathway activation in diabetic retinopathy, complement-driven neurovascular injury, and NF-kappaB-linked autoinflammatory kinase mutations all produce functional visual deficits measurable in rodent models. The challenge for researchers in these fields is to establish whether their intervention of interest produces a biologically meaningful change in retinal circuit function – not just a histological marker of barrier integrity or cell death – and to track this change longitudinally without requiring surgical access or terminal procedures at each time point. For rare genetic autoinflammatory syndromes such as ROSAH syndrome, demonstrating that a selective kinase inhibitor converts a measurable optomotor deficit is critical for establishing translational proof-of-concept.

How Striatech products help

OptoDrum

Provides the non-invasive, longitudinal functional endpoint for visual acuity and contrast sensitivity in diabetic retinopathy, stroke, innate immune disease, and autoinflammatory ocular syndrome models; no anaesthesia or ocular surgery required; suitable for repeated measurements across the full disease course.

Photorefractor

Measures axial refractive state (diopters) to detect lenticular or optical changes co-occurring with neuroinflammatory retinal pathology; provides a structural correlate of anterior segment inflammation in models where uveitis or diabetic lens changes accompany neuroinflammatory disease.

Evidence from the Literature

  • Kinuthia et al (2025) JCI Insight.
  • Ge et al (2025) J Neuroinflammation.

    cGAMP promotes inner blood-retinal barrier breakdown in a diabetic retinopathy model via STING activation, with OptoDrum confirming that iBRB disruption translates to measurable visual acuity loss.

  • Holden et al (2024) J Neurochem.

    Longitudinal neuroinflammatory visual decline in chronic hyperglycaemia was characterised. OptoDrum was used to document progressive retinal visual function decline in a streptozotocin diabetic model, establishing a quantitative natural-history profile for neuroinflammatory DR progression.

  • Colón Ortiz et al (2022) Cell. Death Dis.
    Journal Club →

    Neurovascular neuroinflammation in stroke was examined, showing that neurovascular injury following stroke produces OptoDrum-detectable visual function deficits that serve as a non-invasive biomarker of CNS injury severity and inflammatory sequelae.

  • Sheng et al (2026) Invest Ophthalmol Vis Sci.

    Amyloid-β clearance failure driving retinal neuroinflammation in an Alzheimer’s disease model was studied, quantifying the photopic spatial acuity deficit associated with amyloid accumulation and inflammatory activation.

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

    For genetically defined autoinflammatory disease, gain-of-function mutations in an innate immune signalling gene causing a rare autoinflammatory ocular syndrome were characterised. OptoDrum was used to measure the resulting RGC-level visual functional impairment.

  • Fan et al (2025) Nat Commun.

    Pharmacological blockade of innate immune NF-kappaB activation in ROSAH syndrome protected retinal ganglion cell function as confirmed by OptoDrum.

05
How Does Chronic Neuroinflammation in Rare Inherited Disorders and Aging Drive Progressive Visual Decline, and Can It Be Tracked as a Longitudinal Endpoint?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Chronic neuroinflammation in rare inherited CNS and retinal diseases (ceroid lipofuscinosis, Wolfram syndrome, PMD, hereditary spastic paraplegia) and in normal aging (T cell accumulation, microglial dysregulation) produces progressive visual circuit decline that OptoDrum can track longitudinally, enabling both natural-history profiling and intervention studies with non-invasive serial measurements.

The challenge

Rare inherited neurological disorders are individually uncommon, but collectively they share a common feature: neuroinflammation – whether primary or secondary to metabolic, lysosomal, or structural failure – amplifies the underlying degeneration and accelerates progression. For researchers in these fields, two challenges are paramount. First, the disease course is often slow (months to years in mouse models), requiring a functional endpoint that can be measured repeatedly in the same animal without disease progression confounds introduced by anaesthesia, surgery, or tissue destruction. Second, many rare disease models lack validated functional endpoints: histology and biochemistry describe the mechanism but do not confirm that the pathological process produces a measurable behavioural deficit in the visual or neurological domain. In aging research, the analogous challenge is distinguishing age-related neuroinflammatory visual decline from the broader background of normal aging – requiring the same longitudinal non-invasive measurement capability.

How Striatech products help

OptoDrum

Tracks longitudinal visual acuity and contrast sensitivity decline in rare disease and aging models without anaesthesia or tissue access; can be repeated weekly or monthly across the full natural history; enables treatment arm comparisons within the same cohort using repeated-measures designs.

ScotopicKit

Enables scotopic (rod-mediated) visual function testing where inherited or neuroinflammatory pathology primarily affects rod photoreceptors (e.g. VPS35 rod-specific models, retinitis pigmentosa-like dystrophies); distinguishes rod and cone pathway involvement.

DarkAdapt

Provides the light-tight dark-adaptation environment required before scotopic OptoDrum testing with the ScotopicKit; not a measurement instrument but an essential preparation tool for scotopic testing.

Evidence from the Literature

  • Kinuthia et al (2025) JCI Insight.
  • Groh et al (2021) Nat. Aging
    Journal Club →

    Cytotoxic CD8+ T cells accumulate in aged CNS white matter and drive progressive axon degeneration and functional visual loss, with OptoDrum providing the longitudinal functional biomarker.

  • Karg et al (2023) Immun Ageing.
    Journal Club →
    Feature →

    Microglia serve a neuroprotective function in preserving visual circuit integrity and that microglial dysfunction worsens OptoDrum-measured visual acuity.

  • Groh et al (2021) Brain Commun.
    Journal Club →

    For rare lysosomal disease, it was demonstrated that immune modulation attenuates CLN1 (infantile neuronal ceroid lipofuscinosis) disease and preserves OptoDrum-measured visual function, validating immunosuppression as an approach to treating neuroinflammation-driven rare disease.

  • Rossi et al (2023) Elife

    MCT1-dependent metabolic failure driving secondary neuroinflammation in Wolfram syndrome optic neuropathy was characterised. OptoDrum was used to track visual acuity longitudinally as the disease natural history readout.

  • Hovhannisyan et al (2015) J. Comp. Neurol.

    Established the foundational PMD/leukodystrophy visual phenotype, using OptoDrum in jimpy (Plp1jp/Y) mice, providing a demonstration of OptoDrum-use in a rare inherited CNS disease with secondary neuroinflammation.

  • Hörner et al (2024) Thesis

    Neuroinflammation in hereditary spastic paraplegia was examined using OptoDrum to detect visual pathway impairment arising from inflammatory axon degeneration.

  • Fu et al (2024) Nat Commun.

    For Parkinson’s disease-linked retinal neurodegeneration, OptoDrum (photopic) and ScotopicKit (scotopic) were used to characterise rod and cone pathway dysfunction in VPS35 rod-specific knockout mice, demonstrating that dual photopic/scotopic testing differentiates rod-pathway neuroinflammatory degeneration from cone-mediated function.

  • Shi et al (2024) Int Immunopharmacol.

    Microglial suppression of photoreceptor neuroinflammation in inherited retinal dystrophy was investigated, showing that minocycline-mediated microglial activation suppression preserves photoreceptor function and visual acuity as measured by OptoDrum.

Product Fit

Summary: Striatech Products supporting your research questions

Research Question OptoDrum ScotopicKit AcuiSee Photorefractor DarkAdapt Non-aversive platform
EAE / optic neuritis / MS longitudinal visual tracking Yes Yes Yes
T cell and microglial cellular mechanism attribution Yes Yes
Neuroprotective / immunomodulatory treatment efficacy Yes Yes Yes
STING / complement / innate immune vascular injury Yes Yes Yes
Rare inherited / aging neuroinflammation longitudinal Yes Yes Yes Yes Yes
Measurement Modalities

Measuring Functional Visual Outcomes in Neuroinflammation: How Do Available Methods Compare?

Modality Endpoint Requires anaesthesia? Repeatable longitudinally? Sensitivity to neuroinflammatory change
OptoDrum (optomotor reflex) Photopic spatial acuity, contrast sensitivity No Yes High; detects RGC loss, optic nerve damage, and inflammatory optic neuropathy
ScotopicKit (scotopic optomotor) Scotopic (rod-mediated) spatial acuity No Yes Specific to rod photoreceptor and outer retinal neuroinflammatory pathology
AcuiSee (cortical operant) Suprathreshold visual discrimination, cortical acuity No Yes Captures higher-order visual pathway dysfunction beyond the subcortical reflex
Electroretinography (ERG) Retinal electrical responses (a-wave, b-wave) Yes (typically) Moderate (anaesthesia burden) High for photoreceptor and inner retinal function; limited to retinal layer distinction
Visual evoked potentials (VEP) Cortical response amplitude and latency to visual stimulus Yes (typically) Moderate High for optic nerve and visual cortex conduction; used extensively in EAE/optic neuritis
Optical coherence tomography (OCT) Retinal layer thickness (RNFL, GCL) No (in awake-OCT systems) Yes Structural; does not directly measure function but correlates with RGC loss
Supported by Striatech Products

Publications on Neuroinflammation

Great Research, Interactive

Journal Clubs related to Neuroinflammation

Featured image for “Journal Club: Seeing White Matter Aging Through the Visual System”
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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”
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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: Assessing Neuroinflammation-related Neural Damage by Monitoring the Retinotectal System”
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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.”
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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.
Keep exploring

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

Application Area

Neuroinflammation

A unifying pathological thread running through MS, glaucoma, diabetic retinopathy, age-related decline, stroke, and rare autoinflammatory disorders. Not a disease but a shared mechanism with cross-cutting therapeutic targets.

9
Research Chapters
5
FAQs answered
Main Field where Neuroinflammation is studied
Neuroinflammation and Autoimmune CNS Disease
Other relevant fields
CNS Trauma and Acute Injury: TBI, Optic Nerve Injury, Stroke
Glaucoma and Optic Nerve Neurodegeneration
Neurodegenerative Disease: Alzheimer’s, Parkinson’s and Beyond
Ocular and CNS Toxicity Models
Rare and Inherited CNS and Eye Disorders
Retinal Degeneration and Inherited Retinal Disease
Systemic Aging and CNS decline
Vascular and Metabolic Disease: Diabetic Retinopathy and Stroke