Research Applications for Striatech Products

Blindness

Severe visual loss as a translational endpoint — operationally defined in preclinical research by the absence of measurable optomotor response, and the benchmark against which restoration strategies are evaluated.
Introduction

What is Blindness?

In preclinical visual neuroscience, blindness is not simply a binary label – it is a quantifiable functional endpoint that marks the outer boundary of the visual system's dynamic range. When retinal photoreceptors, retinal ganglion cells (RGCs), or the post-retinal visual pathway are sufficiently damaged, the optomotor reflex falls below a detectable threshold, defining a state of functional blindness in the rodent. Understanding how to measure, characterise, and track that threshold, and how to confirm when a therapy has moved an animal back above it, is a central challenge for translational vision research. This page focuses specifically on blindness as a measurable outcome, independent of the disease mechanism that produces it, addressing how preclinical researchers can define the endpoint, detect the transition from low vision to no vision, and validate restoration of sight. Blindness as a functional endpoint arises across multiple disease contexts: Retinal Degeneration & Inherited Retinal Disease, Glaucoma & Optic Nerve Neurodegeneration, Rare & Inherited CNS and Eye Disorders, Neuroinflammation & Autoimmune CNS Disease, Vascular & Metabolic Disease, Systemic Aging & CNS Decline and Neurodevelopment & Circuit Mechanisms. For the therapeutic strategies that aim to reverse functional blindness (Gene Therapy, Optogenetics, and Cell Replacement) see Maintaining & Restoring Vision. Although blindness most commonly results from primary ocular pathology, it can also arise as a downstream consequence of CNS-primary insults, for example, post-ischaemic demyelination of the visual pathway or inherited CNS disorders affecting optic nerve integrity. In those contexts, functional vision testing provides a non-invasive, quantitative window into CNS white matter status that complements histological endpoints.
Animal Models

What Are Common Animal Models For Blindness?

The following models are restricted to those represented in the published evidence base for this cluster, where functional blindness has been explicitly confirmed by optomotor reflex testing. For the full disease-area model landscape, see the relevant parent application pages linked in the introduction above.
  • rd1 and related inherited retinal dystrophy mice (e.g. rd10, P23H) – Models of rapid or progressive photoreceptor degeneration in which visual acuity declines from near-normal early values to functional blindness within weeks to months. Used in studies by Cha et al. (2022), Shi et al. (2024), Hulliger et al. (2020), Kralik et al. (2022), Brunet et al. (2026), Maddalena et al. (2023), and Lu et al. (2024) to define the blindness endpoint, test scotopic functional loss, and confirm optogenetic or pharmacological rescue.
  • Soluble guanylate cyclase (sGC)-deficient mice – A genetically defined glaucoma-like model in which RGC death and retinal degeneration progress with age, culminating in functional near-blindness as confirmed by OptoDrum longitudinal tracking. Used by Bossardet et al. (2026) to correlate RGC count and structural retinal data with the functional blindness endpoint.
  • RPE metabolic dysfunction models (e.g. MCT2-targeted RPE degeneration) – Models of retinal pigment epithelium failure leading to photoreceptor loss and functional blindness, used by Chandler et al. (2025) and Procyk et al. (2025) to evaluate gene therapy and photoreceptor cell transplantation rescue from a blind baseline.
  • Optogenetically sensitised blind mice (post-degeneration retina expressing channelrhodopsin or novel opsins) – Animals in which endogenous photoreceptors have degenerated to functional blindness and are then re-sensitised to light by viral delivery of optogenetic payloads. Used by van Wyk et al. (2023), Hulliger et al. (2020), Kralik et al. (2022), Maddalena et al. (2023), and Lu et al. (2024) to confirm that optogenetic opsins restore OMR above the functional blindness threshold.
  • Ischaemia-reperfusion injury models – Models of acute retinal or optic nerve ischaemia in which rapid post-injury demyelination and axonal injury drive visual loss to blindness, used by Xue et al. (2023) to confirm that demyelination alleviation prevents functional blindness as measured by OptoDrum.
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
What Functional Threshold Defines "Blindness" in Preclinical Rodent Studies, and How Is It Measured with the Optomotor Reflex?
Audience A - Vision-focused

Quick Answer

In preclinical rodent studies, functional blindness is operationally defined as the absence of a measurable optomotor response at the highest spatial frequencies detectable in healthy controls – typically the inability to track gratings above the noise floor of the optomotor reflex assay. OptoDrum quantifies this endpoint as spatial acuity (cycles per degree) and contrast sensitivity threshold, with stage-mapped inherited degeneration models establishing the correspondence between photoreceptor loss, RGC dropout, and the disappearance of the OMR signal.

The challenge

Preclinical researchers face a definitional problem: unlike clinical visual acuity tests, there is no universal consensus threshold below which a mouse is declared “blind.” The OMR assay is inherently self-limiting – when no response is elicitable, the system reports the noise floor rather than a true acuity value. This ambiguity creates difficulty when comparing across studies, interpreting therapeutic rescue data, or determining whether a rescue treatment has moved an animal from a blind to a sighted state versus from partial loss to partial recovery.

The problem is compounded in longitudinal studies where animals are tested across a disease progression: at what measurement point does the investigator declare that the functional endpoint has been reached? The answer depends on aligning the OMR measurement with parallel structural endpoints – photoreceptor layer thickness, RGC count, electroretinographic amplitude – to anchor the functional endpoint to a biological reference. For a broader overview of how visual function declines in specific inherited retinal diseases, see Retinal Degeneration & Inherited Retinal Disease.

How Striatech products help

OptoDrum

Measures photopic spatial acuity (cycles/degree) and contrast sensitivity threshold via the subcortical optomotor reflex in awake, freely moving rodents. Longitudinal testing across disease stages maps the decline trajectory and defines the measurement-point at which the OMR disappears, anchoring the functional blindness threshold. Non-invasive and repeatable, enabling the same cohort to be followed from normal through blind without a terminal procedure at each timepoint.

AcuiSee

Measures cortical visual acuity via an operant visual-reward paradigm requiring cortical processing. Complements OptoDrum by confirming whether cortical visual representation is also lost at the blindness endpoint, distinguishing complete functional blindness (no OMR and no cortical signal) from a subcortical-only deficit. AcuiSee has no peer-reviewed publications in this specific model context yet; inclusion is based on confirmed cortical-acuity capability.

Non-aversive Animal Platform

Reduces handling stress in aged or severely degenerated animals, where stress-induced suppression of reflexes can confound near-threshold OMR measurements and produce false “blind” readings. Particularly relevant when testing end-stage animals repeatedly.

Evidence from the Literature

  • Kinuthia et al (2025) JCI Insight.
  • Cha et al (2022) Front. Cell. Neurosci.

    Characterised visual acuity and contrast sensitivity at sequential stages of inherited retinal degeneration using OptoDrum, mapping the decline from near-normal early values through the loss of measurable OMR. The study provides a concrete functional timeline aligned with photoreceptor layer thickness measurements, establishing the structural correlates of the functional blindness endpoint.

  • Benkner et al (2013) Behav. Neurosci.
    Journal Club →

    Foundational study mapping optomotor-reflex measured acuity across the lifespan in inherited retinal degeneration mice, demonstrating the assay’s sensitivity from peak normal acuity through functional blindness.

  • Bossardet et al (2026) Sci Rep.

    Longitudinal OptoDrum tracking of a glaucoma-like sGC-deficient mouse model showed progressive age-dependent visual acuity decline to near-blindness, with the blindness tag indicating end-stage functional loss.

02
How Does Scotopic-Specific Testing Detect Night-Blindness and Rod-Mediated Visual Loss Before Complete Blindness Is Reached?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Most inherited retinal dystrophies affect rod photoreceptors before cones, causing scotopic (night) visual loss well before photopic (daytime) acuity disappears. The ScotopicKit extension for OptoDrum enables rod-specific functional testing at multiple reduced luminance levels, identifying scotopic blindness – loss of rod-mediated optomotor responses – as an earlier and more sensitive endpoint than photopic OMR alone. This allows researchers to detect functional blindness specifically in the rod pathway even when cone-driven daytime vision is partially preserved.

The challenge

In most inherited retinal dystrophies, the progression from healthy to blind follows a rod-first pattern: rod photoreceptors degenerate earlier and faster than cones, causing severe night-blindness before photopic acuity is significantly impaired. Standard photopic OMR testing with the OptoDrum (tested at ambient laboratory lighting) is sensitive to cone-mediated vision but may miss the early and often more severe rod-specific component of visual loss. An animal may retain apparently normal photopic optomotor acuity while already being functionally rod-blind – a misleading picture for studies where the therapeutic target is rod rescue.

The distinction matters clinically: most inherited retinal disease patients first present with night vision problems, which is why rod-targeted therapies (gene therapy, neuroprotection) are often evaluated in the context of rod function specifically. A photopic-only functional endpoint understates the severity of functional blindness in the rod pathway and may mask partial rod rescue that does not reach the cone activation threshold. For the broader context of scotopic visual circuit function and rod pathway physiology, see Neurodevelopment & Circuit Mechanisms. For the full landscape of rod-specific inherited diseases, see Retinal Degeneration & Inherited Retinal Disease. For the night-vision-specific cluster context, see the night-vision application page.

How Striatech products help

OptoDrum

ScotopicKit extends OptoDrum testing to scotopic conditions by providing calibrated low-luminance grating stimuli, enabling measurement of rod-mediated optomotor acuity at stepped luminance levels. This allows researchers to generate a scotopic acuity-luminance function and identify the luminance level below which rod-driven OMR is absent – the scotopic blindness threshold – independently of cone-driven photopic performance. Produces the rod-specific functional endpoint needed to validate rod-targeting therapies.

DarkAdapt

Provides a light-tight, controlled dark-adaptation environment prior to ScotopicKit testing. Adequate dark adaptation is essential to ensure that rods are fully recovered before scotopic OMR measurement; premature testing of incompletely dark-adapted animals underestimates rod sensitivity and inflates apparent scotopic acuity loss. DarkAdapt is not a measurement instrument; it is a preparation device that ensures the validity of the scotopic functional endpoint.

Non-aversive Animal Platform

Minimises handling stress during the transition from DarkAdapt housing to the OptoDrum arena, which is particularly important for scotopic testing where stress-induced pupil dilation and heightened motor arousal can affect OMR threshold measurement near the scotopic blindness endpoint.

Evidence from the Literature

  • Kinuthia et al (2025) JCI Insight.
  • Brunet et al (2026) Biomedicines.

    This study evaluated whether AKT pathway activation protects photoreceptors from degeneration in a retinal dystrophy model tagged with blindness, night-vision, and retinal-dystrophy. ScotopicKit confirmed that the SC79 intervention preserved rod-mediated scotopic acuity in treated animals, while OptoDrum confirmed photopic acuity preservation. The dual-modality design demonstrates that rod function can be specifically assessed and the rod-blind endpoint distinguished from cone-blind states.

03
Can Optogenetic Strategies Restore Measurable Visual Function from a Blind Baseline, and How Is the Recovery Quantified by the Optomotor Reflex?
Audience A - Vision-focused

Quick Answer

Yes. Multiple published studies using OptoDrum demonstrate that optogenetic delivery of light-sensitive proteins to surviving inner retinal neurons – bipolar cells, RGCs – restores measurable optomotor acuity in animals that are functionally blind at baseline. The OMR provides a direct, non-invasive, behaviourally meaningful measure of functional rescue that quantifies both whether vision has been restored and the acuity level achieved. For a broader treatment of optogenetic and gene therapy approaches, see Maintaining & Restoring Vision and the optogenetics application page.

The challenge

Optogenetic vision restoration targets inner retinal neurons that survive photoreceptor degeneration – primarily ON-bipolar cells and RGCs – and introduces light-sensitive opsins to re-sensitise the retina to photic stimuli. A critical challenge is that the resulting vision is fundamentally different from rod or cone photoreceptor-mediated vision: the spectral sensitivity, temporal resolution, and spatial resolution of optogenetically restored vision depend entirely on the opsin used, the target cell type, and the AAV dose and tropism. Functional validation therefore requires an assay that (1) can detect the often low-acuity, low-contrast-sensitivity signal produced by optogenetic restoration, and (2) does so non-invasively so that the same animal can be followed across multiple post-treatment timepoints.

A secondary challenge is dose optimisation: AAV-mediated optogenetic delivery is highly dose-dependent, and sub-threshold doses fail to transduce sufficient inner retinal neurons to produce a detectable OMR. Researchers need a quantitative functional endpoint to define the therapeutic dose range and to confirm clinical-grade vector comparability for regulatory submissions. The risk of false-negative results at sub-optimal doses – where histological expression is visible but the functional outcome is absent – underscores the need for behavioural functional endpoints that are orthogonal to and independent of transduction-level histology.

How Striatech products help

OptoDrum

Measures subcortical optomotor acuity before and after optogenetic treatment in the same blind animals, providing a sensitive, repeatable, non-invasive index of restoration. Detects recovery from zero (no OMR) to finite acuity values, allowing researchers to quantify the magnitude of functional rescue as well as the acuity ceiling imposed by the specific opsin and targeting strategy. Critical for dose-response studies: only doses that produce sufficient inner-retinal opsin expression to drive the OMR circuit will yield a positive result.

AcuiSee

Complements OptoDrum by assessing whether optogenetically restored vision reaches the cortical level. Some optogenetic strategies may produce a subcortical OMR response without producing cortical visual signals; AcuiSee operant testing would distinguish this from complete cortical restoration. AcuiSee has no peer-reviewed publications in optogenetic contexts yet; inclusion is based on confirmed cortical-acuity capability.

Non-aversive Animal Platform

Supports repeated testing of post-surgical animals (e.g. intravitreally injected) where conventional restraint may interfere with recovery or stress-suppress OMR thresholds. Particularly important in longitudinal dose-response studies requiring multiple OMR measurements per animal.

Evidence from the Literature

  • Kinuthia et al (2025) JCI Insight.
  • van Wyk et al (2023) Nat. Commun.

    A jellyfish-derived cnidopsin was was expressed in blinded mice and confirmed by OptoDrum that treated animals regained measurable optomotor acuity, including responses to near-UV wavelengths outside the native mammalian photoreceptor range.

  • Lu et al (2024) Gene Ther
    Feature →

    The dose-response relationship between AAV titre and the functional OMR outcome in optogenetic restoration was established, demonstrating that only doses above a threshold produce measurable acuity recovery in blind mice. OptoDrum (Striatech) was the functional endpoint that defined therapeutic dose sufficiency.

  • Kralik et al (2022) Commun. Biol.

    Demonstrated that bipolar cell-targeted optogenetics prevents the decline to functional blindness in a retinal degeneration model, with OptoDrum confirming measurable acuity preservation. Bipolar cell targeting is clinically relevant because these cells survive longer than photoreceptors in late-stage degeneration.

  • Maddalena et al (2023) Front. Drug Deliv.

    Combined CRISPR-mediated gene editing with optogenetic payload delivery for precision-targeted retinal expression, with OptoDrum confirming OMR restoration from a blind baseline. Demonstrates that the functional endpoint is compatible with combined editing-optogenetics platforms as well as pure viral delivery strategies.

  • Hulliger et al (2020) Mol. Ther. Methods Clin. Dev.
    Journal Club →

    Validated a bipolar-cell-specific human promoter for optogenetic transgene expression, with OptoDrum confirming restoration of measurable visual acuity in blind mice.

04
How Can Gene Therapy and Photoreceptor Cell Transplantation Rescue Vision from a Blind Baseline, and What Does the Optomotor Reflex Reveal About the Quality of Functional Recovery?
Audience A - Vision-focused

Quick Answer

AAV-mediated gene therapy targeting metabolic support pathways in the RPE, clinical-grade vector preparations for rare retinal diseases, and human photoreceptor transplantation have each been shown to preserve or restore measurable optomotor acuity in rodent models starting from a blind or near-blind functional baseline. OptoDrum provides the primary in vivo functional endpoint that determines whether a molecular or cellular intervention translates to behaviourally meaningful vision – the threshold question that histological readouts alone cannot answer. For broader gene therapy and cell-based strategy coverage, see Maintaining & Restoring Vision and the gene-therapy application page.

The challenge

Gene therapy and cell transplantation studies in advanced retinal degeneration face a fundamental translational challenge: histological and molecular measures of success (photoreceptor survival counts, RPE integrity, transgene expression levels, transplanted cell markers) do not necessarily predict whether the surviving or restored cells are functionally integrated into the visual circuit at a level sufficient to drive behaviour. A retina that retains more photoreceptors than an untreated control is not necessarily a retina that sees.

The problem is especially acute for rare disease models and clinical-grade vector preparations: regulators require functional evidence of efficacy, not only structural evidence. The OMR provides an appropriate primary functional endpoint because it is non-terminal, repeatable, and sensitive to low-acuity vision, which is the range relevant for animals starting from a blind or near-blind baseline. For rare inherited retinal disorders specifically, see Rare & Inherited CNS and Eye Disorders and Retinal Dystrophy. For models with co-occurring cell death mechanisms, see the Retinal Degeneration & Inherited Retinal Disease application page.

How Striatech products help

OptoDrum

Measures photopic visual acuity and contrast sensitivity before and after gene therapy or cell transplantation, providing the non-invasive longitudinal functional endpoint. In rescue studies starting from a blind baseline, a positive OptoDrum outcome confirms that the intervention has restored circuit-level visual signal propagation through the retina and retino-brainstem pathway – a conclusion unavailable from histology alone.

AcuiSee

Provides the cortical-level complement to OptoDrum’s subcortical OMR measure. In gene therapy rescue studies, a key question is whether restored retinal photoreceptor function translates all the way to cortical visual representation; AcuiSee operant testing would confirm this for studies that require cortical-level evidence of restoration. AcuiSee has no peer-reviewed publications in this context yet; inclusion is based on confirmed cortical-acuity capability.

Non-aversive Animal Platform

Critical for post-surgical animals recovering from subretinal or intravitreal injection, where conventional restraint is inappropriate and stress can suppress OMR thresholds, producing false-negative results in the early post-treatment period.

Evidence from the Literature

  • Kinuthia et al (2025) JCI Insight.
  • Chandler et al (2025) Proc Natl Acad Sci U S A.
    Journal Club →
    Feature →

    Demonstrated that AAV-mediated RPE-specific overexpression of monocarboxylate transporter 2 (MCT2) preserves visual acuity above an untreated near-blind degeneration control in a retinal degeneration model bearing the blindness, retinal-dystrophy, and cell-death tags. OptoDrum confirmed functional preservation as the primary outcome.

  • Presa et al (2025) Commun Med (Lond).
    Journal Club →

    Evaluated clinical-grade versus research-grade AAV vector preparations in a rodent retinal degeneration model, using OptoDrum to confirm that clinical-grade manufacturing produces functional visual benefit comparable to the research-grade preparation. A rare translational validation using a functional outcome measure appropriate for regulatory submission in rare retinal disease.

  • Procyk et al (2025) Stem Cell Reports.
    Journal Club →
    Feature →

    Human cone photoreceptors were transplanted into a degenerated rodent retina and used OptoDrum to confirm whether transplanted human cones produced a functional recovery of photopic visual acuity above a blind baseline. An improvement in OMR-measured acuity confirms functional integration of transplanted cells into the host visual circuit.

05
How Do Histological Endpoints – RGC Count, Photoreceptor Layer Thickness, Microglial Activation – Correlate with the Functional Blindness Endpoint Measured by the Optomotor Reflex?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Functional blindness measured by the OMR correlates with quantifiable structural endpoints including photoreceptor outer nuclear layer (ONL) thickness, RGC density, and markers of neuroinflammation. Studies in both inherited retinal dystrophy and glaucoma-like models show that when ONL thickness or RGC count falls below a critical fraction of healthy control values, the OMR disappears. This structural-functional correlation enables histological endpoints to serve as surrogate markers for functional blindness and allows researchers to predict functional outcome from terminal tissue analysis in studies where behavioural testing is not possible at all stages.

The challenge

Histological endpoints are terminal and provide a structural snapshot, not a functional reading. For many studies – particularly those with complex surgical designs, post-mortem tissue requirements, or regulatory submissions – the question arises: what structural measurement corresponds to functional blindness? Conversely, when a therapeutic intervention preserves retinal structure, does structural preservation necessarily translate to functional vision, or can structurally intact photoreceptors be functionally silent due to synaptic, glial, or inflammatory disruption?

The two-directional correlation is important: researchers need to know both (1) below what structural threshold is functional blindness certain, so that tissue analysis can substitute for OMR in some cohorts, and (2) whether structural rescue translates to functional rescue, so that positive histological outcomes do not overstate a therapy’s efficacy. Neuroinflammation – microglial activation and cytokine-mediated photoreceptor stress – can impair visual function before photoreceptors are lost, creating a functional impairment disproportionate to the structural damage. For the neuroinflammatory context, see Neuroinflammation & Autoimmune CNS Disease and the neuroinflammation cluster. For glaucoma-specific RGC count and IOP correlation, see Glaucoma & Optic Nerve Neurodegeneration and the retinal-ganglion-cell-death cluster. For ischaemic blindness where demyelination is the structural correlate, see Vascular & Metabolic Disease and the retinal-ischemia-reperfusion-injury cluster.

How Striatech products help

OptoDrum

Provides the functional endpoint against which histological measurements are calibrated. Longitudinal OptoDrum tracking across disease stages, combined with terminal histology at selected timepoints, generates the structural-functional correlation curve that anchors blindness to a specific ONL thickness, RGC density, or microglial activation level. The OMR outcome is the ground truth that validates or challenges a structural surrogate.

Non-aversive Animal Platform

Enables OptoDrum testing to be reliably performed on animals that are approaching the terminal disease stage and may be debilitated or weight-reduced, where conventional restraint would suppress OMR responses and inflate false-blindness readings. Ensuring valid OMR measurements at end-stage is critical for the structural-functional correlation at the blindness end of the scale.

Evidence from the Literature

  • Kinuthia et al (2025) JCI Insight.
  • Shi et al (2024) Int Immunopharmacol.

    Demonstrated that minocycline-mediated suppression of microglial activation preserved photoreceptor layer thickness and visual acuity in inherited retinal dystrophy bearing the blindness tag. Provides a direct correlation between histological endpoints (photoreceptor survival, microglial marker expression) and OptoDrum-measured functional outcome at the near-blind endpoint.

  • Bossardet et al (2026) Sci Rep.

    Longitudinal OptoDrum tracking in a glaucoma-like model with progressive RGC death and retinal degeneration demonstrates the correlation between age-related structural decline and the loss of optomotor function to a near-blind level. Provides a non-dystrophy context for structural-functional correlation at the glaucoma-related blindness endpoint.

  • Xue et al (2023) Brain Pathol.

    Showed that demyelination of the post-retinal visual pathway following ischaemia drives functional visual loss to the blindness endpoint, and that a demyelination-alleviating intervention preserves OMR performance. Provides a CNS-primary structural-functional correlation: myelin integrity of the visual pathway, not retinal photoreceptor survival, is the structural correlate of functional blindness in this model.

Product Fit

Summary: Striatech Products supporting your research questions

Research Question OptoDrum ScotopicKit AcuiSee Photorefractor Keratometer DarkAdapt Non-aversive platform
Blindness threshold definition Yes Yes Yes
Scotopic / night-blindness detection Yes Yes Yes Yes
Optogenetic rescue from blindness Yes Yes Yes
Gene therapy / cell transplantation rescue Yes Yes Yes
Histological endpoint correlation Yes Yes
Measurement Modalities

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

The table below compares the primary methods used to assess the blindness endpoint in preclinical rodent studies. Striatech tools are listed alongside complementary modalities to provide an honest picture of where each fits.
Method What It Measures Invasiveness Repeatable in Same Animal Automation Detects Near-Zero Vision 3Rs Benefit
OptoDrum (OMR) Subcortical optomotor reflex; photopic spatial acuity and contrast sensitivity Non-invasive Yes – unlimited repeats High Yes – floor is noise, not zero High – no anaesthesia, no surgery
ScotopicKit (scotopic OMR) Rod-mediated scotopic acuity at low luminance Non-invasive Yes High Yes – scotopic-specific near-zero detection High
AcuiSee (operant acuity) Cortical visual acuity via operant discrimination Non-invasive Yes Medium (training phase required) Yes – can distinguish sub-OMR cortical signals High
ERG (electroretinography) Retinal photoreceptor and bipolar cell electrical activity Minimally invasive (electrode, dilating drops) Yes – but requires anaesthesia Medium Yes – flat ERG defines outer retinal blindness Moderate – anaesthesia required
VEP (visual evoked potential) Cortical visual response amplitude and latency Invasive (cortical electrode implant or skull screw) Limited by electrode integrity Low Yes – absent VEP confirms cortical blindness Low – surgical preparation required
Histology (ONL thickness, RGC count) Structural retinal cell survival Terminal No – single endpoint Low Indirect – structure does not guarantee function Low – terminal procedure
Supported by Striatech Products

Publications on Blindness

Great Research, Interactive

Journal Clubs related to Blindness

Featured image for “Journal Club: Photoreceptor Cell Therapy to Treat Advanced Retinal Degeneration”
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Thursday, 05 Feb 2026

Journal Club: Photoreceptor Cell Therapy to Treat Advanced Retinal Degeneration

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Rachael Pearson, Ph.D. - Ocular Cell and Gene Therapy Group, Centre for Gene Therapy and Regenerative Medicine, King’s College London
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This Journal Club highlights research by Rachael Pearson et al. on photoreceptor transplantation. Photoreceptor transplantation has long been proposed as a strategy to restore vision, but in advanced retinal degeneration it remained unclear whether the inner retinal neurons could still accept and process new inputs from donor cells. The study shows that human pluripotent stem cell–derived cone photoreceptors can integrate into end-stage mouse retinas, drive retinal function, and induce behavioral responses, revealing that even severely degenerated retinas retain the capacity to remodel in response to healthy photoreceptors.
Featured image for “Journal Club: Gene-Agnostic Gene Therapy to Preserve Vision”
Q&A available
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Thursday, 11 Dec 2025

Journal Club: Gene-Agnostic Gene Therapy to Preserve Vision

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Constance Cepko, Ph.D. - Harvard Medical School: Genetics & Ophthalmology (Blavatnik Institute) • HHMI
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This Journal Club features innovative research by Harvard’s Cepko lab, exploring gene-independent strategies to preserve vision in retinitis pigmentosa and other genetic forms of blindness. Using AAVs to enhance metabolic support, including MCT2 expression in retinal pigment epithelial cells, they preserved cone photoreceptors and maintained color and daylight vision across diverse genotypes.
Featured image for “Journal Club: RIP1 Inhibition Protects Retinal Ganglion Cells in Preclinical Glaucoma Models”
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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: The Impact of Lateral Inhibition on Healthy Vision and Retinal Degeneration”
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Thursday, 05 Dec 2024

Journal Club: The Impact of Lateral Inhibition on Healthy Vision and Retinal Degeneration

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Matteo Rizzi, Ph.D. - UCL Institute of Ophthalmology – Moorfields Eye Hospital, Visual Perception and Repair Laboratory
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This Journal Club provides insights into Matteo Rizzi’s research on lateral inhibition in the retina, highlighting its impact on visual function and the development of gene therapy for age-related macular degeneration.
Featured image for “Journal Club: Developing a Novel Gene Therapy for Kcnv2 Retinopathy”
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Wednesday, 24 Jan 2024

Journal Club: Developing a Novel Gene Therapy for Kcnv2 Retinopathy

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Livia Carvalho, Ph.D. - University of Melbourne
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This Journal Club demonstrates the effectiveness of an AAV-based gene therapy in rescuing vision and restoring normal retinal responses in a mouse model of KCNV2 retinopathy, a genetic form of irreversible blindness caused by mutations in the Kv8.2 subunit of voltage-gated potassium channels. Efficacy tests were carried out with Striatech’s OptoDrum and ScotopicKit, among others.
Featured image for “Symposium: Opportunities, Hopes, and Challenges in Translating Visual Restoration from Mouse to Human”
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Sunday, 17 Sep 2023

Symposium: Opportunities, Hopes, and Challenges in Translating Visual Restoration from Mouse to Human

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Professor Eberhart Zrenner - Institute for Ophthalmic Research, Centre for Ophthalmology, University of Tübingen
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Constance Cepko, PhD - Harvard Medical School
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Miikka Terho, MBA - Pioneer Retina Implant Patient, Finland
Striatech celebrates its 5th anniversary with a top-class Symposium on the topic of translating visual restoration from mouse to human. Presentations will be given by Professor Eberhart Zrenner (University of Tübingen), Professor Constance Cepko (Harvard Medical School) and Miikka Terho (Pioneer Retina Implant Patient, Finland). In addition, the speakers will highlight important aspects and directions in this area of research in a moderated panel discussion.
Featured image for “Journal Club: Postsynaptic Neuronal Activity Promotes Retinal Axon Regeneration”
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Wednesday, 21 Jun 2023

Journal Club: Postsynaptic Neuronal Activity Promotes Retinal Axon Regeneration

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Supraja Varadarajan, Ph.D. - Stanford University, School of Medicine, Huberman Lab
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This Journal Club provides insights into mechanisms that promote retinal ganglion cell (RGC) axon regeneration in vertebrates after optic nerve injury.
Featured image for “Journal Club: Inherited Retinal Dystrophy: Chronic Proinflammatory Signaling Accelerates the Rate of Degeneration”
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Wednesday, 05 Apr 2023

Journal Club: Inherited Retinal Dystrophy: Chronic Proinflammatory Signaling Accelerates the Rate of Degeneration

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T.J. Hollingsworth, PhD - University of Tennessee Health Science Center
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T.J. Hollingsworth presents his work where he characterized a new polygenic mouse model of inherited retinal dystrophies, the BXD32 mouse strain. He presents evidence that a proinflammatory environment in the retina supports and accelerates the degeneration of the retina and the loss of visual function.
Featured image for “Journal Club: Developing Retinal Gene Therapy for Zellweger Spectrum Disorder (ZSD)”
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Wednesday, 25 Jan 2023

Journal Club: Developing Retinal Gene Therapy for Zellweger Spectrum Disorder (ZSD)

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Catherine Argyriou, PhD - McGill University, Dept of Human Genetics
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Peroxisomal disorders and the PEX1-G844D mouse model for mild Zellweger Spectrum Disorder (ZSD), leads to retinal degeneration and vision loss. Catherine Argyriou will describe how her team used AAV8-mediated gene delivery to robustly and durably improve functional vision, retinal response, retinal structure, and biochemical metabolites in ZSD-mice.
Featured image for “Journal Club: In Vivo Modeling of Immune-mediated Optic Neuropathies”
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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: Restoring vision – Optogenetic gene therapy targeted at human ON-bipolar cells”
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Thursday, 25 Mar 2021

Journal Club: Restoring vision – Optogenetic gene therapy targeted at human ON-bipolar cells

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Dr. Elmar Hulliger - Institute of Physiology, University of Bern
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Optogenetic gene therapy holds great promise for healing blindness. Hulliger et al have developed a new promoter that effectively targets human ON bipolar cells. This is an important step towards clinical applications of optogenetic gene therapy for restoring vision.
Featured image for “Webinar: Visual Acuity as a Relevant Phenotype in Mouse Models of Rare Disease”
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Thursday, 08 Oct 2020

Webinar: Visual Acuity as a Relevant Phenotype in Mouse Models of Rare Disease

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Zoë Bichler, PhD - The Jackson Laboratory
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Maximiliano Presa, PhD - The Jackson Laboratory
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The Jackson Laboratory will introduce their Neurobehavior Phenotyping Core, in which they also do visual acuity measurements. They will present two examples where the OptoDrum has been used to characterizte vision in animal models for rare disease: The Charcot-Marie-Tooth-disease, and Multiple-Sulfatase-Deficiency.
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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.
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Related application areas, neighbouring research chapters, and the questions researchers ask most.

Application Area

Blindness

Severe visual loss as a translational endpoint — operationally defined in preclinical research by the absence of measurable optomotor response, and the benchmark against which restoration strategies are evaluated.

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Research Chapters
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FAQs answered
Main Field where Blindness is studied
Maintaining and Restoring Vision
Other relevant fields
Glaucoma and Optic Nerve Neurodegeneration
Neurodevelopment and Circuit Mechanisms
Neuroinflammation and Autoimmune CNS Disease
Rare and Inherited CNS and Eye Disorders
Vascular and Metabolic Disease: Diabetic Retinopathy and Stroke