Research Applications
A guided index to visual function across neuroscience research.
Striatech's automated visual-function platforms — the OptoDrum optomotor system, AcuiSee operant testing, and supporting accessories — are used in preclinical research spanning the eye, the central nervous system, and foundational disease modelling. Browse our applications by research field, chapter, or specific topic.
Visual Function:
The Common Readout
The Common Readout
Research Field · 01
CNS & Neurodegeneration
Neurodegenerative disease, neuroinflammation, aging, trauma, and vascular injury. Visual readouts as a non-invasive CNS probe.
5
chapters
28
areas
162
FAQs
Research Field · 02
Eye & Retinal Disease
Models and applications focused on the eye, retina, and visual system.
5
chapters
26
areas
154
FAQs
Research Field · 03
Foundations & Models
Developmental mechanisms, rare-disease paradigms, and safety pharmacology — the foundational paradigms behind translational work.
3
chapters
18
areas
104
FAQs
Neurodegenerative disease, neuroinflammation, aging, trauma, and vascular injury. Visual readouts as a non-invasive CNS probe.
01
CNS Trauma and Acute Injury: TBI, Optic Nerve Injury, Stroke →
Mechanical, ischemic, and blast injuries that drive rapid, often irreversible damage to CNS neurons and axons. Optic nerve crush, retinal I/R, and TBI models share core injury cascades and yield directly quantifiable visual outcomes.
02
Neurodegenerative Disease: Alzheimer’s, Parkinson’s and Beyond →
Progressive neuronal loss across Alzheimer's, Parkinson's, tauopathies, and related disorders. The retina and optic nerve carry the same molecular lesions as the brain and offer accessible, longitudinal readouts of CNS disease progression.
03
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
Age-Related Macular Degeneration
Aging
Alzheimer's Disease
Autoimmune Demyelinating Diseases
Axon Degeneration
Blindness
Experimental Autoimmune Encephalomyelitis
Glaucoma
Glial Suppression
MOG Antibody-Associated Disorder
Multiple Sclerosis
Neuroinflammation
Optic Nerve Damage
Optic Nerve Regeneration
Optic Neuritis
Parkinson's Disease
PLP defects
Rare Disease
Retinal Degeneration
Retinal Ischemia-Reperfusion Injury
04
Systemic Aging and CNS decline →
Aging as the dominant risk factor for neurodegeneration. The retina and optic nerve age in parallel with the brain, offering longitudinal in vivo readouts where most CNS biomarkers remain terminal.
05
Vascular and Metabolic Disease: Diabetic Retinopathy and Stroke →
Disruption of blood flow and glucose homeostasis driving retinal and CNS visual pathway injury. Diabetic retinopathy and ischemic stroke share neurovascular mechanisms and converge on quantitative visual endpoints.
Models and applications focused on the eye, retina, and visual system.
01
Glaucoma and Optic Nerve Neurodegeneration →
The leading cause of irreversible blindness, driven by progressive retinal ganglion cell loss. Models span IOP-dependent and pressure-independent mechanisms, microglial and complement activation, and the search for neuroprotective therapies beyond pressure-lowering.
02
Myopia, Refractive Development and Eye Growth →
Excessive axial elongation of the eye, projected to affect half the global population by 2050. Research targets the visual feedback loops controlling emmetropisation and the genetic and environmental disruptors that drive pathological eye growth.
2 Application areas
03
Ocular Inflammation and Immune-Mediated Eye Disease →
Uveitis, optic neuritis, and the ocular manifestations of systemic and rare inflammatory disorders. Research targets the immune mechanisms behind a major share of preventable blindness in high-income countries.
04
Restoring Vision: Gene Therapy, Optogenetics and Regeneration →
Gene therapy, optogenetics, and regenerative strategies for vision restoration. Each requires non-invasive, quantitative functional readouts to confirm that a treated eye actually sees better.
05
Retinal Degeneration and Inherited Retinal Disease →
Progressive loss of photoreceptors, RPE, and retinal ganglion cells across roughly 280 genetically distinct conditions. The proving ground for ocular gene therapy and the clinical entry point for retinal regenerative medicine.
Developmental mechanisms, rare-disease paradigms, and safety pharmacology — the foundational paradigms behind translational work.
01
Neurodevelopment and Circuit Mechanisms →
The visual system as a tractable entry point into neural circuit assembly, from progenitor specification through activity-dependent refinement. Disruptions of this developmental programme illuminate broader principles of CNS wiring and disease.
02
Ocular and CNS Toxicity Models →
Chemical, pharmacological, and genetic insults that produce defined, reproducible damage to the visual system and CNS. Indispensable for mechanistic studies, safety pharmacology, and the preclinical evaluation of neuroprotective interventions.
03
Rare and Inherited CNS and Eye Disorders →
Genetic and congenital disorders of the CNS and visual system — individually rare, collectively affecting hundreds of millions. Models span inherited retinal dystrophies, leukodystrophies, rare optic neuropathies, and metabolic disease with ocular involvement.
Index
All application areas, A to Z
A flat alphabetical index of every application area on stria.tech. Each entry links to its dedicated page, with a brief description shown alongside.
The leading cause of irreversible central vision loss in adults over 50, driven by RPE dysfunction, complement dysregulation, and choroidal neovascularisation. Preclinical models span dry geographic atrophy and wet neovascular forms with quantifiable functional readouts.
Aging as a cross-context modifier — not a disease itself, but a pervasive shifter of disease susceptibility, progression, and therapeutic window across glaucoma, neurodegeneration, demyelinating disease, and refractive change.
Progressive amyloid-β plaques, tau tangles, and synaptic loss extending from the brain into the retina. Visual dysfunction emerges as both a direct retinal pathology and a non-invasive window onto CNS disease state.
Multiple sclerosis, NMOSD, MOGAD, and their experimental analogues — distinct immunopathologies that converge on shared cascades of complement activation, microglial myelin stripping, and secondary axon degeneration.
The actively programmed self-destruction of the axonal compartment, with unifying mechanisms across optic nerve crush, glaucoma, demyelinating disease, and chronic CNS injury.
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.
Pre- and postnatal maturation of retinal circuits, retinothalamic projections, and visual cortex into a fully calibrated visual pathway. Disruption produces measurable acuity and contrast deficits trackable across the first weeks of life.
The leading cause of preventable blindness in working-age adults. Neurodegeneration of the inner retina precedes or parallels the classical microvascular pathology, opening a functional biomarker window before fundoscopic lesions appear.
The principal rodent paradigm for multiple sclerosis. Model variants (MOG, PLP, B-cell-dependent, passive transfer) differ in disease course and visual phenotype, with optic neuritis as a near-universal feature.
AAV-delivered gene replacement, silencing, and metabolic-support strategies for inherited and acquired visual disease. The retina serves as the field's proof-of-concept arena for CNS gene therapy more broadly.
Glaucoma as a cross-context model — its core RGC degeneration intersects with aging, axial myopia, neuroinflammation, and inherited susceptibility, making it both a disease and a methodological lens onto CNS neurodegeneration.
Targeted modulation of pathologically reactive microglia and astrocytes to limit secondary neurodegeneration. A therapeutic strategy with applications across glaucoma, demyelinating disease, and acute CNS injury.
A distinct demyelinating CNS disease defined by autoantibodies against myelin oligodendrocyte glycoprotein. Recurrent optic neuritis is its defining manifestation, making functional visual outcomes the central preclinical endpoint.
Chronic immune-mediated demyelination, neuroinflammation, and axonal loss across the brain, spinal cord, and optic nerves. Visual endpoints translate directly between rodent EAE models and clinical MS trials.
Pathological axial elongation of the eye driven by retinal–scleral signalling. Preclinical research targets the dopaminergic and growth-factor pathways governing emmetropisation, with refractive, axial, and functional readouts in parallel.
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.
Coordinated damage to the vascular and neural components of the retina and optic nerve. A convergent endpoint across ischaemic, metabolic, and inflammatory disease, organised around the retinal neurovascular unit.
Scotopic visual function — mediated almost exclusively by rods and the rod-bipolar synapse. A sensitive functional readout for inherited retinal disease, photoreceptor toxicity, and gene therapy efficacy.
Axonopathy across acute trauma, chronic glaucomatous pressure, and demyelinating injury. Defined molecular cascades, like SARM1 activation, zinc toxicity, RGC soma death, produce functional consequences detectable before structural loss is irreversible.
Experimental induction of axon regrowth from injured RGCs back toward central visual targets. The translational challenge is showing that anatomical regrowth produces a measurable recovery of behavioural visual function.
Inflammatory demyelination of the optic nerve — the most common presenting feature of MS and a defining manifestation of NMOSD and MOGAD. Visual outcomes are clinically meaningful endpoints accepted in phase II MS trials.
Opsin-based vision restoration, targeting surviving inner-retinal neurons after photoreceptor loss. Post-rescue acuity is the central preclinical benchmark for translation toward clinical sight restoration.
Progressive dopaminergic neuron loss and α-synuclein pathology extending beyond the substantia nigra into the retina. Dopaminergic amacrine cell dysfunction produces measurable contrast sensitivity deficits that mirror CNS disease progression non-invasively.
PLP1 mutations and duplications producing the X-linked hypomyelinating leukodystrophy spectrum, from severe Pelizaeus-Merzbacher disease to milder spastic paraplegia type 2. The optic nerve is a primary CNS white-matter readout of dysmyelination.
Individually uncommon, collectively affecting 300 million people — and uniquely tractable in preclinical research because the causal molecular lesion is known. The visual system is often a primary target or an early indicator of CNS pathology.
Progressive, largely irreversible loss of photoreceptors, RPE, and retinal ganglion cells across inherited, age-related, toxic, ischaemic, and inflammatory contexts. A cross-cutting mechanistic theme rather than a single disease entity.
Genetically heterogeneous monogenic disorders driving predictable, gene-defined photoreceptor degeneration. The natural history is reproducible in rodent models, making them benchmark systems for gene therapy and rescue strategies.
Death and dysfunction of the projection neurons linking eye to brain. RGC-targeted assays detect functional loss before histological cell death, expanding the therapeutic window across glaucoma, axon injury, and neurodegeneration.
Acute IOP-elevation ischemia followed by reperfusion — a preclinical analogue of retinal artery occlusion and ischemic optic neuropathy. Mechanistically aligned with stroke and CNS ischemia research.
A selective RPE toxin producing reproducible, dose-dependent outer retinal degeneration — the benchmark chemical model for AMD-like geographic atrophy. Bridges retinal degeneration research with toxicology methodology.
Ischemic and hemorrhagic cerebrovascular events producing a wide spectrum of visual deficits, from homonymous hemianopia to subtle perceptual loss. Detected in 73% of acute stroke survivors and a major contributor to acquired visual disability.
Chemical, viral, and reporter-construct insults that produce defined retinal and CNS damage. The visual system serves as a sensitive, non-invasive readout for safety pharmacology beyond ophthalmology proper.
Mechanical, blast, and closed-head injury producing primary axonal damage and a delayed cascade of neuroinflammation and neurovascular disruption. Visual deficits are reported by 30–70% of survivors yet often missed by standard acuity tests.
Research Applications
Where your research goes from here.
Specific application areas, neighbouring research chapters, and open questions in this field. Our application experts cover vision science, neuroinflammation, and circuit neuroscience — tell us about your study design.