Research Applications for Striatech Products

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.
Introduction

What is Axon Degeneration?

Axon degeneration is the active, molecularly programmed self-destruction of the axon compartment – a process distinct from classical apoptosis of the neuronal soma and governed by its own intrinsic executioner machinery. The central pathway, Wallerian degeneration, is initiated when axon injury or metabolic stress tips the balance of NAD+ metabolism: the axon-protective enzyme NMNAT2 is depleted and the pro-degenerative NAD+-hydrolase SARM1 is activated, triggering a catastrophic collapse of axonal NAD+ levels and ultimately cytoskeletal disassembly. This programme operates in acute traumatic injury (optic nerve crush, peripheral nerve transection), in chronic pressure-dependent glaucoma, and in immune-mediated demyelinating diseases – making it a unifying mechanism across multiple CNS and peripheral nervous system pathologies. Secondary axon degeneration can also arise from immune effectors acting on otherwise intact axons, as occurs in progressive multiple sclerosis and related leukodystrophies where cytotoxic T lymphocytes drive axonopathy in myelin-deficient CNS tracts. This page focuses on axon degeneration as a molecular mechanism and therapeutic target – covering the SARM1/NMNAT axis, NAD+ metabolic vulnerability, axonal transport failure, and the diversity of cellular triggers that converge on the same axon self-destruction programme. While the optic nerve serves as a primary experimental model, the mechanisms discussed are broadly conserved across CNS and peripheral axons, including in spinal cord injury, motor neuron disease, and inherited axonopathies. The Optic Nerve Damage field complements this view by focusing on tissue- and anatomical-level consequences and disease classifications, rather than the molecular biology of axon self-destruction. Further related application areas: Glaucoma and Optic Nerve Neurodegeneration, Neuroinflammation and Autoimmune CNS Disease, Ocular Inflammation and Immune-Mediated Eye Disease, Rare and Inherited CNS and Eye Disorders, Retinal Degeneration and Inherited Retinal Disease, Neurodegenerative Disease, Systemic Aging and CNS Decline, Trauma and Acute Injury and Maintaining and Restoring Vision.
Vision: A Window into the brain 

Why Are Visual Endpoints Relevant in Axon Degeneration Research?

If your primary research object is peripheral axons, corticospinal tract neurons, or spinal motor axons rather than the visual system, the optic nerve offers practical advantages as an experimental window on CNS axon biology. Retinal ganglion cell (RGC) axons are long, myelinated CNS projection neurons with no peripheral nervous system component and no capacity for spontaneous regeneration – recapitulating the biology of spinal cord and supraspinal axons. The retina is optically accessible for non-invasive imaging, and the visual function driven by RGC axon integrity can be measured repeatedly, non-invasively, and quantitatively in awake freely moving rodents using the optomotor reflex. Optic nerve crush is technically simpler and more reproducible than spinal cord contusion, and SARM1-knockout or Wlds mice validated in peripheral nerve biology produce measurable functional readouts in the optic nerve system using the same genetic constructs. For researchers studying axon degeneration in ALS, hereditary spastic paraplegia, or peripheral neuropathy, the optic nerve provides a tractable CNS model in which the same molecular mechanisms can be studied alongside a direct, non-invasive, circuit-level functional endpoint.
Animal Models

What Are Common Animal Models For Axon Degeneration?

The following models are represented in the Striatech publication evidence base specifically in the context of axon degeneration mechanisms. Models present in the parent application overviews only for broader disease reasons, without cluster-specific axon mechanism evidence, are omitted.
  • Optic nerve crush (ONC) – wild-type and genetic backgrounds: The optic nerve crush model produces synchronised, reproducible acute Wallerian-like degeneration of all RGC axons distal to the crush site. In ZnT3-knockout mice (Liu et al., 2023) ONC was used to test whether presynaptic zinc release modulates post-injury axon degeneration; in Varadarajan et al. (2023) the same ONC model was used to study whether activity-dependent mechanisms in downstream brain targets promote axon regeneration. OptoDrum measured functional vision recovery at defined post-ONC time points in both studies.
  • SARM1-knockout in chronic glaucoma (bead occlusion model): Zeng et al. (2024) used a microbead occlusion model of elevated intraocular pressure in SARM1-knockout mice to directly test the Wallerian self-destruction programme in chronic pressure-dependent glaucoma. This model pairs the molecular specificity of a genetic null with the clinically relevant chronic glaucoma induction method, and OptoDrum quantified whether SARM1-pathway targeting preserves functional vision under sustained elevated IOP.
  • PLP1-deficient mouse (Pelizaeus-Merzbacher disease model): PLP1-mutant mice model the X-linked leukodystrophy Pelizaeus-Merzbacher disease and exhibit progressive secondary axon degeneration driven by dysfunctional myelin and exacerbated by cytotoxic T cell infiltration. Groh et al. (2023) and Abdelwahab et al. (2023) used this model to dissect the protective vs damaging roles of microglia and CTLs in CNS axon degeneration, with OptoDrum providing longitudinal functional tracking across disease stages.
  • Aged mouse (immunosenescence-driven axon degeneration): Groh et al. (Nat Aging, 2021) documented progressive axon degeneration in naturally aged mice associated with accumulation of cytotoxic CD8+ T cells, validated by OptoDrum visual acuity measurements across age cohorts. This model distinguishes age-driven immune-mediated axonopathy from acute injury or genetic mutation models.
  • EAE and NMOSD/MOGAD variants: Experimental autoimmune encephalomyelitis (EAE) and its NMOSD/MOGAD-specific variants (Remlinger et al., 2023) produce immune-mediated optic nerve axon degeneration through complement-dependent or T cell-dependent mechanisms. OptoDrum tracked the functional visual phenotype of each variant, distinguishing the OMR consequences of different upstream immune mechanisms acting on the same axon substrate.
  • CLN1/INCL mouse (Ppt1-knockout): The CLN1 disease mouse model (Groh et al., Brain Commun 2021) exhibits lysosomal storage-driven neuroinflammation that triggers secondary axon degeneration and visual loss. OptoDrum tracked the functional benefit of immune modulation as a treatment strategy targeting the neuroinflammatory upstream of axon degeneration.
  • Alzheimer's disease models with optic nerve amyloid: Matynia et al. (2024) and Oh et al. (2025) used AD mouse models to characterise amyloid-driven RGC axon vulnerability and functional OMR loss, addressing axon degeneration in the context of proteinopathy rather than injury or immune attack.
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 Is SARM1 and How Does the Optomotor Reflex Detect the Functional Onset of Wallerian Axon Self-Destruction?
Audience A - Vision-focused

Quick Answer

SARM1 is a TIR-domain NAD+ hydrolase that executes the intrinsic Wallerian axon self-destruction programme when axonal NMNAT2 levels fall below a critical threshold. Its activation produces a catastrophic local depletion of NAD+, triggering cytoskeletal disassembly and axon fragmentation. Genetic deletion of SARM1 or its upstream activator MKAK2 strongly delays Wallerian degeneration in multiple injury and disease models. The optomotor reflex (OMR), measured by OptoDrum, detects the functional consequence of this programme at the circuit level – reporting the integrated output of surviving RGC axons through the accessory optic system and nucleus of the optic tract without requiring cortical processing, making it sensitive to early axon loss before complete circuit failure.

The challenge

The SARM1/NMNAT2 pathway is increasingly recognised as a causal driver of axon degeneration in glaucoma, traumatic optic neuropathy, and peripheral neuropathies, and SARM1 inhibitors are in active preclinical development. A central challenge for translational studies is demonstrating that genetic or pharmacological suppression of SARM1 rescues not only axon structural integrity (as assessed by histology or OCT) but also circuit-level visual function. Structural endpoints measure axon count; functional endpoints measure whether surviving axons transmit information. Relating the two requires a sensitive, non-invasive, longitudinal functional assay that can detect partial axon loss before complete circuit failure. In glaucoma models, the slow progressive loss of RGC axons under elevated intraocular pressure further demands an endpoint with low test-retest variance to distinguish disease progression from noise across multiple time points. Additionally, because the SARM1 programme operates in RGC axons (which project to the brain via the optic nerve), the relevant functional readout is one that captures the retino-recipient pathway – a subcortical reflex-based measurement is ideally suited because it does not require corticospinal circuit integrity and can reflect partial axon loss quantitatively.

How Striatech products help

OptoDrum

Measures spatial visual acuity (cycles per degree) and contrast sensitivity threshold via the subcortical optomotor reflex in awake, unrestrained mice. In SARM1-KO glaucoma experiments, OptoDrum detects whether SARM1 pathway targeting preserves circuit-level visual output under chronic elevated IOP, providing the functional counterpart to structural RGC counts. Serial testing is possible without animal training, enabling longitudinal monitoring across disease progression.

AcuiSee

Measures visual acuity via cortical operant discrimination – complementary to OMR testing where researchers additionally need to assess cortical visual pathway integrity downstream of surviving RGC axons. AcuiSee can differentiate subcortical from cortical circuit recovery in studies combining structural axon rescue with downstream target remodelling.

Evidence from the Literature

02
How Does NAD+ Metabolism Determine the Fate of the Degenerating Axon, and What Does the Optomotor Reflex Reveal About Metabolic Rescue?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

The axon’s survival decision is controlled by the local ratio of NAD+ synthesis (NMNAT2) to NAD+ hydrolysis (SARM1). When NMNAT2 supply falls – due to axonal transport arrest, injury, or disease – SARM1 constitutively depletes local NAD+, initiating a self-amplifying collapse. Wlds (Wallerian degeneration slow) mice express a fusion protein that includes NMNAT activity in the axon compartment, replacing the transport-dependent NMNAT2 supply and dramatically delaying degeneration. NAD+ precursor supplementation (NMN, NR) or SARM1 small-molecule inhibitors can pharmacologically replicate this effect. The OMR detects the functional benefit of NAD+ metabolic rescue by measuring whether preserved axons transmit subcortical visual signals after intervention.

The challenge

NAD+-based axon protection is a field that has produced compelling structural evidence from Wlds genetics and SARM1 knockout experiments, but the translation from structural axon preservation to functional circuit recovery is not guaranteed – surviving axons must also maintain correct synaptic connectivity and transmission fidelity to produce a measurable functional benefit. Researchers targeting the NAD+ metabolic axis face the need to demonstrate functional, not merely structural, rescue. In addition, NAD+ has pleiotropic roles in neuronal metabolism beyond the SARM1 programme (mitochondrial function, PARP activation, sirtuin signalling), creating interpretive challenges when using systemic NAD+ precursor supplementation: does a functional readout improvement reflect axon preservation specifically or a broader metabolic improvement? Genetic models (SARM1-KO, Wlds) allow mechanistically cleaner experiments, and the OMR provides the circuit-level endpoint needed to determine whether genetic or pharmacological axon protection translates to functional vision.

How Striatech products help

OptoDrum

Provides repeated non-invasive visual acuity and contrast sensitivity measurements in the same animal across longitudinal treatment windows, enabling within-subject comparison of NAD+-targeted intervention effects on OMR output. Contrast sensitivity may be a more sensitive endpoint than peak acuity for detecting partial axon preservation, as it reflects the ability of surviving axons to transmit lower-contrast signals at threshold.

AcuiSee

If cortical visual processing is also an endpoint of interest (for example, in models where axon rescue is expected to preserve downstream visual cortex function), AcuiSee measures operant visual discrimination that requires intact cortical processing, providing a complementary endpoint to the subcortical OMR.

Evidence from the Literature

03
How Can Functional and Structural Endpoints Distinguish Axonal Degeneration from Somal Retinal Ganglion Cell Loss?
Audience A - Vision-focused

Quick Answer

Axon degeneration (Wallerian-like, distal-to-proximal) and somal apoptosis (retrograde, affecting the cell body first) produce different structural and temporal signatures on histology and OCT, but both ultimately reduce RGC counts and axon density. Functional endpoints – particularly the optomotor reflex – integrate the output of all surviving RGC axons through the retino-collicular pathway; they report the net functional consequence of axon loss regardless of whether it is axon-intrinsic or soma-driven. Comparing OMR trajectories to longitudinal soma counts (IHC) or nerve fibre layer thickness (OCT) allows researchers to determine whether functional deficits precede or follow structural loss, and whether a given intervention restores axon connectivity independently of soma rescue.

The challenge

A persistent interpretive problem in RGC biology is that not all RGC subtypes are equivalently vulnerable to a given injury or disease stimulus. Intrinsically photosensitive RGCs (ipRGCs), for example, are relatively preserved in several models of chronic neurodegeneration while other RGC subtypes are severely depleted. Because ipRGCs express melanopsin and contribute to circadian and pupillary responses rather than the pattern-detection optomotor reflex, their preservation does not sustain OMR output. Conversely, selective loss of the RGC subtypes that project to the nucleus of the optic tract (NOT) and superior colliculus – the drivers of the OMR – will reduce OptoDrum readouts even if total soma counts decline only modestly. This population-specific mapping of structural loss to functional output is a crucial consideration when comparing structural (IHC/OCT) and functional (OMR) endpoints in axon degeneration experiments: divergence between these measures can indicate subtype-selective vulnerability rather than instrument insensitivity. AcuiSee, which measures cortical operant discrimination, provides an additional tier sensitive to different RGC projection pathway integrity.

How Striatech products help

OptoDrum

Measures the OMR – a reflex specifically driven by RGC axon projections to the NOT and superior colliculus. Its output reports the functional integrity of retino-collicular axon connectivity, allowing researchers to track axon-level functional loss even when soma histology shows only partial degeneration. Longitudinal serial measurements allow functional onset to be timed relative to structural endpoints, distinguishing axon-first degeneration from soma-first models.

AcuiSee

Measures visual acuity via cortical operant conditioning, which depends on retino-geniculate-cortical pathway integrity. Comparing AcuiSee and OptoDrum outcomes in the same model allows inference about whether axon degeneration has differentially affected retinocollicular vs retinogeniculate projections – a distinction relevant to models where RGC subtype vulnerability is asymmetric across projection targets.

Evidence from the Literature

04
Do Different Upstream Triggers of Axon Degeneration – Trauma, Chronic Pressure, Immune Attack, and Inherited Myelin Defects – Converge on Shared Molecular Executioners?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Multiple upstream triggers can activate the same downstream axon self-destruction programme. Traumatic crush activates SARM1 acutely through NMNAT2 loss of transport; chronic elevated IOP in glaucoma activates SARM1 through sustained metabolic stress on long RGC axons; CTL-driven secondary axonopathy in demyelinating disease may activate SARM1 through disruption of axolemmal integrity and local NAD+ supply; complement-mediated NMOSD attack damages axons through a distinct antibody-dependent mechanism but still converges on cytoskeletal disassembly. The Wlds and SARM1-KO experiments demonstrate that blocking the shared executioner provides protection across multiple trigger types, supporting the idea of a universal axon degeneration checkpoint downstream of diverse pathological inputs. The OMR detects the functional output of whichever subset of triggers and mechanisms is operative in a given model, providing a common phenotypic readout across mechanistic diversity.

The challenge

Researchers designing axon-protection experiments face the question of which upstream mechanism dominates in their model and whether targeting a shared downstream executioner is sufficient when the upstream trigger is chronic or multifactorial. In EAE and demyelinating disease models, axon degeneration co-occurs with active inflammation, and suppressing SARM1 alone may not address the immune effector damage. In NMOSD, complement-dependent rapid axon damage may proceed on a timescale too fast for SARM1 programme inhibition to be protective. Distinguishing mechanism-specific from shared-executioner contributions requires model systems with defined single-mechanism triggers (ONC, genetic pressure elevation, CTL-depletion experiments) that can be cross-compared using the same functional readout. The OMR provides this shared functional denominator: the same OptoDrum protocol can be applied across ONC, glaucoma, EAE, NMOSD, PMD, HSP, and CLN1 models, enabling cross-model comparison of functional axon loss trajectories as a surrogate for comparing molecular mechanism severity.

How Striatech products help

OptoDrum

Applies the same subcortical OMR protocol across all mechanistically distinct models, enabling cross-model functional comparison. Contrast sensitivity and acuity thresholds serve as the common functional denominator across acute (ONC), chronic (glaucoma), immune-driven (EAE/NMOSD/PMD), and metabolic (CLN1/AD) axon degeneration paradigms. Serial measurements allow timeline comparison of functional onset and progression rate across mechanisms.

AcuiSee

Adds a cortical visual endpoint for models where researchers want to determine whether immune-driven axon degeneration also disrupts cortical circuit integrity (relevant to progressive MS models with cortical lesion involvement), beyond the subcortical OMR readout.

Evidence from the Literature

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

    CTL-driven axon degeneration (PLP1-mutant): Abdelwahab et al. – OptoDrum measured visual loss produced by CTL-mediated secondary axonopathy in PLP1-deficient mice.

  • Groh et al (2023) Nat Commun.

    Microglial-protective demyelination (PLP1-mutant): Groh et al. – OptoDrum quantified functional preservation in the context of controlled microglial demyelination as a protective response.

  • Groh et al (2021) Nat. Aging

    Age-related CTL accumulation: Groh et al. – OptoDrum tracked progressive immune-driven functional decline across aging cohorts.

  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.

    NMOSD/MOGAD antibody-mediated axon degeneration: Remlinger et al. – OptoDrum documented the distinct functional phenotype of antibody-driven vs T cell-driven optic nerve axon degeneration.

  • Hörner et al (2024) Thesis

    HSP corticospinal axon degeneration with visual readout: Horner et al. – OptoDrum measured visual pathway consequences of neuroinflammation-driven axon degeneration in an upper motor neuron disease model, illustrating the broader CNS axon applicability of OMR endpoints.

05
Which Pharmacological and Genetic Axon-Protective Strategies Have Demonstrated Functional Visual Rescue, and What Readouts Detect the Effect?
Audience A - Vision-focused

Quick Answer

Several orthogonal strategies have demonstrated axon protection in preclinical visual-system models: SARM1 genetic deletion (Zeng et al.), zinc transporter deletion (ZnT3-KO; Liu et al.), immune modulation targeting neuroinflammation-driven axonopathy (Groh Brain Commun 2021), and activity-dependent promotion of axon regeneration (Varadarajan et al.). In each case, OptoDrum-measured OMR provided the circuit-level functional validation that structural axon rescue translates to restored or preserved visual output. These strategies target distinct nodes in the axon-degeneration cascade: intrinsic executioner suppression (SARM1), modulation of axon-damaging presynaptic signalling (ZnT3/zinc), upstream neuroinflammation reduction (immune modulation), and post-degeneration regenerative re-growth (activity-dependent).

The challenge

A fundamental translational gap in axon protection research is the disconnect between structural rescue (counts of surviving axons, RNFL thickness, RBPMS-positive soma) and functional rescue (behavioural visual acuity, optomotor performance). Structural endpoints are necessary but not sufficient: a therapy that preserves RGC somata but fails to maintain the axon-to-target connection, or that restores axon number without restoring synaptic function, will not produce a functional benefit. Conversely, a partial functional readout improvement (for example, a 20% improvement in contrast sensitivity threshold) may not cross significance in a structural count that has high biological variance. The OMR is uniquely positioned to bridge this gap because it is a circuit-level endpoint: it reports whether surviving axons are transmitting actionable visual signals through the retino-collicular pathway, not merely surviving in histological sections. For regeneration experiments specifically, the critical question is whether re-grown axons form functional synapses with their targets – a question that only a behavioural endpoint can answer.

How Striatech products help

OptoDrum

Provides the circuit-level functional readout needed to validate axon-protective and axon-regenerative strategies beyond structural endpoints. In longitudinal treatment studies, serial OptoDrum measurements detect the functional onset of rescue effects and can establish the therapeutic window within which intervention must occur to preserve function. Non-invasive design allows the same animals to contribute both functional (OptoDrum) and structural (OCT, IHC) endpoints, improving statistical power and reducing animal numbers per experiment.

AcuiSee

Measures cortical operant visual acuity – relevant for regeneration studies where the question is whether re-grown RGC axons form functional geniculocortical connections in addition to collicular synapses. AcuiSee provides the cortical endpoint that confirms whether functional axon regeneration has reached higher visual processing centres.

Evidence from the Literature

Product Fit

Summary: Striatech Products supporting your research questions

Research Question OptoDrum AcuiSee Photorefractor ScotopicKit (with OptoDrum) DarkAdapt Non-aversive Platform
SARM1 and axon self-destruction: functional onset Yes – OMR detects circuit-level functional consequence of SARM1-driven axon loss Yes – cortical operant endpoint for downstream circuit integrity No No – axon degeneration studies use photopic OMR; scotopic extension not indicated by cluster evidence No Yes – reduces handling stress in aged or glaucomatous animals undergoing serial OMR testing
NAD+ metabolism and axon metabolic rescue Yes – serial OMR tracks functional benefit of NAD+-targeted interventions across treatment windows Yes – cortical endpoint for downstream functional rescue validation No No No Yes – facilitates longitudinal repeated-measures design in chronic models
Differentiating axonal vs somal RGC loss Yes – OMR reports retino-collicular axon projection integrity; temporal comparison with structural data distinguishes axon-first from soma-first models Yes – cortical operant endpoint sensitive to retino-geniculate pathway; comparison with OMR distinguishes projection target-specific loss No No No No
Mechanism comparison: trauma vs glaucoma vs immune-driven axon degeneration Yes – single standardised OMR protocol applicable across all mechanistically distinct models enabling cross-model functional comparison Yes – by capability; cortical complement to subcortical OMR in models with cortical involvement No No No Yes – facilitates testing of aged or post-surgical animals in longitudinal cross-model comparisons
Pharmacological and genetic axon-protective strategies Yes – circuit-level functional validation of axon-protective and axon-regenerative interventions; detects partial functional recovery not visible in structural endpoints Yes – cortical operant endpoint for regeneration studies assessing whether re-grown axons reach and form functional geniculocortical synapses No No No Yes – non-aversive design supports welfare-compliant serial testing in genetic models and aged cohorts
Measurement Modalities

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

Modality What It Measures Sensitivity to Axon-Specific Loss Longitudinal Feasibility Structural vs Functional
OptoDrum (OMR) Spatial visual acuity and contrast sensitivity via subcortical optomotor reflex (retino-collicular pathway) High for retinocollicular axon loss; integrates across surviving axon population; sensitive to partial degeneration High – serial measurement without training; 4 min per animal; daily if needed Functional (circuit output)
AcuiSee Visual acuity via cortical operant discrimination (retino-geniculate-cortical pathway) High for retinogeniculate axon loss; sensitive to cortical circuit disruption Moderate – requires initial training phase (10-14 days); session-based Functional (cortical)
OCT (retinal nerve fibre layer) RNFL thickness as a structural proxy for RGC axon number Structural – detects bulk axon loss; limited subtype resolution High – non-invasive imaging; compatible with longitudinal design Structural
Histology / IHC (RBPMS, TUNEL) RGC soma counts; axon density in nerve cross-section; apoptotic markers High for soma loss; requires tissue extraction; endpoint is terminal Low – terminal endpoint; cannot repeat in same animal Structural (terminal)
Flash VEP / Pattern ERG Electrical response of retina (ERG) or visual cortex (VEP) to patterned stimuli Moderate – pattern ERG reflects RGC function; VEP requires cortical integrity Moderate – requires anaesthesia; more invasive than OMR; repeatable Functional (electrophysiological)
Supported by Striatech Products

Publications on Axon Degeneration

Keep exploring

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

Application Area

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.

8
Research Chapters
5
FAQs answered
Main Field where Axon Degeneration is studied
Neurodegenerative Disease: Alzheimer’s, Parkinson’s and Beyond
Other relevant fields
CNS Trauma and Acute Injury: TBI, Optic Nerve Injury, Stroke
Glaucoma and Optic Nerve Neurodegeneration
Neuroinflammation and Autoimmune CNS Disease
Ocular Inflammation and Immune-Mediated Eye Disease
Rare and Inherited CNS and Eye Disorders
Restoring Vision: Gene Therapy, Optogenetics and Regeneration
Retinal Degeneration and Inherited Retinal Disease