Research Applications for Striatech Products

Aging

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.
Introduction

What is Aging?

Biological aging is not a disease in itself, but it acts as a pervasive modifier that shifts disease susceptibility thresholds, accelerates pathological progression, and narrows the window in which therapeutic interventions remain effective. In the visual system, this modifier role plays out across at least ten distinct research domains: aging accelerates intraocular-pressure-driven retinal ganglion cell (RGC) degeneration in glaucoma, compounds axial elongation and optic nerve stretch in progressive myopia, drives ciliary muscle senescence that alters refractive state, provides the immune context in which neuroinflammation and demyelinating optic nerve disease emerge, and primes the retina for amyloid and tau accumulation that mirrors CNS Alzheimer's pathology. These are not isolated aging effects – they are mechanistic overlaps in which age reshapes the landscape of each disease studied on the parent research domains. Further related applications cover:
Vision: A Window into the brain 

Why Are Visual Endpoints Relevant in Aging Research?

For researchers whose primary interest is systemic or CNS aging – rather than ophthalmology per se – visual function endpoints offer a compelling advantage: the retina and optic nerve are CNS tissue accessible without surgery, anaesthesia, or invasive sampling. The retina's transparency, its direct anatomical connection to the brain via the optic nerve, and the existence of validated, automated behavioral tests for retinal circuit output mean that visual acuity and contrast sensitivity can serve as repeated, non-invasive biomarkers of CNS aging processes that are otherwise measured only at terminal time points. Groh et al. (2021), published in Nature Aging, exemplify this principle directly: cytotoxic T cell accumulation in the aging CNS – a process of immunosenescence with implications far beyond ophthalmology – was quantified functionally through longitudinal visual acuity measurement with OptoDrum. Similarly, retinal amyloid deposition (Sheng et al., 2026, IOVS) and tau-associated visual pathway changes (Rodriguez et al., 2020, Neurobiology of Aging) have been detected via optomotor testing in AD models where retinal tissue provides a non-invasive proxy for CNS proteinopathy burden. Automated optomotor testing is the practical instrument enabling this approach: it requires no animal training, no anaesthesia, and approximately four minutes per animal, making it feasible across large longitudinal aging cohorts. For CNS aging researchers asking whether the retina can serve as a window onto brain aging, the answer from the literature collected here is: yes, and OptoDrum is the tool that makes that window quantitative.
Animal Models

What Are Common Animal Models For Aging?

The models listed here are restricted to those for which aging-specific findings are documented in the publications on this page. Models used on parent research domains for non-aging reasons are not repeated here; see the relevant parent pages for comprehensive model descriptions.
  • Aged C57BL/6 mice (12 to 24 months) – The canonical healthy aging cohort used across multiple studies on this page. Groh et al. (2021, Nat Aging) and Groh et al. (2025, Nat Neurosci) used aged C57BL/6-background mice to characterise cytotoxic T cell accumulation and microglial CX3CR1 activation respectively, with OptoDrum documenting the progressive visual acuity decline associated with these aging processes. Karg et al. (2023, Immun Ageing) used aged mice to characterise microglial neuroprotective roles in aging-associated retinal degeneration. This background is used across the aging cohort literature as the standard reference for age-dependent visual acuity baseline shifts.
  • DBA/2J mice (6 to 18 months) – A hereditary glaucoma model in which aging is the primary driver of iris disease and progressive IOP elevation, making it intrinsically an age-modified glaucoma model. The aging-glaucoma interaction is central to this strain's phenotype; Bossardet et al. (2026) and Insignares et al. (2025) provide complementary evidence for age-dependent functional visual decline in glaucoma-relevant models, and the DBA/2J is the reference model for longitudinal OptoDrum profiling across age-related IOP escalation. For a full model description, see Glaucoma and Optic Nerve Neurodegeneration.
  • APP/PS1 and related amyloid-tau Alzheimer's disease mouse cohorts (aged) – Used in Sheng et al. (2026), Matynia et al. (2024), Oh et al. (2025), and Rodriguez et al. (2020) to document aging-associated retinal and optic nerve amyloid-β accumulation, tau pathology, and differential RGC subtype vulnerability. These cohorts are studied at ages (typically 9 to 18 months) when amyloid and tau burden are maximal, and OptoDrum provides the non-invasive functional correlate of cumulative proteinopathy. For fuller neurodegenerative disease model characterisation, see Neurodegenerative Disease.
  • Senescent ciliary muscle models (aged rodents, Photorefractor endpoint) – Gao et al. (2024a) used aged mice with oxidative-toxicity-induced ciliary muscle senescence as a model for presbyopia-like refractive change. The Photorefractor measured refractive state (diopters) to document the functional consequences of ciliary senescence and the refractive-preserving effects of lutein. This is the primary evidence for a Photorefractor endpoint in aging-related accommodative and refractive biology on this page.
  • Soluble guanylate cyclase (sGC) deficiency mice (aged progression cohorts) – Bossardet et al. (2026) characterised this model across aging time points, demonstrating that sGC pathway disruption produces an age-accelerated glaucoma-like trajectory with progressive OptoDrum-measurable visual decline. The age-dependent progression trajectory makes this model a mechanistic case study in gene-environment-age interaction in glaucoma. For full model characterisation, see Glaucoma and Optic Nerve Neurodegeneration.
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 Does Aging Modify Disease Susceptibility and Functional Trajectories in Glaucoma and Optic Nerve Disease?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Chronological aging acts as an independent risk multiplier in glaucoma and optic nerve disease: it accelerates RGC loss at any given level of intraocular pressure, narrows the IOP threshold below which RGC degeneration can be avoided, and amplifies the functional visual acuity decline detectable by OptoDrum. In genetic models with age-dependent phenotype onset, aging is the disease clock. OSK epigenetic reprogramming can partially reverse this age-related RGC vulnerability, with OptoDrum as the readout.

The challenge

Most preclinical glaucoma studies use young adult animals (2 to 4 months) where the aging co-variable is absent or minimal. Yet the overwhelming clinical burden of glaucoma falls in patients aged 60 and above, in whom aging-associated changes – mitochondrial dysfunction in RGC soma, epigenetic drift in RGC chromatin, reduced axon transport capacity, microglial senescence, and altered trabecular meshwork physiology – combine with elevated IOP to produce neurodegeneration at rates far exceeding those in young animals. Mapping the functional trajectory of this age-IOP interaction requires longitudinal functional data across age cohorts, not single-time-point histology. The key question for this research area is distinct from what the parent Glaucoma and Optic Nerve Neurodegeneration page addresses broadly: here the question is specifically how much does aging shift the functional outcome, and can that shift be measured and reversed?

The age-glaucoma interaction is also a frequent topic of interest for the Glaucoma and Optic Nerve Neurodegeneration research community, where aging-glaucoma interaction is among the most searched mechanistic angles. For RGC-specific vulnerability in aging, including age-related shifts in RGC subtype sensitivity, see also the RGC Pathology content within Retinal Degeneration and Inherited Retinal Disease.

How Striatech products help

OptoDrum

Measures photopic spatial visual acuity (cycles per degree) and contrast sensitivity via the subcortical optomotor reflex in awake, freely moving mice and rats. Enables longitudinal profiling of visual acuity across aging cohorts (monthly time points from 3 to 18+ months), detecting age-dependent baseline shifts, disease-accelerated declines, and post-treatment recovery. Each eye is assessed independently; no training or anaesthesia required; test duration approximately 4 minutes per animal.

AcuiSee

Measures visual acuity and contrast sensitivity via a cortical operant forced-choice paradigm. Appropriate when the research question requires assessment of suprathreshold visual perception or cognitive dimensions of visual function – for example, whether age-related RGC loss that spares the optomotor reflex nonetheless impairs cortical visual processing and visual discrimination. Note that AcuiSee requires a training phase of 10 to 14 days; aged animals may require adapted training protocols.

Non-aversive Animal Platform

Allows animals to voluntarily enter the OptoDrum testing environment from their home cage via a tunnel-lid design. Particularly relevant for aged cohorts: older mice have reduced locomotor activity and elevated stress responses, and minimising handling stress reduces test-to-test variability and welfare concerns in long-duration aging studies spanning 12 to 24 months.

Evidence from the Literature

  • Kinuthia et al (2025) JCI Insight.
  • Bossardet et al (2026) Sci Rep.

    Used OptoDrum to track progressive visual acuity decline across aging time points in sGC-deficient mice, demonstrating that NO-cGMP pathway disruption produces an age-accelerated glaucoma-like trajectory.

  • Insignares et al (2025) Int J Mol Sci.

    Characterised age-dependent progressive axial elongation with secondary optic nerve damage and RGC dysfunction in a model spanning glaucoma, myopia, and rare inherited eye disease. OptoDrum documented visual acuity decline as the functional correlate of these compounding age-dependent structural changes.

  • Karg et al (2023) Cell Reprogram.
    Journal Club →

    Demonstrated that AAV-OSK epigenetic reprogramming achieves sustained visual recovery in aged glaucoma-model mice. OptoDrum measured the magnitude and durability of functional recovery, establishing that aging-related epigenetic drift is both a disease driver and a reversible therapeutic target.

02
How Does Immunosenescence and Age-Related Neuroinflammation Compound Visual Pathway Damage Across Disease Contexts?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

The aging immune system accumulates cytotoxic T cells in CNS white matter and undergoes microglial phenotypic shifts (including CX3CR1 dysregulation) that collectively amplify neuroinflammation and axon degeneration in the visual pathway. These immunosenescence-driven mechanisms operate independently of – and additively with – primary disease triggers such as IOP elevation or amyloid deposition. OptoDrum has been used in landmark studies to document the resulting functional visual acuity decline as a biomarker of this immune-aging interface.

The challenge

Neuroinflammation research in the visual system typically examines young adult animals or acute inflammatory challenges. The immunosenescence context – in which the aging immune environment actively promotes chronic, low-grade CNS inflammation even in the absence of acute injury – is a distinct mechanistic regime requiring aged cohorts and longitudinal functional tracking. The questions are also different: not “does neuroinflammation cause visual loss?” (addressed on the parent Neuroinflammation and Autoimmune CNS Disease page) but rather “does the aging immune environment produce neuroinflammation-driven visual loss even without a superimposed acute inflammatory trigger, and is the pathway targeting innate or adaptive immune senescence?” The dual microglia story further complicates experimental design: Karg et al. (2023, Immun Ageing) demonstrated that microglia are neuroprotective in aging-associated retinal degeneration at baseline, while Groh et al. (2025, Nat Neurosci) showed that CX3CR1-mediated microglial activation drives optic nerve demyelination in an aging context. Longitudinal OptoDrum tracking across these experimental conditions is what separates protective from pathological microglial aging states at the functional level.

How Striatech products help

OptoDrum

Provides non-invasive, weekly or monthly visual acuity and contrast sensitivity measurements in aged cohorts undergoing immunosenescence. Longitudinal data from OptoDrum can distinguish: (1) baseline age-related acuity decline in control animals, (2) accelerated decline in animals with superimposed neuroinflammatory burden, and (3) recovery or stabilisation following immune-targeted interventions. Subcortical endpoint is appropriate for studies of optic nerve demyelination, axon degeneration, and RGC loss – all outputs of the immunosenescence cascade.

AcuiSee

Complements OptoDrum for studies that also wish to assess whether age-related immune-driven CNS changes impair cortical visual processing beyond what the optomotor reflex captures. Particularly relevant in studies modelling the intersection of immunosenescence and cognitive aging, where cortical visual endpoints may diverge from subcortical ones.

Non-aversive Animal Platform

Reduces handling-related stress variability in aged cohorts, which is especially important in immunosenescence studies where glucocorticoid stress responses interact with immune function. Voluntary entry from home cage minimises confounds in aged animals with altered stress physiology.

Evidence from the Literature

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

    Cytotoxic CD8+ T cells accumulate in aging CNS white matter and drive age-related axon degeneration and visual pathway decline. OptoDrum documented progressive visual acuity loss as the functional biomarker of this immunosenescence-driven process across aging cohorts.

  • Groh et al (2025) Nat Neurosci.
    Journal Club →
    Feature →

    Demonstrates that microglial CX3CR1 activation in aged animals orchestrates optic nerve demyelination and RGC death. OptoDrum confirmed the functional visual circuit consequences, linking a specific aging-activated glial signalling pathway to measurable optomotor acuity loss. Directly extends Groh et al. (2021) to the glial mechanism downstream of T cell-driven inflammatory priming.

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

    OptoDrum tracked visual acuity longitudinally to correlate microglial functional states with visual outcomes, establishing that microglial aging involves context-dependent dual roles (neuroprotective at baseline, potentially pathological when dysregulated).

03
Can the Aging Retina and Optic Nerve Serve as a Non-Invasive Window onto CNS Neurodegeneration in Alzheimer's Disease Models?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Yes. Retinal amyloid-β accumulation, optic nerve amyloid deposition, tau-associated visual pathway changes, and differential RGC subtype vulnerability are all detectable in aged Alzheimer’s disease mouse models, and OptoDrum provides the non-invasive functional correlate – visual acuity and contrast sensitivity – that bridges structural amyloid and tau burden to circuit-level output. For CNS aging researchers, this means the retina is not merely an ophthalmic endpoint: it is a spatially and functionally accessible piece of CNS tissue that reports on the same proteinopathy burden driving cognitive decline.

The challenge

CNS aging researchers studying Alzheimer’s disease typically quantify brain amyloid load by immunostaining at terminal time points, or by PET imaging in clinical studies. Non-invasive longitudinal biomarkers of amyloid and tau burden in small-animal models are scarce. The retina has attracted attention as a potential biomarker tissue – retinal amyloid can be visualised by fundus fluorescence imaging and OCT – but the functional correlate of retinal amyloid burden (i.e., what visual circuit output does accumulated amyloid impair, and by how much?) is rarely addressed. The publications here directly fill this gap: Sheng et al. (2026) link retinal amyloid clearance to OptoDrum-measurable visual acuity, Oh et al. (2025) extend the amyloid story to the optic nerve specifically, Matynia et al. (2024) provide RGC subtype granularity (which cell populations drive the optomotor signal in aged AD models), and Rodriguez et al. (2020) establish the tau-optomotor connection. Together they build the evidentiary basis for OptoDrum visual acuity as a functional correlate of CNS proteinopathy in aged rodents. This angle is distinct from – and not duplicated by – the parent Systemic Aging and CNS Decline page’s treatment of these studies as biomarker evidence within a broader aging context, or from the Neurodegenerative Disease page’s focus on disease mechanism rather than aging as the modifier.

How Striatech products help

OptoDrum

Measures spatial visual acuity (cycles per degree) and contrast sensitivity via the subcortical optomotor reflex in awake, freely moving mice. In aged AD model cohorts, OptoDrum provides a repeated non-invasive functional correlate of retinal and optic nerve proteinopathy burden, enabling correlation of structural amyloid and tau measurements with circuit-level functional output across aging time points. No training, no anaesthesia, no surgical access required.

AcuiSee

Measures cortical visual processing via an operant forced-choice paradigm. Appropriate for AD aging studies that also wish to assess whether proteinopathy impairs cortical visual discrimination and perception beyond what the subcortical optomotor reflex captures – for example, studies examining the visual cortex in parallel with retinal amyloid imaging. Note: AcuiSee measures a cortical endpoint; cortical visual plasticity changes documented in the literature (e.g., Rodriguez et al., 2020) are within AcuiSee’s scope, not OptoDrum’s.

DarkAdapt

Provides controlled dark adaptation for aged rodents prior to scotopic (dark-adapted) optomotor testing with the ScotopicKit. In AD aging models, dark-adapted contrast sensitivity may detect rod pathway dysfunction earlier than photopic measurements, since rods are reported to be more vulnerable in early AMD and aging-associated outer retinal degeneration.

Non-aversive Animal Platform

Minimises handling stress in aged AD-model cohorts. Cognitive dysfunction in AD models may interact with handling-induced anxiety, confounding behavioral measurements; voluntary entry from home cage reduces this confound in long-duration aging studies.

Evidence from the Literature

04
How Does Ciliary Muscle Senescence Affect Refractive State, and Can Age-Related Refractive Shifts Be Detected by the Photorefractor?
Audience A - Vision-focused

Quick Answer

Aging-associated cellular senescence in the ciliary muscle – driven by oxidative stress and cumulative DNA damage – impairs the accommodative mechanism and produces measurable refractive shifts in rodents. The Striatech Photorefractor detects these shifts as changes in spherical equivalent (diopters), providing a quantitative in vivo readout of ciliary aging. Lutein supplementation has been shown to protect senescent ciliary muscle cells and preserve refractive state in this model.

The challenge

Presbyopia – the progressive loss of accommodative amplitude with age – is the most universal age-related visual change in humans, affecting virtually all individuals by their fifth decade. In rodents, the accommodative mechanism differs anatomically, but ciliary muscle senescence produces detectable refractive changes that serve as a functional proxy. Establishing that these changes are measurable non-invasively by photorefraction, and that they can be modified by nutritional or pharmacological interventions, is relevant both to understanding age-related refractive biology and to screening compounds with cytoprotective effects on ciliary tissue. This question is distinct from the age-related refractive progression discussed on the Myopia, Refractive Development, and Eye Growth page, which focuses on axial growth mechanisms; here the mechanism is ciliary senescence rather than axial elongation. The Photorefractor measures diopters only – specifically the refractive state of the eye – and is not used to assess visual acuity or optic nerve integrity.

How Striatech products help

Photorefractor

Measures the spherical equivalent refractive state of the rodent eye (diopters) non-invasively using photoretinoscopy. In aging models with ciliary muscle senescence, provides a quantitative readout of accommodative-tone-related refractive change. Enables detection of age-related refractive shifts and their modulation by cytoprotective interventions. Measures diopters only; does not assess visual acuity or contrast sensitivity.

Keratometer

Measures corneal surface curvature. In aging models where corneal shape changes are a potential confound for refractive interpretation (e.g., secondary to changes in scleral or limbal mechanics with age), Keratometer data can separate corneal from non-corneal contributions to refractive state. Measures curvature only.

Non-aversive Animal Platform

Enables low-stress voluntary positioning for photorefraction and keratometry measurements in aged animals. Reduces measurement variability from handling-induced locomotor arousal, which is particularly relevant for aged animals where stress responses may be exaggerated and repeated measurements over months require stable baseline conditions.

Evidence from the Literature

05
Does Biological Aging Narrow the Therapeutic Window for Vision Rescue, and Can Epigenetic Reprogramming Reopen It?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Aging reduces the efficacy of neuroprotective and regenerative interventions in the visual pathway: RGCs in aged animals show reduced axon regeneration capacity, greater baseline epigenetic drift, more depleted mitochondrial reserve, and a more inflammatory retinal environment. OSK epigenetic reprogramming directly targets aging-related epigenetic drift in RGCs and has achieved sustained visual recovery in aged glaucoma-model mice, as measured by OptoDrum – providing proof-of-concept that the aging therapeutic window can be re-expanded rather than merely managed around.

The challenge

A fundamental and largely unresolved question in translational vision research is whether neuroprotective and regenerative strategies validated in young adult animal models retain efficacy when applied in aged animals – the population most relevant to clinical glaucoma, AMD, and Alzheimer’s-associated retinal degeneration. The therapeutic window question operates on two levels: (1) does aging worsen baseline RGC vulnerability such that more cells are lost before treatment is initiated? (2) does aging reduce intrinsic RGC regenerative and survival capacity such that treatments that work at 2 months fail at 12 months? The OSK gene therapy result (Karg et al., 2023) addresses both by targeting the epigenetic mechanism of aging itself rather than a downstream consequence, and demonstrating sustained functional recovery in aged animals. OptoDrum is what makes this question answerable in living animals: without a non-invasive, longitudinal functional readout, the question of whether rescue efficacy declines with age would require separate terminal cohorts at each time point rather than within-animal tracking. This angle is distinct from the therapeutic restoration content on the parent Maintaining and Restoring Vision page, which covers therapeutic modalities broadly; here the focus is specifically on age as a modulator of whether rescue works.

How Striatech products help

OptoDrum

Measures visual acuity (cycles per degree) and contrast sensitivity longitudinally in aged animals before, during, and after therapeutic intervention. Enables within-animal comparison of pre-treatment baseline, post-injury decline, and post-treatment recovery – critical for detecting partial or transient rescue effects in aged cohorts where baseline drift and disease progression are simultaneously occurring. Subcortical endpoint is directly relevant for RGC-targeting and optic nerve interventions.

AcuiSee

Provides a cortical operant visual function endpoint complementary to OptoDrum for therapeutic window studies in which cortical-level integration of the visual signal is specifically targeted (e.g., cortical gene therapies, cortical neurotrophic factor delivery). Absence of a training-free measurement makes it less suited to aged animals unless a pre-training period is factored into study design.

Non-aversive Animal Platform

Enables voluntary, low-stress OptoDrum measurements in aged animals across the full duration of therapeutic trials spanning 6 to 18 months. Reduces cumulative handling-related stress, which is a confound in therapeutic studies where treatment effects on immune and inflammatory pathways may interact with stress physiology.

Evidence from the Literature

  • Kinuthia et al (2025) JCI Insight.
  • Karg et al (2023) Cell Reprogram.
    Journal Club →

    Demonstrated sustained visual recovery following AAV-mediated OSK (Oct4, Sox2, Klf4) epigenetic reprogramming in both aged mice and glaucomatous eyes. OptoDrum measured the magnitude and durability of visual acuity recovery, establishing that reversal of RGC epigenetic aging drift produces functional – not merely structural – rescue detectable non-invasively.

Product Fit

Summary: Striatech Products supporting your research questions

Research Question OptoDrum ScotopicKit AcuiSee Photorefractor Keratometer DarkAdapt Non-aversive platform
Longitudinal acuity tracking in aged glaucoma cohorts Yes Yes
Age-dependent baseline acuity shifts (photopic) Yes Yes
Age-dependent baseline acuity shifts (scotopic, rod pathway) Yes Yes Yes
Cortical visual function and discrimination in aging/AD models Yes
Ciliary senescence and age-related refractive shifts Yes Yes Yes
Immunosenescence-driven neuroinflammation and visual decline Yes Yes
Retinal and optic nerve amyloid / tau as CNS aging biomarker Yes Yes Yes
Therapeutic window and rescue efficacy in aged animals Yes Yes Yes
Dark adaptation for aged scotopic testing Yes
Measurement Modalities

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

Modality What It Measures Suitability for Aged Cohorts Key Limitation in Aging Studies
OptoDrum (optomotor reflex) Photopic spatial acuity and contrast sensitivity; subcortical retino-brainstem circuit High: no training, no anaesthesia, 4-minute sessions; no age-related compliance decline Does not capture cortical or cognitive dimensions of visual aging; subcortical circuit only
ScotopicKit + DarkAdapt Scotopic (rod-mediated) spatial acuity and contrast sensitivity after dark adaptation High: same advantages as OptoDrum; DarkAdapt controls the dark-adaptation variable Requires DarkAdapt dark-adaptation period prior to testing; test room must be maintained in darkness
AcuiSee (operant cortical) Suprathreshold visual acuity and discrimination; cortical visual processing Moderate: requires 10-14 day training phase; aged animals may need adapted protocols Training duration and cognitive requirements may introduce confounds in aged or cognitively impaired animals
Electroretinography (ERG) Rod and cone photoreceptor responses; Muller cell (b-wave) integrity Moderate: anaesthesia required; pupil dilation required; age-related anaesthesia risk Requires anaesthesia; single or limited time points practical; photoreceptor-level only
Visual evoked potentials (VEP) Cortical visual pathway integrity Low to moderate: electrode implantation or transcranial recording; anaesthesia often required Invasive; single or limited time points; technical expertise requirements high in aged cohorts
Optical coherence tomography (OCT) Structural: retinal layer thickness, optic nerve head morphology Moderate: anaesthesia typically required; excellent structural resolution Structural only; does not provide circuit-level functional output; does not detect subclinical functional decline
Photorefractor Refractive state (spherical equivalent, diopters) High: non-invasive, rapid; relevant specifically to ciliary senescence and presbyopia models Measures optics only; does not assess visual acuity, contrast sensitivity, or neural pathway integrity
Supported by Striatech Products

Publications on Aging

Great Research, Interactive

Journal Clubs related to Aging

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: 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: Aging and Injured Retinal Ganglion Cells Can Be Rejuvenated by Epigenetic Reprogramming”
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Thursday, 27 Feb 2025

Journal Club: Aging and Injured Retinal Ganglion Cells Can Be Rejuvenated by Epigenetic Reprogramming

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Bruce R. Ksander, Ph.D. - Schepens Eye Institute of Mass Eye & Ear, Harvard Medical School, Department of Ophthalmology
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This Journal Club highlights groundbreaking work by Harvard Medical School scientist Bruce R. Ksander and his team. They were able to reverse aging in retinal ganglion cells, improving visual function after injury or in disease.
Featured image for “Journal Club: Visual Function with Aging in Normal and Alzheimer’s Disease Model Mice”
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Thursday, 11 Jul 2024

Journal Club: Visual Function with Aging in Normal and Alzheimer’s Disease Model Mice

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Anna Matynia, Ph.D. - University of Houston College of Optometry
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This Journal Club highlights the conservation of rod, cone, and melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs) between mice and humans, facilitating the translation of visual function studies to clinical settings. It examines early degeneration of ipRGCs in Alzheimer’s models and human post-mortem retinas, and discusses how non-invasive assessments of visual acuity, contrast sensitivity, and pupillary light reflex in both species may serve as early biomarkers for Alzheimer’s Disease. Visual acuity and contrast sensitivity measurements were conducted using Striatech’s OptoDrum.
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.
Keep exploring

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

Application Area

Aging

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.

6
Research Chapters
5
FAQs answered
Main Field where Aging is studied
Systemic Aging and CNS decline
Other relevant fields
Glaucoma and Optic Nerve Neurodegeneration
Maintaining and Restoring Vision
Neurodegenerative Disease: Alzheimer’s, Parkinson’s and Beyond
Neuroinflammation and Autoimmune CNS Disease
Ocular and CNS Toxicity Models