Stargardt Disease

Stargardt disease belongs to a group of conditions called inherited retinal dystrophies (IRDs)—progressive genetic conditions in which mutations cause the gradual degeneration of the photoreceptors (the light-sensing cells of the retina) and/or the retinal pigment epithelium (RPE), the supportive cell layer directly beneath the photoreceptors. Inherited retinal dystrophies range widely in severity, from mild central vision loss to complete blindness, and genetic testing is available for many forms. Stargardt disease is the most common and well-studied of all the inherited macular dystrophies.

Stargardt macular dystrophy—also known simply as Stargardt disease, STGD, or STGD1 for the most common form—is a progressive hereditary condition in which the central part of the retina, called the macula, gradually deteriorates due to the toxic accumulation of fatty waste products in the RPE cells. It is named after Karl Stargardt, the German ophthalmologist who first described it in 1909. An older alternate name, fundus flavimaculatus (from the Latin for “yellowish spots on the fundus”), was historically used for the same disease spectrum, based on the characteristic yellow-white spots visible on the retina during eye examination. Stargardt disease is the most prevalent inherited macular dystrophy and one of the most common causes of inherited visual impairment in both children and young adults.

Stargardt disease affects approximately 1 in 8,000 to 10,000 people—roughly 8 to 10 per 100,000 persons—making it a relatively rare but clinically significant condition. The condition progresses slowly and irreversibly, with no spontaneous remission. A critically important feature of the typical form of Stargardt disease is that peripheral (side) vision is preserved throughout the disease course, and night blindness is not a typical feature. Central vision—used for reading, recognizing faces, and seeing fine detail—is what is progressively lost. Prognosis varies by the age at which symptoms begin: patients with onset before age 20 are more likely to reach legal blindness (vision of 20/200 or worse) over their lifetime, while those with onset after age 20 are more likely to maintain functional vision above the legal blindness threshold. In one well-studied patient group, the median time from symptom onset to legal blindness was 25 years—a slow progression that spans decades. There is currently no U.S. Food and Drug Administration (FDA)-approved disease-modifying treatment, but Stargardt disease has the most active clinical trial pipeline of any inherited retinal disease globally, with gene therapy, cell therapy, and several pharmacological agents now in advanced human trials.

Physicians classify Stargardt disease by the gene causing it, the age at which symptoms begin, the pattern of electrical responses on specialized eye tests (electroretinogram—ERG classification), and the appearance of the retina on imaging (Fishman staging). The gene-based classification identifies biologically distinct subtypes with different inheritance patterns, while the age-of-onset classification best predicts how the disease will progress.
By gene and inheritance pattern, four main forms are recognized:

• STGD1 (ABCA4 gene, autosomal recessive): the most common form, accounting for the great majority of all Stargardt cases. It is caused by mutations in the ABCA4 gene, which encodes a protein that transports toxic retinoid byproducts out of photoreceptor cells. Both copies of the ABCA4 gene must be abnormal to cause disease (recessive inheritance). Each parent of an affected child is typically an unaffected carrier. The carrier frequency in the general population is approximately 1 in 20, making this gene one of the most commonly mutated in all of ophthalmology.
• STGD3 (ELOVL4 gene, autosomal dominant): a rare Stargardt-like form caused by mutations in a gene that produces a fatty acid enzyme essential for photoreceptor function. Only one abnormal copy of the gene is needed to cause disease. A key distinguishing feature on fluorescein angiography is that STGD3 lacks the “dark choroid sign” that is characteristic of STGD1.
• STGD4 (PROM1 gene, autosomal dominant): STGD4 is a very rare Stargardt-like macular dystrophy caused by mutations in prominin-1, a protein on the surface of photoreceptor outer segments important for normal disc formation.
• PRPH2-associated Stargardt-like dystrophy (autosomal dominant): Mutations in the peripherin-2 gene cause a similar macular dystrophy that can be distinguished from STGD1 by imaging features, including the absence of characteristic peripapillary sparing on autofluorescence imaging.

By age of onset—the most clinically useful guide to prognosis—three groups are recognized:

• Early-onset STGD1 (symptoms beginning at age 10 or younger): the most severe subtype. Vision decline can begin before any retinal changes are visible on examination. Patients are often visually impaired by their teenage years. Classic pisciform (fish-shaped) retinal flecks may be absent early in this group.
• Intermediate-onset STGD1 (symptoms beginning between ages 11 and 45): the classic form most commonly described in medical textbooks. Progressive central vision loss develops alongside the appearance of characteristic yellow-white retinal flecks over years to decades.
• Late-onset STGD1 (symptoms beginning at age 45 or older): the mildest form. Central visual acuity may be preserved for years to decades after symptoms begin. This form is frequently misdiagnosed as age-related macular degeneration (AMD) because of the patient’s age at presentation, and it is significantly underdiagnosed in clinical practice.

By electrophysiological testing (Lois ERG classification), three groups reflect the extent of retinal involvement beyond the macula. Group 1 has dysfunction limited to the macula with a normal full-field ERG—the best prognosis. Group 2 shows additional generalized cone involvement—intermediate prognosis, with 47% progressing to Group 3 over time. Group 3 has both cone and rod involvement throughout the retina—the worst prognosis, with 100% showing significant electrophysiological deterioration on long-term follow-up.

Stargardt disease is caused by inherited genetic mutations that disrupt the normal recycling of vitamin A (retinoid recycling) within the photoreceptors and the retinal pigment epithelium. When this recycling process fails, toxic fatty waste products accumulate progressively in the RPE cells, eventually destroying them and causing the secondary death of the overlying photoreceptors.

In STGD1—the most common form—the affected protein is ABCA4, a transporter that sits at the rim of the membrane discs inside rod and cone photoreceptors. After each cycle of light detection, the visual pigment in photoreceptors releases a byproduct called all-trans retinal. In a normal eye, ABCA4 transports this byproduct safely out of the disc interior so it can be recycled back into functional visual pigment by the RPE. When ABCA4 is absent or dysfunctional, all-trans retinal accumulates inside the disc. It chemically combines with other molecules to form a toxic compound called A2E—a component of lipofuscin, the “wear-and-tear” pigment that RPE cells cannot break down. Over years and decades, A2E accumulates in RPE lysosomes (the cell’s waste-disposal system), generates damaging reactive oxygen species, triggers an abnormal immune (complement) response, and ultimately causes RPE cell death. When RPE cells die, the photoreceptors above them—which depend on the RPE for oxygen, nutrition, and daily maintenance—follow in progressive cell death. The result is the expanding zone of central macular atrophy that defines Stargardt disease. How severe the disease is and when it begins depends on the specific ABCA4 mutations present: patients with two complete loss-of-function mutations have the earliest and most severe disease, while those with milder missense mutations (which produce some partially working protein) tend to develop symptoms later in life.

Two environmental factors can influence the rate of this toxic accumulation. High-dose vitamin A supplementation provides more substrate for the toxic A2E-forming reaction, potentially accelerating damage—for this reason, high-dose vitamin A supplements are specifically contraindicated in Stargardt disease. Bright light and ultraviolet exposure increase phototoxic stress on the RPE, and avoidance of prolonged intense light is widely recommended. In STGD3, the mechanism is different: mutations in the ELOVL4 enzyme deplete the retina of very long chain fatty acids that photoreceptors need to maintain their outer segment structure. The mutant ELOVL4 protein also exerts a dominant negative effect—it pulls the normal protein out of its correct location in the cell, amplifying the functional loss.

Stargardt disease is a genetic condition. The primary risk factors are genetic, and there is currently no way to reduce the underlying biological risk of inheriting the disease.

• Biallelic pathogenic ABCA4 mutations (STGD1): Having two copies of a disease-causing ABCA4 mutation is the necessary and sufficient cause of STGD1. When both parents are carriers, each child has a 25% chance of inheriting both mutations and developing the disease. The ABCA4 carrier frequency is approximately 1 in 20 in the general population, making carrier couples more common than might be expected.
• Heterozygous ELOVL4 truncating mutations (STGD3): This is autosomal dominant; each child of an affected parent has a 50% chance of inheriting the mutation and developing disease.
• Heterozygous PROM1 mutations (STGD4): This is autosomal dominant; 50% transmission risk per child.
  Two null (complete loss-of-function) ABCA4 alleles: associated with the earliest disease onset (before age 10), the most severe course, and the fastest rate of retinal atrophy progression. These individuals are at highest risk for legal blindness at a young age.
• Early age of onset (before 20 years): the strongest clinical predictor of eventually reaching legal blindness. Patients with symptom onset before age 20 are significantly more likely to reach vision of 20/200 or worse over their lifetime compared to those with later onset.
• FAF Type 3 baseline pattern (multifocal atrophy): a finding on fundus autofluorescence imaging indicating multiple areas of RPE cell loss at baseline, associated with the fastest disease progression regardless of visual acuity. Eyes with this pattern show atrophy growth of approximately 4.37 mm² per year versus only 0.06 mm² per year in the mildest pattern.
• Larger baseline atrophic lesion area: Larger atrophic areas at diagnosis expand faster than smaller ones.
• Family history and consanguinity: Siblings of affected individuals have a 25% recurrence risk (assuming both parents are ABCA4 carriers). Consanguineous families have higher rates of STGD1.
• Excessive ultraviolet (UV) and bright light exposure: may accelerate lipofuscin accumulation based on animal model data. Patients are advised to use UV-blocking eyewear.
• High-dose vitamin A supplementation: This provides an additional substrate for the toxic A2E-forming reaction; patients should avoid vitamin A supplements and high-dose multivitamins containing vitamin A.

There is no population-wide screening program for Stargardt disease. Screening is targeted to individuals with a known family history or clinical suspicion based on symptoms. Siblings and children of known STGD1 patients should receive a baseline comprehensive ophthalmological evaluation, including fundus autofluorescence imaging and optical coherence tomography (OCT), which can detect subtle structural changes before any drop in visual acuity. Genetic testing—using next-generation sequencing of the full ABCA4 gene and other relevant inherited retinal disease genes—is recommended for all confirmed patients and their first-degree family members. Once a causative mutation is identified in the family, targeted carrier testing is available for relatives considering family planning. The earliest detectable structural change on OCT imaging—thickening of the external limiting membrane—has been identified in genetically confirmed children as young as 5 years of age, before any visual symptoms or visible retinal changes appear, underscoring the value of surveillance in at-risk children.

Stargardt disease is a genetic condition and cannot be prevented. However, the following evidence-based steps may slow disease progression or reduce the impact of modifiable risk:

• Avoid high-dose vitamin A supplements: Patients should specifically avoid supplements containing vitamin A and should not take Age-Related Eye Disease Study (AREDS)-formula vitamins (used for age-related macular degeneration), as the vitamin A components can accelerate toxic A2E formation in ABCA4-mutant eyes.
• Wear UV-blocking sunglasses outdoors: UVA- and UVB-blocking wraparound sunglasses with lateral shields are strongly recommended for daily use to reduce phototoxic stress on the macula.
• Reduce prolonged bright light exposure: While evidence is primarily from animal studies, avoidance of sustained intense light is a widely recommended precaution.
• Genetic counseling for family planning: Couples in which both partners carry ABCA4 mutations face a 25% chance with each pregnancy of having an affected child. Preconception genetic counseling clarifies the risk and reviews reproductive options.
• Stop smoking: General evidence supporting retinal health supports smoking cessation, though Stargardt-specific human data are limited.

The most characteristic symptom of Stargardt disease is progressive bilateral loss of central vision—the ability to see fine detail directly ahead for tasks such as reading, recognizing faces, and seeing color. This central vision loss occurs gradually and symmetrically in both eyes, caused by the progressive destruction of macular photoreceptors and the underlying RPE. Peripheral (side) vision is typically preserved throughout the disease course, and patients do not typically experience night blindness—features that distinguish Stargardt disease from retinitis pigmentosa and many other inherited retinal conditions. The common primary symptoms include:

• Reduced central visual acuity: gradual decrease in the sharpness of straight-ahead vision, most often first noticed as difficulty reading, seeing a computer screen, or recognizing faces at a distance. The decline is slow—measured in terms of decades—but cumulative and irreversible.
• Central blind spot (central scotoma): an area of missing, darkened, or blurred vision at the center of the visual field. As the scotoma enlarges, patients unconsciously adopt a strategy of looking slightly to the side of a target—using a peripheral retinal area called the preferred retinal locus (PRL)—rather than looking directly at it. Each additional degree of eccentricity of the PRL from the center corresponds to approximately a 2.3-letter loss in best-corrected visual acuity.
• Difficulty with color discrimination (dyschromatopsia): This is an impaired ability to distinguish between colors, particularly similar shades; present in most patients and detectable with standardized color vision testing.
• Delayed dark adaptation: slower-than-normal adjustment when moving from bright to dim environments. This becomes particularly noticeable as the disease progresses to intermediate and advanced stages.
• Photophobia and glare sensitivity: This is increased discomfort or difficulty seeing in bright light conditions; a common and often early complaint that can be partially managed with tinted lenses.
• Distorted central vision (metamorphopsia): Straight lines may appear wavy or bent when viewed centrally, caused by disruption of the photoreceptor arrangement at the macula.
• Difficulty reading: This is one of the earliest and most functionally disabling symptoms; central scotoma and reduced acuity combine to make sustained reading progressively more challenging.

On eye examination, the ophthalmologist looks for specific signs that confirm the diagnosis. The most characteristic finding is the presence of yellow-white pisciform (fish-shaped or spindle-shaped) flecks at the level of the RPE, spread across the macula and sometimes extending further. These flecks represent lipofuscin-laden RPE cells and are the pathognomonic (disease-defining) sign of Stargardt disease. The macula itself may have a “beaten bronze,” “beaten metal,” or “snail-slime” mottled appearance from abnormal RPE pigmentation. It is important to know that up to one-third of children with early-onset STGD1 do NOT show visible flecks at their initial presentation—flecks develop over time as the disease progresses, and their absence should not rule out the diagnosis in a child with an appropriate history and ERG findings.

• In children with early-onset disease (symptoms beginning before age 10): Vision decline may begin before any visible retinal changes can be detected on examination. Children may have difficulty seeing the classroom board, reading printed text, or recognizing faces. School performance may suffer. Parents are often the first to notice that something is wrong before any specific diagnosis is made.
• In young adults with intermediate-onset disease (symptoms beginning between ages 11 and 45): Central vision loss becomes gradually but meaningfully functionally impaired during these prime working and learning years. Loss of driving ability typically occurs during this phase. The characteristic yellow-white flecks are visible on examination. Reading speed and reading endurance decline progressively.
• In older adults with late-onset disease (symptoms beginning at age 45 or older): Central visual acuity may be relatively preserved for years to decades after symptoms begin, but subtle central scotoma may impair reading ability even when the standard eye chart shows reasonable acuity. This form is the most likely to be misdiagnosed as age-related macular degeneration, and genetic testing is essential for correct diagnosis.

Stargardt disease is diagnosed by a retinal specialist or ophthalmologist. Diagnosis can be challenging because the retina may appear entirely normal in early disease, up to one-third of children lack the characteristic flecks at presentation, and late-onset disease closely mimics age-related macular degeneration. The current standard of care combines multimodal retinal imaging with genetic testing, which provides the definitive molecular diagnosis and is required for enrollment in clinical trials. The key diagnostic tools are:

• Fundus autofluorescence (FAF): the primary imaging tool for Stargardt disease. FAF detects the autofluorescence signal emitted by lipofuscin in RPE cells, making it possible to map disease activity before changes are visible on standard ophthalmoscopy. Areas of excess lipofuscin (active RPE stress) appear brighter than normal (hyperautofluorescent), while areas where RPE cells have already died appear darker (hypoautofluorescent atrophy). FAF reveals the characteristic hyperautofluorescent flecks, tracks their evolution, maps the expanding zone of central atrophy, and predicts the rate of progression based on the distribution pattern. The autofluorescence pattern is also used to classify disease severity into three types (type 1, 2, and 3) with different prognostic implications.
• Spectral-domain optical coherence tomography (SD-OCT): high-resolution cross-sectional imaging of the retinal layers that detects the loss of the ellipsoid zone (the outer segment layer of the photoreceptors) and the external limiting membrane—the two structural hallmarks of photoreceptor degeneration in Stargardt disease. The earliest detectable OCT change is thickening of the external limiting membrane in children as young as five years, before any visual symptoms. Serial OCT measurements track the expanding zone of photoreceptor loss over time and provide objective structural endpoints for clinical trials.
• Full-field electroretinography (ffERG): measures the electrical response of the entire retina to standardized light flashes, assessing both rod and cone photoreceptor function. In Stargardt disease, the ERG is used for the Lois classification (Groups 1, 2, and 3) that predicts long-term disease trajectory. Group 1 (macular dysfunction with a normal full-field ERG) carries the best prognosis; Group 3 (dysfunction extending to rods across the entire retina) carries the worst. ERG is essential for prognosis counseling and clinical trial stratification.
• Fundus fluorescein angiography (FFA): a dye-based retinal vascular imaging technique in which intravenous fluorescein is injected, and photographs of the retinal circulation are taken. In STGD1, FFA reveals the “dark choroid sign”—the masking of normal choroidal fluorescence by the lipofuscin-laden RPE—a finding pathognomonic for STGD1. The dark choroid sign is absent in STGD3, helping distinguish these two forms.
• Microperimetry: a fundus-guided visual field test that maps the sensitivity of individual points across the macula with high spatial precision, correlating sensitivity measurements to exact retinal locations on a fundus image. It quantifies the loss of macular sensitivity, measures the stability of the preferred retinal locus (PRL), and can be used to train patients to use the most functional eccentric retinal location through biofeedback.
• Genetic testing (next-generation sequencing): the definitive diagnostic test. Next-generation sequencing of the full ABCA4 coding region and flanking intronic sequences identifies disease-causing mutations and confirms the molecular diagnosis. Standard coding-region sequencing detects approximately 60–80% of STGD1 disease alleles; whole-exome sequencing is used for unsolved cases. Identifying both causative mutations establishes the specific STGD subtype, guides prognosis by allele severity class, and is required for clinical trial enrollment. Genetic testing also enables accurate carrier testing of family members.
• Adaptive optics scanning light ophthalmoscopy (AOSLO): a research-grade imaging technique that achieves cellular-resolution visualization of individual photoreceptors in the living eye. AOSLO can detect “dark cones”—photoreceptors that have lost their outer segments but whose inner segments still survive—before changes are visible on standard OCT or FAF. While not yet a routine clinical tool, AOSLO-based cone counting is emerging as a sensitive outcome measure in clinical trials of therapies aimed at preserving photoreceptors.

As of 2026, there is no FDA-approved disease-modifying treatment for any form of Stargardt disease. The condition is not currently curable. The goals of management are to protect remaining vision from modifiable harm, maximize functional independence through low vision rehabilitation, and connect patients with the advanced clinical trials that offer the realistic prospect of approved therapies in the coming years. Stargardt disease currently has the most active investigational treatment pipeline of any inherited retinal disease in the world, with multiple approaches in advanced human trials.

Low vision rehabilitation is the primary treatment for all patients with Stargardt disease and the intervention with the most consistent impact on daily function and quality of life. A certified low vision specialist, occupational therapist, and orientation and mobility specialist work together to maximize independence. Specific interventions include:

• Optical magnification devices: Handheld magnifiers, stand magnifiers, clip-on telescopes for distance tasks, and spectacle-mounted magnifiers help patients read, see faces, and perform close work.
• Electronic magnification systems: Desktop closed-circuit television (CCTV) magnifiers, electronic portable magnifiers, and tablet-based magnification apps provide adjustable contrast, size, and brightness control.
• Head-mounted display (HMD) devices: Electronic devices worn like glasses that capture video and project an enlarged, enhanced image directly onto the patient’s functional peripheral retina. Multiple commercial HMDs have been studied in home-use trials in Stargardt patients with promising patient-reported outcomes.
• Absorptive and tinted lenses: Yellow or amber filter lenses significantly reduce glare sensitivity and photophobia and are well accepted by patients with Stargardt disease.
• Microperimetry biofeedback training: A specialized technique that uses real-time retinal mapping to train patients to use their most functional eccentric preferred retinal locus (PRL) consistently and stably. Documented improvements in fixation stability, reading speed, and contrast sensitivity have been reported.
• Digital accessibility technology: Screen readers, voice assistants (Siri, Google Assistant), smartphone accessibility features, and computer magnification software (ZoomText, Magnifier) maintain access to information and communication as central vision decreases.
• Orientation and mobility training: White cane instruction, eccentric viewing technique practice, and low-light navigation strategies help maintain safe independent movement.

No pharmacological agent has received FDA approval for Stargardt disease. The following drugs are in active clinical trials and represent the most advanced investigational pharmacological approaches:

• Emixustat hydrochloride (ACU-4429): an oral drug that inhibits RPE65, the key enzyme that converts retinoid compounds in the RPE visual cycle, thereby reducing the substrate available for toxic A2E formation. A Phase 2 dose-finding trial confirmed strong biological activity—near-complete suppression of the rod visual recovery rate at 10 mg—but the drug caused dose-dependent color disturbance (chromatopsia) in 57% of treated patients and delayed dark adaptation in 48%. Emixustat is currently in a Phase 3 randomized, placebo-controlled trial (the SeaSTAR trial) evaluating its ability to slow macular atrophy progression over 24 months.
• ALK-001 (deuterium-modified vitamin A): an oral modified version of vitamin A in which hydrogen atoms are replaced with deuterium (heavy hydrogen). This modification prevents two vitamin A molecules from combining to form the toxic A2E byproduct while preserving the molecule’s normal role in the visual cycle. Preclinical studies in ABCA4 mouse models showed significantly reduced lipofuscin accumulation and stabilized ERG amplitudes. The Phase 2 TEASE-2 trial is ongoing.
• Avacincaptad pegol (Izervay™): an intravitreal (into-the-eye) injection that blocks complement component C5, a protein in the immune system’s complement cascade. A2E and other lipofuscin components activate this cascade in RPE cells, contributing to RPE death. Izervay™ was FDA-approved in August 2023 for geographic atrophy in age-related macular degeneration—but it is not approved for Stargardt disease, where it is under investigation in a Phase 2b trial.

Replacing the defective ABCA4 gene with a functional copy is the most conceptually direct approach to treating STGD1. The main technical challenge is that the ABCA4 gene is unusually large (approximately 6.8 kilobases of coding sequence), exceeding the cargo capacity of the adeno-associated virus (AAV) vectors used in most successful retinal gene therapies. Researchers have addressed this by using a lentiviral vector—a type of virus with greater cargo capacity—to deliver the gene. SAR422459 (StarGen) uses a lentiviral vector to deliver a functional ABCA4 gene by subretinal injection (a surgical procedure that places the gene therapy directly beneath the retina). A Phase I/II clinical trial enrolled patients in four ascending dose cohorts, with no safety concerns reported in initial cohorts. Nanoparticle-based gene delivery approaches for ABCA4 are also in preclinical development, with encouraging results in mouse models.

A Phase I/IIa clinical trial transplanted RPE cells derived from human embryonic stem cells (hESC-RPE) into the subretinal space of 13 patients with advanced STGD1, with immunosuppression to prevent rejection. The primary endpoint of safety and tolerability was met, with no serious adverse events attributable to the transplanted cells and five-year follow-up ongoing. The limitation of RPE replacement alone is that in advanced disease, the photoreceptors above the RPE have also been lost—ultimately, combination RPE and photoreceptor replacement strategies may be needed for the most advanced cases.

A small proportion of Stargardt patients develop choroidal neovascularization (CNV)—abnormal new blood vessel growth beneath the macula—as a rare complication. CNV causes rapid additional central vision loss if untreated. It is managed with intravitreal anti-vascular endothelial growth factor (VEGF) injections (ranibizumab or bevacizumab) using the same approach as for neovascular age-related macular degeneration. While anti-VEGF treatment can slow CNV progression, significant visual improvement from this complication is limited.

Stargardt disease is a lifelong condition, but the majority of patients retain their peripheral vision throughout their lives and can achieve meaningful independence and quality of life with the right support. The severity of daily life impact varies considerably. Patients with early-onset disease may experience significant visual impairment by their teenage years, affecting schooling, driving, and early career choices. Those with late-onset disease may retain functional central vision well into middle age and beyond. Central vision loss—affecting reading, face recognition, and driving—is the primary disability. However, with appropriate low vision devices, accessible technology, orientation and mobility training, and strong support networks, many individuals with Stargardt disease continue to work, participate in recreational activities, maintain their independence, and live full lives. Life expectancy is entirely normal, as Stargardt disease affects only the eye in its primary forms.

Understanding your specific genetic diagnosis matters in practical ways. Knowing which ABCA4 mutations you have allows your specialist to give a more accurate prognosis, determines clinical trial eligibility for the most promising therapies, and enables targeted genetic counseling for your family. The Macular Society (macularsociety.org) and the Foundation Fighting Blindness (fightingblindness.org) provide patient education resources, peer support communities, information on clinical trials, and advocacy for research funding. Connecting with these communities provides both practical resources and the peer support that makes an enormous difference when navigating a progressive visual condition.

To further your understanding of your diagnosis and to contribute to cutting-edge research, consider participating in a clinical trial so clinicians and scientists can learn more about causes, symptoms, treatment, and prevention of Stargardt disease and related disorders. Clinical research uses human volunteers to help researchers learn more about a disorder and perhaps find better ways to safely detect, treat, or prevent disease.

All types of volunteers are needed—those who are healthy or may have an illness or disease—of all different ages, sexes, races, and ethnicities to ensure that study results apply to as many people as possible, and that treatments will be safe and effective for everyone who will use them.