Regional choroidal atrophy and alopecia (also called Moloney syndrome or choroidal atrophy–alopecia syndrome) is a very rare inherited condition. In this condition, part of the choroid (the blood-rich layer under the retina) becomes thin and wasted, and the person also has hair loss and other “ectodermal” problems such as thin hair, missing eyelashes or eyebrows, and abnormal nails.
The eye problem (choroidal atrophy) can cause slowly progressive vision loss, problems seeing in dim light, and sometimes blind spots in the visual field. The skin, hair, and nails can look different from birth or early childhood. Only a very small number of families have been reported worldwide, so most of what we know comes from single case reports.
Doctors believe this syndrome is a form of ectodermal dysplasia. “Ectodermal dysplasia” means that tissues that come from the outer layer of the embryo (skin, hair, nails, parts of the eye) did not develop in the usual way. The exact gene change for this syndrome has not yet been clearly found, and the pattern of inheritance is still uncertain.
Other names
Doctors and books may use different names for the same condition. Common “other names” include:
Choroidal atrophy–alopecia syndrome
Regional choroidal atrophy and alopecia
Moloney syndrome (named after the author who first described it)
Choroidal atrophy; alopecia syndrome
These names all point to the same core idea: damage and thinning of the choroid in the eye together with hair loss and other ectodermal changes.
Types
Because this is so rare, there is no strict official “type” classification. However, doctors sometimes describe practical types based on how the disease looks in the eye and on the body:
Type by choroidal involvement (regional vs more widespread)
In some patients only a specific region of the choroid is atrophic (regional), while in others the atrophy spreads more widely around the back of the eye. This pattern is described in reports of regional choroidal atrophy and other diffuse choroidal atrophies.Type by severity of eye disease (mild, moderate, severe)
Some people keep fair central vision for many years, while others develop significant vision loss, large areas of choroidal thinning, and big visual field defects. Doctors may informally grade this by vision level and extent of atrophy on eye scans.Type by hair involvement (scalp only vs generalized)
In some patients hair loss mainly affects the scalp, but in others the eyelashes, eyebrows, and body hair are also sparse or missing. This is similar to other ectodermal dysplasia patterns.Type by nail and skin changes (with or without nail dystrophy)
Many reports mention thick, grooved, or dysplastic nails together with fine sparse hair. Some patients may have mainly eye and hair findings, while others also have marked nail changes and dry skin.Type by age at diagnosis (childhood-onset vs adult-diagnosed)
The condition starts early, but some people are only diagnosed in adolescence or adulthood when eye tests finally explain their visual problems. Others are recognized as children because the hair and nail changes are obvious.
These “types” are more like clinical descriptions than true genetic subtypes, because the exact gene defect is still unknown.
Causes (20)
Remember: because this syndrome is extremely rare, many causes listed here are probable or associated factors, not all are fully proven. Doctors use knowledge from this syndrome plus similar choroidal atrophy and ectodermal dysplasia diseases.
Underlying genetic mutation in an ectodermal gene
The main suspected cause is a change (mutation) in a gene that controls development of ectoderm tissues such as hair, nails, skin, and parts of the eye. The exact gene for Moloney syndrome is not yet found, but similar choroidal atrophy and ectodermal dysplasia conditions are clearly genetic.Autosomal recessive inheritance in some families
Case reports describe affected siblings with healthy parents, which suggests a possible autosomal recessive pattern (two faulty copies of a gene). This means each parent carries one silent copy, and the child gets both.De novo (new) mutation
In very rare diseases, a gene change can appear for the first time in a child without being present in the parents. This “new” mutation can still affect eye and hair development even though the family history is negative.Abnormal development of the choroidal blood vessels
The choroid is full of tiny blood vessels that feed the retina. In choroidal atrophy syndromes, these vessels can develop poorly or regress over time, leading to thinning and scarring.Abnormal development of the retinal pigment epithelium (RPE)
The RPE is a pigmented layer on top of the choroid. Genetic problems that damage the RPE can secondarily lead to atrophy of the choroid, especially in regional patterns of choroidal atrophy.Shared ectodermal origin of hair, skin, and eye tissues
Hair follicles, nails, parts of the cornea, lens, and retina all come from ectoderm. A single defect in ectodermal development can thus show as both alopecia and choroidal atrophy.Possible involvement of photoreceptor-related genes
In some diffuse and regional choroidal atrophy conditions, mutations in the photoreceptor protein peripherin/RDS have been found. This shows that gene defects in the retina can ultimately cause choroidal thinning, although this specific link is not confirmed for Moloney syndrome.Ectodermal dysplasia mechanisms
The syndrome is classified among ectodermal dysplasia syndromes. In these disorders, pathways that control hair shaft formation, nail plates, and sweat glands are disturbed, and similar pathways may affect the eye tissues.Abnormal collagen and connective tissue in the eye wall
Some chorioretinal atrophies in high myopia or hereditary dystrophies involve abnormal sclera and connective tissue, which may affect choroidal stability and blood supply. This general mechanism might also contribute here.Defective cell survival pathways in the choroid and RPE
Gene problems can make cells more likely to die early (apoptosis). In retinal and choroidal dystrophies, this slow, programmed cell death leads to progressive thinning of tissues.Shared immune or inflammatory pathways with alopecia areata (possible)
Alopecia areata itself is an autoimmune disease. Some chorioretinal atrophy patterns have been reported with alopecia areata or immune disease, though this is not proven in Moloney syndrome and may represent different entities.Epigenetic factors (gene regulation without DNA change)
In rare eye-hair syndromes, not only the DNA sequence but also the regulation of genes (epigenetics) may be abnormal, affecting how strongly key development genes are turned on or off.Possible consanguinity (parents related by blood)
Many rare recessive syndromes occur in families where the parents are related (for example, cousins). This increases the chance that both carry the same rare gene change.Modifier genes that change disease severity
People with the same main mutation can still show different severity. Other genes, called “modifier genes,” can make choroidal atrophy or alopecia milder or more severe. This is seen in other hereditary eye dystrophies.Oxidative stress and damage over time
Some ectodermal and mitochondrial disorders increase oxidative stress, which damages cells. Long-term oxidative damage can worsen choroidal and retinal thinning.Abnormal development of hair follicles
In many hair loss syndromes, the hair follicles are small, twisted, or poorly anchored. This structural defect explains fine, sparse scalp hair, absent lashes, and thin eyebrows in this syndrome.Abnormal nail matrix and nail plate formation
Grooved, thick, or dysplastic nails suggest defects in nail matrix cells, which are also ectodermal. The same developmental pathway problems may also affect the eye.Possible overlap with other chorioretinal dystrophies
Some authors have reported patients with both alopecia and different forms of choroidal or chorioretinal dystrophy. This suggests that the Moloney pattern may sit on a spectrum with other genetic retinal diseases.Environmental factors that may modify expression (not primary cause)
Light exposure, smoking, poor nutrition, or systemic illness can worsen retinal and choroidal health in general. They are not the primary cause of this syndrome but may influence how fast vision declines.Still-unknown disease-specific gene
Finally, the most honest statement is that the exact gene and molecular pathway for Moloney syndrome are still unknown. Future genetic studies are needed to define the precise cause.
Symptoms (15)
Progressive decrease in vision
Many patients notice that their vision slowly gets worse over years. This can involve both central vision (for reading and faces) and peripheral vision (side vision), because the atrophic areas in the choroid and retina no longer support normal sight.Difficulty seeing in dim light (night blindness)
When the choroid and retina are damaged, rod cells (for night and dark vision) may not work well. People can struggle to see at dusk, in poorly lit rooms, or when moving from bright to dark areas.Blind spots or patches of missing vision
Regional choroidal atrophy can create areas where the person cannot see, called scotomas. These may show as missing patches in the field of vision, which the person may notice as “blank” or “grey” spots.Fine, sparse scalp hair (alopecia)
Hair on the head may be very thin, soft, and sparse, or there may be clear areas of baldness. This finding is typical and often appears early in life.Loss or reduction of eyelashes and eyebrows
Many patients have few or no eyelashes and very thin or absent eyebrows. This is part of the ectodermal dysplasia pattern and is included in the original description of the syndrome.Abnormal nails (dysplastic, thick, or grooved nails)
Nails may look thick, ridged, or oddly shaped. Some nails may break easily or grow slowly. These nail changes are often mentioned along with hair and eye findings.Mild to moderate visual field constriction
Visual field testing may show narrowing of the field, like looking through a tunnel or losing parts of side vision. This relates to the pattern of atrophic choroidal and retinal areas.Possible reduction in visual acuity from childhood or adolescence
Some patients already have lower-than-normal visual acuity when they are young adults. Others may have a long stable phase before the vision gradually worsens.Light sensitivity (photophobia) in some patients
Damaged retina and RPE can make the eyes more sensitive to light. People may feel discomfort or glare in bright sunlight or harsh indoor lights, though this is not described in every case.Difficulty with detailed tasks (reading, fine work)
Because central vision can be involved, patients might find it harder to read small print, sew, or do other detailed work, especially if the macular region is affected by atrophy.Cosmetic distress due to hair loss and nail changes
The visible alopecia, missing lashes and brows, and nail abnormalities can cause emotional and social distress. People may feel self-conscious or anxious about their appearance.Possibly mild visual loss rather than complete blindness
GARD and other references describe “mild visual loss” in many patients, so severe blindness is not inevitable, though this may vary between individuals and families.Dry or abnormal skin in some ectodermal dysplasia patterns
While not described in all reports of this exact syndrome, ectodermal dysplasia conditions often have dry, thin, or easily scarred skin, which might be present in some individuals with regional choroidal atrophy and alopecia.Possible mild refractive errors (myopia or hyperopia)
Many chorioretinal dystrophies coexist with refractive errors such as myopia. The case literature in choroidal atrophy often mentions high myopia, though the exact pattern in Moloney syndrome is not fully defined.Psychological impact (anxiety, low mood)
Living with a rare disease that affects both vision and appearance can lead to worry, sadness, or low self-esteem. This is common in patients with alopecia and chronic eye disease in general.
Diagnostic tests (20)
Doctors use many tests to confirm regional choroidal atrophy and alopecia and to rule out other conditions. Below they are grouped as requested.
Physical examination tests
Full general physical and skin examination
The doctor looks at the whole body, including skin, scalp, face, and nails. In this syndrome, they may see fine, sparse hair, missing lashes and eyebrows, and nail changes, which support an ectodermal dysplasia pattern.Detailed scalp and hair inspection
The scalp is checked for diffuse thinning, patchy bald areas, or abnormal hair shafts. The pattern of alopecia helps distinguish this rare syndrome from common causes like androgenetic alopecia or alopecia areata.Nail examination (hands and feet)
Nails are inspected for thickness, grooves, color changes, and shape abnormalities. Dysplastic or grooved nails are a key sign that hair and nail problems come from a shared ectodermal defect.Basic eye examination with visual acuity testing
Standard letter chart testing (like Snellen chart) measures how well the person can see at distance and near. Decreased acuity that cannot be corrected fully with glasses raises concern for retinal or choroidal disease.Confrontation visual field testing
The doctor checks the person’s side vision by moving fingers or objects in from the edge of the visual field. Areas where the patient cannot see may correspond to regions of choroidal atrophy.
Manual / clinical office tests
Color vision testing
Simple color plates (for example, Ishihara charts) are used to see if color vision is normal. In some chorioretinal atrophies, color vision is surprisingly preserved, which can help in differential diagnosis.Amsler grid testing
The patient looks at a grid of straight lines to see if any lines look wavy, blurred, or missing. Distortion or missing boxes may indicate macular involvement from choroidal or retinal atrophy.Slit-lamp examination of the anterior eye
Using a microscope with a bright beam, the eye doctor examines the cornea, anterior chamber, lens, and front of the eye. This helps rule out other structural problems and prepares for a better view of the back of the eye.Dilated fundus examination (indirect ophthalmoscopy)
After putting drops to widen the pupil, the doctor looks at the retina and choroid with special lenses. They may see pale, thinned, or patchy areas of choroidal atrophy and sometimes pigment changes along vessels.Family examination and pedigree drawing
Eye and hair examinations of parents and siblings, along with a diagram of family history, help decide if the pattern suggests autosomal recessive inheritance, dominant traits, or sporadic disease.
Laboratory and pathological tests
Targeted or panel genetic testing for retinal/choroidal dystrophy genes
A blood sample can be used for DNA testing. Panels for chorioretinal dystrophies or ectodermal dysplasia may detect known disease genes, help confirm a hereditary basis, and allow genetic counseling, even if the specific MolONEY gene is not yet mapped.Whole-exome or whole-genome sequencing in research settings
When standard panels are negative, more extensive genetic sequencing can be done, often as part of research. This approach has discovered genes for other rare chorioretinal conditions, and may eventually identify the gene for this syndrome.Basic blood tests to exclude metabolic or inflammatory causes
Tests like complete blood count, inflammatory markers, and sometimes specific metabolic tests (for example, plasma ornithine for gyrate atrophy) help rule out other conditions that also cause choroidal atrophy.Skin or hair biopsy (in selected cases)
A small sample of skin or hair follicles may be examined under the microscope. It can show structural hair shaft or follicle abnormalities typical of ectodermal dysplasia and helps distinguish inherited alopecia from acquired autoimmune types.Nail biopsy or histology (rarely needed)
Nail matrix or plate samples are rarely taken but can show dysplastic nail formation. This provides extra proof of ectodermal involvement when the diagnosis is uncertain.
Electrodiagnostic tests
Full-field electroretinography (ERG)
ERG measures the electrical responses of rod and cone cells when light flashes are given. In chorioretinal atrophy, the ERG often shows reduced amplitudes or delayed responses, proving that the retina is functionally impaired.Multifocal ERG
Multifocal ERG maps function in many small regions across the central retina. Areas of choroidal and retinal atrophy show reduced signals, helping map which parts of the macula work and which do not.Visual evoked potentials (VEP)
VEP tests the pathway from the eye to the visual cortex in the brain. Abnormal VEP results show that visual signals are not being transmitted normally, which can happen when retinal or choroidal diseases are advanced.
Imaging tests
Optical coherence tomography (OCT)
OCT is a key imaging test that uses light waves to make cross-section pictures of the retina and choroid. In choroidal atrophy, OCT shows thinning of the choroid and outer retina and can measure how much tissue has been lost over time.Fundus autofluorescence and angiography (FA / ICGA / OCT-A)
Fundus autofluorescence maps the health of the retinal pigment epithelium. Fluorescein angiography (FA) and indocyanine green angiography (ICGA) show blood flow in the retina and choroid. OCT-angiography (OCT-A) is a non-dye method to image vessels. Together, these tests highlight areas of choroidal atrophy and help distinguish this syndrome from other retinal diseases.
Non-pharmacological treatments (therapies and other approaches)
Because this syndrome is very rare, the non-drug treatments below are adapted from evidence in inherited retinal diseases, pathologic myopia, dry eye disease and alopecia areata, not from large trials in this exact condition.
1. Low-vision rehabilitation
Low-vision rehab teaches the person how to use their remaining sight more effectively in daily life. Training can include using magnifiers, high-contrast reading materials, special lighting and smartphone accessibility tools. The goal is not to “fix” the damaged retina, but to make school, work and self-care easier and safer. Early referral improves independence and quality of life in inherited retinal disease.
2. Optical aids and tinted lenses
High-plus reading glasses, magnifying glasses, handheld or stand magnifiers, and telescopic lenses can help enlarge print or distant objects. Photochromic or tinted lenses cut glare and may protect the fragile retina from excessive light. People with choroidal atrophy often report disabling glare and contrast loss, so these simple tools can make a big difference in comfort and function.
3. Orientation and mobility training
If peripheral vision or depth perception is affected, walking outdoors, crossing roads or climbing stairs may feel unsafe. Orientation and mobility specialists teach safe travel skills, such as scanning, using landmarks, and sometimes using a mobility cane. This training reduces the risk of falls and boosts confidence in children and adults with low vision.
4. Electronic magnifiers and digital tools
Closed-circuit television (CCTV) readers, tablet cameras with zoom, screen-magnifier apps, large fonts and high-contrast display settings can all help with reading and screen work. Unlike fixed magnifiers, digital tools allow adjustable magnification and contrast, which is helpful when contrast sensitivity is reduced by choroidal atrophy.
5. Environmental modifications at home and school
Good lighting, high-contrast markings on steps, big-print labels on medicine bottles, and clutter-free floors lower the risk of accidents. In classrooms, seating close to the board, printed notes and digital copies of slides can support learning. These changes are simple but strongly improve participation for people with retinal disease.
6. Sun and UV protection for eyes
People with retinal and choroidal thinning may be more sensitive to light and theoretically more vulnerable to cumulative light damage. Wearing good-quality sunglasses with UV-A and UV-B protection, plus a brimmed hat outdoors, is advised. This is standard advice in macular and choroidal degenerations to protect remaining retinal tissue.
7. Scalp and skin photoprotection
Areas without hair burn easily. Daily broad-spectrum sunscreen, hats, scarves or wigs help shield the scalp, eyebrows and exposed skin from UV damage and sunburn. Dermatology guidelines for alopecia and ectodermal dysplasias stress strict sun protection to reduce skin cancer risk and discomfort.
8. Eyelid hygiene and ocular surface care routines
Gentle lid hygiene, warm compresses and regular artificial tears can stabilise the tear film, which is often disturbed in people with lash abnormalities or ocular surface disease. A stable tear film protects the cornea over areas of poor corneal innervation or exposure, as seen in many complex eye syndromes.
9. Wigs, hairpieces and cosmetic solutions
Custom wigs, partial hairpieces, scalp micropigmentation, and cosmetic eyebrow techniques help many people feel more comfortable in social situations. These options do not treat the root cause of alopecia, but they can greatly improve self-image and reduce anxiety or depression linked to hair loss.
10. Cosmetic eyebrow and eyelash options
Eyebrow pencils, powders, microblading and false eyelashes can soften the appearance of missing brows or lashes. Care is needed to avoid glues or dyes that irritate the eyes or skin. Dermatology literature shows that cosmetic camouflage is an important supportive therapy in severe alopecia areata and other hair disorders.
11. Psychological counselling and support groups
Visible hair loss combined with visual disability can be emotionally heavy, especially for teenagers. Short-term counselling, cognitive-behavioural therapy and peer support groups help people process grief, build coping skills and manage social anxiety. Studies in alopecia areata show that emotional support improves quality of life even when hair regrowth is limited.
12. Genetic counselling for the family
A genetic counsellor explains what is known about inheritance, offers testing when available, and discusses options such as carrier testing, prenatal testing or preimplantation genetic testing. This does not change current symptoms but can help families plan and reduces uncertainty about future children.
13. Educational support and accommodations
Individualised education plans (IEPs) or similar supports can provide extra time for exams, access to enlarged print, digital textbooks, and note-taking assistance. These accommodations are widely recommended for children with inherited retinal diseases and can prevent academic under-performance due to vision rather than ability.
14. Occupational therapy for daily living skills
Occupational therapists teach adaptive ways to cook, manage money, dress, use devices and travel safely with reduced vision. For a person who also has cosmetic and self-esteem challenges from alopecia, mastering daily living skills can restore a sense of control and independence.
15. Healthy physical activity with eye-safe choices
Regular exercise supports heart and brain health, which also benefits the eyes. Non-contact sports and activities with low risk of head or eye trauma are usually preferred. For degenerative retinal conditions, avoiding activities with a high chance of direct eye injury is commonly advised.
16. Screen-use hygiene
Frequent breaks (for example, 20–20–20 rule), good screen distance, and avoiding very bright or very dim screens can reduce eye strain and dryness. While screens do not cause choroidal atrophy, comfortable use helps people with low vision keep up with school and work without extra discomfort.
17. Sleep and general health optimisation
Good sleep, balanced diet, hydration and control of systemic illnesses (like diabetes or hypertension) support eye health in general. Many retinal disease guidelines include systemic risk-factor control to slow overall vascular and neural damage.
18. Smoking avoidance and alcohol moderation
Smoking increases oxidative stress and is a risk factor for age-related macular degeneration and other retinal diseases. Heavy alcohol intake also worsens overall health. Avoiding smoking and keeping alcohol low is a simple, evidence-based way to protect remaining vision.
19. Regular specialist follow-up
Scheduled visits with a retina specialist and dermatologist allow early detection of complications such as choroidal neovascularization, retinal tears, corneal damage, or skin cancers on sun-exposed, hairless areas. In many degenerative retinal conditions, timely treatment of complications is crucial to preserving vision.
20. Family and caregiver education
Teaching family members about the condition, its visual and cosmetic effects, and the need for protection and follow-up reduces blame, misunderstanding and unsafe behaviours at home. Education is a core part of care in rare hereditary eye and hair syndromes.
Drug treatments
Important: No medicine is currently approved specifically to cure “regional choroidal atrophy and alopecia” as a single syndrome. Medicines are used to treat complications: macular or choroidal atrophy similar to geographic atrophy or pathologic myopia, choroidal neovascularization, severe dry eye, neurotrophic keratitis, and alopecia areata-like hair loss. Many uses are off-label, and every drug must be chosen and dosed by a specialist.
1. Pegcetacoplan intravitreal injection (Syfovre)
Pegcetacoplan is a complement C3 inhibitor approved to slow the growth of geographic atrophy (GA) from age-related macular degeneration. The FDA label recommends 15 mg (0.1 mL) injected into the eye every 25–60 days by a retina specialist. It does not restore lost tissue but can slow atrophy expansion. Possible side effects include eye inflammation, increased intra-ocular pressure and rare retinal vascular events. In a patient with similar atrophic macular changes, a specialist might consider whether GA-type treatment is appropriate.
2. Avacincaptad pegol intravitreal injection (Izervay)
Avacincaptad pegol is a complement C5 inhibitor also approved for geographic atrophy secondary to AMD. The prescribing information describes 2 mg intravitreal injections every 28 days. Like pegcetacoplan, it aims to slow atrophy growth, not cure the disease. Side effects include conjunctival haemorrhage, increased intra-ocular pressure and rare retinal detachments. Its role in hereditary choroidal atrophy is unknown, so it should only be used under expert guidance if retinal findings overlap GA.
3. Ranibizumab (Lucentis) – anti-VEGF for choroidal neovascularization
Ranibizumab is an anti-vascular endothelial growth factor (anti-VEGF) antibody fragment approved for neovascular AMD, diabetic macular edema and other retinal vascular diseases. Typical dosing is 0.5 mg intravitreal monthly at first, then less often. It blocks VEGF to reduce leakage and abnormal new vessels. If choroidal atrophy areas develop secondary choroidal neovascular membranes, ranibizumab or similar anti-VEGF drugs can help preserve central vision.
4. Aflibercept (Eylea) – anti-VEGF trap
Aflibercept is a fusion-protein “VEGF trap” approved for neovascular AMD, diabetic macular edema and retinal vein occlusion. Labels describe 2 mg intravitreal injections every 4 weeks initially, then every 8 weeks in many regimes. It binds VEGF-A, VEGF-B and placental growth factor, drying macular fluid and stabilising vision. As with ranibizumab, its role in this syndrome is to treat secondary neovascular complications, not the underlying choroidal atrophy.
5. Faricimab (Vabysmo) – dual Ang-2 / VEGF inhibitor
Faricimab is a bispecific antibody targeting both VEGF-A and angiopoietin-2, approved for neovascular AMD, diabetic macular edema and retinal vein occlusion. The label supports injections every 4 weeks initially, then every 8–16 weeks depending on response. By stabilising both vascular growth and vascular leakage pathways, it can provide longer treatment intervals. Again, it would only be considered in this syndrome if neovascular complications develop.
6. Triamcinolone acetonide suprachoroidal injection (Xipere)
Xipere is a formulation of triamcinolone acetonide approved for macular edema associated with uveitis. The label describes 4 mg delivered in the suprachoroidal space using a special injector. Corticosteroids reduce inflammation and vascular leakage. In severely inflamed choroidal or macular tissue in related conditions, similar steroid approaches may help, but they carry risks such as raised intra-ocular pressure and cataract.
7. Cyclosporine ophthalmic emulsion 0.05% (Restasis and generics)
Topical cyclosporine ophthalmic emulsion is approved to increase tear production in patients with inflammatory dry eye (keratoconjunctivitis sicca). The usual dose is one drop in each eye twice daily, about 12 hours apart. It works by locally suppressing T-cell driven inflammation on the ocular surface. For patients with this syndrome who have chronic dry eye and ocular surface disease, cyclosporine can improve comfort and protect the cornea. Burning on instillation is the most common side effect.
8. Lifitegrast ophthalmic solution 5% (Xiidra)
Lifitegrast is a lymphocyte function–associated antigen-1 (LFA-1) antagonist approved for the signs and symptoms of dry eye disease. It is used as one drop in each eye twice daily. By blocking LFA-1/ICAM-1 interaction, it reduces T-cell activation and ocular surface inflammation. In patients with chronic dry eye not controlled with lubricants, lifitegrast can reduce burning, grittiness and redness, though it may cause temporary irritation or a metallic taste.
9. Artificial tears and lubricating gels (OTC)
Non-prescription artificial tears based on carboxymethylcellulose, hyaluronic acid or other polymers are first-line for dry eye and exposure keratopathy. They create a protective moist layer over the cornea and reduce friction when blinking. In complex ocular surface disease, frequent use of preservative-free tears and night gels is often recommended to protect the epithelium and improve comfort.
10. Cenegermin ophthalmic solution 0.002% (Oxervate)
Cenegermin is recombinant human nerve growth factor approved for neurotrophic keratitis, a condition where corneal nerves are damaged and the surface fails to heal. The label indicates one drop in the affected eye(s) six times per day at 2-hour intervals for eight weeks. It supports corneal nerve regeneration and epithelial healing. In a person with this syndrome who develops neurotrophic ulcers, cenegermin may be considered by a cornea specialist.
11. Baricitinib (Olumiant) for severe alopecia areata
Baricitinib is an oral Janus kinase 1/2 inhibitor approved for adults with severe alopecia areata. Labels describe once-daily dosing, commonly 2 mg or 4 mg, with careful monitoring for serious infections, blood clots, laboratory changes and malignancy risk. Clinical trials show meaningful scalp hair regrowth in a proportion of patients. In a patient whose alopecia in this syndrome behaves like severe alopecia areata, a dermatologist may consider baricitinib, but only after discussing the risks.
12. Ritlecitinib (Litfulo) for severe alopecia areata
Ritlecitinib is an oral JAK3/TEC family kinase inhibitor approved for severe alopecia areata in adults and adolescents from 12 years of age. The FDA label and press materials describe a once-daily 50 mg dose, with warnings about serious infections, malignancy, cardiovascular events and thrombosis. Trials show improved hair regrowth compared with placebo. In any child or teen, this drug must be managed strictly by a dermatologist experienced with JAK inhibitors.
Dietary molecular supplements
There is no specific supplement proven to stop regional choroidal atrophy and alopecia. However, data from age-related macular degeneration (AREDS/AREDS2) and general eye-health research support some nutrients for retinal and choroidal health. These should never replace medical treatment, and high doses can be harmful, so they must be discussed with a doctor.
1. Lutein
Lutein is a carotenoid concentrated in the macula. It filters blue light and acts as an antioxidant. AREDS2-style supplements often use about 10 mg per day, but doses must follow product labels and medical advice. Lutein may help protect photoreceptors and the retinal pigment epithelium in degenerative macular diseases, though it does not reverse existing atrophy.
2. Zeaxanthin
Zeaxanthin works together with lutein in the macular pigment. Typical supplement doses are around 2 mg per day in AREDS2 formulations. It helps absorb harmful blue light and neutralise free radicals. In AMD, higher lutein/zeaxanthin intake is linked to slower disease progression, so some retina specialists suggest them as supportive therapy in other macular degenerations.
3. Vitamin C (ascorbic acid)
Vitamin C is a water-soluble antioxidant used at about 500 mg per day in AREDS formulations. It helps regenerate other antioxidants and supports collagen in blood vessels and connective tissue. In retinal disease, it mainly acts as part of an antioxidant network rather than a stand-alone treatment. Very high doses can upset the stomach or kidneys, so medical guidance is needed.
4. Vitamin E
Vitamin E is a fat-soluble antioxidant often included at 400 IU per day in eye-health formulas. It protects cell membranes from oxidative damage. Some studies show benefit in AMD, but others raise concerns about high-dose vitamin E and cardiovascular risk, so dose and personal risk factors must be checked with a doctor.
5. Zinc with copper
Zinc is important for many retinal enzymes. AREDS used 80 mg zinc oxide plus 2 mg copper; AREDS2 showed similar benefit with 25 mg zinc. High zinc can deplete copper, so these two are combined. In intermediate AMD, this mix reduced progression risk. For a rare choroidal dystrophy, zinc/copper may be used cautiously as a supportive antioxidant, under supervision.
6. Omega-3 fatty acids (DHA/EPA)
Omega-3 fatty acids from fish oil help build retinal cell membranes and reduce inflammation. Dietary intake of fatty fish at least once per week has been linked to a lower risk of AMD, though supplement trials are mixed. Typical supplement doses are 500–1000 mg combined DHA/EPA daily, adjusted for age and bleeding risk.
7. Vitamin A (within safe limits)
Vitamin A is essential for the visual cycle. True deficiency causes night blindness and retinal dysfunction. However, many inherited retinal dystrophies are not due to deficiency, and high vitamin A can be toxic, especially to the liver or in certain genetic conditions. If dietary intake is low, modest supplementation within recommended daily allowances may be considered after checking liver function and overall diet.
8. B-vitamins and folate for general nerve and vascular health
B-vitamins (B6, B9, B12) support nerve function and control homocysteine levels, which may influence vascular health. Typical doses come from balanced multivitamins or diet. There is no direct trial in this syndrome, but maintaining normal B-vitamin status is a standard part of general neurovascular health support.
Regenerative / stem-cell-related and “immunity-supporting” therapies
True regenerative or stem-cell drugs for this exact syndrome do not exist yet. Some therapies aim to improve healing or nerve function in the eye, and stem-cell approaches are being studied for inherited retinal diseases. These treatments are highly specialised and available only in specific centres or clinical trials.
1. Autologous serum eye drops
Autologous serum eye drops are made from the patient’s own blood serum, diluted and used as eye drops. They contain growth factors, vitamins and proteins similar to natural tears. Studies show benefit in severe dry eye and persistent epithelial defects when standard drops are not enough. Dosing schedules vary (often several times per day), and preparation must follow strict protocols in a specialised lab.
2. Platelet-rich plasma (PRP) eye drops
PRP drops are prepared from the patient’s blood and contain concentrated platelets and growth factors. Research suggests that PRP can improve dry eye symptoms, enhance epithelial healing, and improve meibomian gland function in resistant ocular surface disease. Dosing is typically multiple times daily for several weeks. PRP is still considered an advanced therapy and is not available everywhere.
3. Cenegermin (Oxervate) as a regenerative corneal therapy
Although listed earlier under drugs, cenegermin deserves mention here because it is a recombinant human nerve growth factor that stimulates regeneration of corneal nerves and epithelium in neurotrophic keratitis. By restoring corneal sensitivity and promoting healing, it can prevent ulcers and perforation in eyes with nerve damage. Treatment is intensive (six times daily for eight weeks) and must be supervised by a cornea specialist.
4. Experimental retinal stem-cell therapies (clinical trials)
Several early-phase trials test transplantation of retinal pigment epithelium (RPE) or photoreceptor precursor cells derived from stem cells into eyes with retinal degeneration such as retinitis pigmentosa, Stargardt disease or atrophic AMD. Early results suggest potential safety and small visual gains, but evidence is still limited and long-term outcomes are unknown. These approaches remain experimental and are only available in controlled trials.
Surgical options
Surgery in this syndrome is usually aimed at treating complications rather than the primary choroidal atrophy or alopecia. Below are five important types.
1. Cataract surgery
If cataracts develop and significantly blur vision, standard phacoemulsification with intra-ocular lens implantation can improve clarity. In eyes with retinal thinning, realistic counselling is vital: the surgery can clear the “dirty window,” but it cannot repair damaged retina or choroid, so visual gain may be limited.
2. Vitrectomy and macular surgery
In some degenerative retinal diseases, tractional changes or macular holes can occur. Pars plana vitrectomy, sometimes with internal limiting membrane peeling, can relieve traction and close macular holes. Surgeons must weigh benefits against risks, especially in eyes with thin choroid and retina where complications are more likely.
3. Laser or cryotherapy for retinal tears
If peripheral retinal thinning leads to retinal tears or small detachments, laser photocoagulation or cryotherapy can “spot-weld” the retina to underlying tissue and prevent progression. This is standard care in many retinal degenerations with lattice or atrophic holes and may also be applied here if similar lesions occur.
4. Corneal transplantation or limbal stem-cell procedures
Severe ocular surface damage or scarring may occasionally require corneal grafts or limbal stem-cell transplantation. These surgeries are complex, with variable success, and usually reserved for cases where other treatments fail to restore a clear, stable corneal surface.
5. Hair transplantation and scalp procedures
Where enough donor hair exists, scalp or eyebrow hair transplantation can improve cosmetic appearance. Results depend on the pattern and type of alopecia; in some ectodermal or syndromic alopecias donor hair may also be abnormal, limiting success. Nonetheless, carefully selected patients can experience meaningful improvement in appearance and confidence.
Prevention of complications
You cannot prevent being born with a genetic syndrome. However, you can lower the risk of later complications and rapid worsening.
Consistent UV and light protection for eyes and scalp – Use sunglasses, hats and sunscreen every day outdoors.
Avoid eye trauma and rubbing – Protect the eyes during sports and avoid rubbing, which can worsen corneal problems.
Treat dry eye early and aggressively – Use tears, lids hygiene and prescribed drops to prevent corneal breakdown.
Do not smoke; avoid second-hand smoke – Smoking accelerates many retinal and vascular diseases.
Control systemic diseases (diabetes, blood pressure, cholesterol) – These conditions worsen vascular damage, including in the eye.
Keep regular eye and skin check-ups – Scheduled visits allow early treatment of neovascularisation, retinal tears, corneal ulcers or skin cancers.
Use protective helmets or headgear for risky sports – Protecting the head and eyes lowers risk of retinal and scalp trauma.
Genetic counselling before pregnancy – Families can understand recurrence risks and options such as prenatal or preimplantation testing.
Maintain a nutrient-rich diet – Emphasise fruits, vegetables, fish and whole grains that support overall and eye health.
Vaccinate as recommended – Preventing severe infections (for example, herpes zoster, measles) reduces risks of certain eye inflammations that could further harm vision.
What to eat and what to avoid
1. Eat colourful fruits and leafy green vegetables
Spinach, kale, collard greens, oranges, berries and carrots supply lutein, zeaxanthin, vitamin C and beta carotene, all helpful for eye health. Try to include at least five portions of fruits and vegetables per day.
2. Eat fatty fish regularly
Salmon, mackerel, sardines and trout provide omega-3 fatty acids (DHA/EPA), which support retinal cell membranes and may reduce risk of some degenerative changes. Aim for one to two servings of oily fish per week if not restricted.
3. Choose whole grains and lean proteins
Whole-grain bread, brown rice, lentils, beans, eggs and lean meats help keep blood sugar and blood pressure stable. Stable vascular health supports the retina and choroid over the long term.
4. Include nuts and seeds in moderation
Almonds, walnuts, sunflower seeds and flaxseeds offer vitamin E and healthy fats. Small daily portions can add antioxidant and anti-inflammatory benefits without too many calories.
5. Limit highly processed and sugary foods
Sugary drinks, sweets, white bread, instant noodles and fast food can worsen obesity, diabetes and vascular disease if eaten often. Because these conditions can harm the retina, it is safer to keep such foods as occasional treats.
6. Keep salt and trans-fats low
Very salty snacks and foods high in trans-fats raise blood pressure and damage blood vessels, including those in the eye. Choose home-cooked meals, use herbs and spices instead of too much salt, and avoid deep-fried fast food when possible.
7. Avoid smoking and heavy alcohol
Smoking introduces toxins and increases oxidative stress. Heavy alcohol intake can damage the liver and nerves. Both can indirectly worsen eye health and overall healing, so avoiding them is one of the simplest “dietary” protections.
8. Be careful with “mega-dose” supplements
Very high, unsupervised doses of vitamin A, vitamin E or herbal mixtures can be harmful. Because this syndrome is rare, there is no proof that high-dose supplements reverse it, so any supplement plan must be checked with the treating doctors.
9. Stay well hydrated
Drinking enough water supports tear production and general health. While it will not fix dry eye alone, dehydration can make symptoms worse.
10. Tailor diet to other health conditions
If the person also has kidney, liver, heart or metabolic disease, standard dietary rules for those conditions must be followed first. An ophthalmologist and dietitian can then adjust eye-health advice safely on top.
When to see a doctor
You should see an eye doctor or go to emergency care immediately if there is sudden loss of vision, new dark curtain in the vision, flashes of light, many new floaters, severe eye pain, or strong redness. These may signal retinal tear, detachment, infection, or acute glaucoma, which need urgent treatment.
You should arrange a prompt appointment if there is gradual worsening of central or side vision, new blind spots, trouble reading, double vision, persistent eye dryness or burning that does not improve with artificial tears, or any non-healing sore on the eye surface. Regular six- to twelve-monthly check-ups with a retina or cornea specialist are wise even when things feel stable.
For hair and skin, see a dermatologist if there is rapid new hair loss, scalp pain, ulceration, hard or bleeding skin lesions on hairless areas, or if you are considering systemic medications such as JAK inhibitors. A mental-health professional should be consulted if sadness, anxiety, or social withdrawal become persistent.
Frequently asked questions (FAQs)
1. Is regional choroidal atrophy and alopecia curable?
Right now there is no cure that can completely reverse the genetic changes or fully restore lost retina or hair. Treatment focuses on protecting remaining vision, treating eye and scalp complications, and supporting appearance and mental health. Research on gene and cell therapies for inherited retinal diseases is ongoing, so future options may become available.
2. Will I definitely go blind?
Not everyone becomes totally blind. Vision often gets worse slowly over years, and many people keep useful central or peripheral vision for a long time. With low-vision aids, environmental changes and regular specialist care, many tasks can still be done independently even if the retina is thin.
3. Does hair ever grow back in this condition?
Because hair problems are part of the syndrome’s structure, full regrowth is uncommon. However, some people may have patchy growth, and modern treatments for alopecia areata (like JAK inhibitors) might help when the pattern resembles that disease. Cosmetic options such as wigs and eyebrow techniques can also give a satisfying appearance.
4. Are the new drugs for alopecia areata safe for teenagers?
Ritlecitinib is approved down to age 12 for severe alopecia areata, while baricitinib is currently approved for adults. Both carry serious risks such as infections, blood clots and possible increased cancer risk, so they require close monitoring and are not simple “hair pills.” Only a dermatologist experienced with these drugs should decide if benefits outweigh risks.
5. Can special diets cure my eye disease?
No diet has been proven to cure this syndrome. A healthy eating pattern rich in vegetables, fruits, fish and whole grains may support overall and eye health and is recommended for almost everyone, but it cannot rebuild destroyed retinal tissue. Avoid extreme or “miracle” diets that promise to “reverse blindness.”
6. Are stem-cell or gene therapies available for me now?
Stem-cell and gene therapies are in clinical trials for several inherited retinal diseases and for specific gene defects such as RPE65, but not yet for this exact syndrome. Joining a trial is only possible if you meet very strict criteria. Your retina specialist can tell you if any relevant studies exist in your region.
7. Is it safe to play sports?
Many non-contact sports like swimming, cycling with a helmet, walking, or yoga are usually fine and good for health. High-impact contact sports that risk head and eye trauma, like boxing, are often discouraged in people with fragile retina. Your eye doctor can give personalised advice after examining your eyes.
8. Will using screens make my eyes worse?
Screen use does not cause choroidal atrophy, but it can make eyes feel dryer and more tired. Using good lighting, keeping a proper distance, taking regular breaks, and using lubricating drops as advised can keep screen use more comfortable.
9. Should my family members be tested?
Because this is likely genetic, close relatives may benefit from eye exams and, if a specific gene is found, genetic testing. Genetic counselling helps decide who should be tested, when, and what the results might mean for future children.
10. Can I wear contact lenses?
Some people can wear contact lenses, especially specialty lenses that protect the cornea and improve vision. Others, particularly those with severe dry eye or neurotrophic keratitis, may not be good candidates. Your cornea specialist will check the ocular surface and advise you safely.
11. Are over-the-counter “eye vitamins” useful?
AREDS-type eye vitamins may help certain patients with macular degeneration. For this rare syndrome, they can be considered as supportive antioxidants but are not proven treatments. They should be chosen with your doctor to avoid unsafe dosing, especially of zinc, vitamin A or vitamin E.
12. Is it safe to colour or style my hair?
Hair that is thin or fragile may be more easily damaged by harsh chemicals and heat. Gentle colouring methods and low-heat styling are safer, but always test for scalp sensitivity and get advice from your dermatologist, especially if you are on systemic medications.
13. Can stress make my condition worse?
Stress does not change the underlying gene defect, but it can worsen sleep, dry eye symptoms, and how you cope with hair loss or visual limits. Good stress management, exercise, counselling and support groups can improve day-to-day functioning and mood.
14. How often should I see my eye doctor?
Many specialists recommend at least yearly visits, and more often (every 3–6 months) if there are active problems such as macular changes, dry eye, or corneal issues. Your doctor will adjust the interval based on age, severity and any new symptoms.
15. What is the most important thing I can do right now?
The most important steps are: stay under regular care with an experienced eye team, protect your eyes and scalp from UV and injury, treat dry eye carefully, consider psychological support, and involve your family or caregivers in education and planning. These simple actions, repeated over time, often matter more than any single medicine.
Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.
The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: January 14, 2026.
Moloney Syndrome
