Reticular Drusen ( Subretinal Drusenoid Deposits)

Reticular drusen are tiny, yellow-white bumps that sit above the retinal pigment epithelium (RPE), in the shallow space just under the light-sensing cells. Doctors also call them reticular pseudodrusen or subretinal drusenoid deposits (SDD). They look like an interlacing, net-like pattern—often superotemporal to the fovea—and they are most often seen in people with age-related macular degeneration (AMD). They matter because their presence signals a higher risk of moving to the late, vision-threatening stages of AMD, especially geographic atrophy, and sometimes to a particular “type 3” neovascular pattern. Modern imaging (especially OCT and near-infrared reflectance) is the best way to find them. EyeWikiPubMed CentralLippincott JournalsOphthalmology Retina

Reticular drusen—also called reticular pseudodrusen or subretinal drusenoid deposits (SDD)—are tiny yellow-white spots that collect above the retinal pigment epithelium (RPE), in the subretinal space, near the light-sensing cells. Regular (“soft”) drusen usually sit under the RPE; reticular drusen sit on the other side, which is why doctors see them best with special imaging like near-infrared reflectance, fundus autofluorescence, and optical coherence tomography (OCT). On OCT, they often look like small bumps or mounds right over the RPE. This different location is the key thing that makes reticular drusen special. Review of OptometryPubMed

Reticular drusen matter because they are strongly linked with age-related macular degeneration (AMD) and can signal a higher chance of progression to late AMD, including geographic atrophy (GA) or neovascular (“wet”) AMD in the future. They are also often associated with thinning of the choroid (the blood vessel layer under the retina). In plain terms: if you have reticular drusen, the retina may be more fragile, so careful follow-up and healthy-vision habits are extra important. Review of OptometryPubMed Central

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Types

By the look on fundus images (clinical patterns).
Clinicians describe three common patterns when they look at the back of the eye with multimodal imaging: dot-type spots, ribbon-type interconnected bands, and peripheral clusters beyond the central macula. These patterns help doctors recognize the condition because some show up better on infrared scanning laser images while others show up better on color photos. EyeWikiAjo

By the layer-by-layer OCT appearance (stages).
On spectral-domain OCT, reticular pseudodrusen are above the RPE. A widely used staging system describes: Stage 1—fine, grainy reflective material between the RPE and the ellipsoid zone; Stage 2—small mounds that gently push on the ellipsoid zone; Stage 3—conical deposits that poke into the outer retina. This staging tells us where the deposits sit and how they disturb nearby photoreceptors. PubMed CentralLippincott Journals

By where they live in the retina.
They often favor the superotemporal macula and spare the fovea early. In some inherited disorders, they can extend far into the retinal periphery. EyeWikiPubMed Central

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Causes

Reticular drusen form because the outer retina and its support system (RPE–Bruch’s membrane–choriocapillaris) struggle to handle lipids, waste, and blood supply with age and disease. Below are factors and conditions linked to their presence. Each item explains the “why” in simple terms.

1. Ageing. With age, waste and lipids build up around the RPE/Bruch’s membrane, and the outer retina’s clean-up system slows, encouraging deposit formation above the RPE. Nature

2. Intermediate AMD phenotype. Reticular drusen are a recognized AMD feature and mark a higher risk of progression, especially toward geographic atrophy. PubMed Central

3. ARMS2/HTRA1 risk variants and higher genetic risk scores. These common AMD risk genotypes are associated with having reticular drusen. PubMed

4. Female sex (epidemiologic association). Several cohorts find reticular drusen more frequently in women. EyeWiki

5. Thinning or poor perfusion of the choroid. A thinner or under-perfused choroid delivers less oxygen and nutrients to the outer retina, favoring deposits. PubMed Central

6. Choriocapillaris flow deficits on OCT angiography. Subtle blood-flow reduction right under the retina (choriocapillaris) is linked to reticular drusen. PubMed

7. Reticular macular disease spectrum. Reticular drusen sit within a broader phenotype that reflects outer retinal/choroidal insufficiency. Ophthalmology Retina

8. Pseudoxanthoma elasticum (PXE). A diseased, stiff Bruch’s membrane in PXE is linked to reticular drusen. PubMedJAMA Network

9. Sorsby fundus dystrophy (TIMP3). An inherited macular dystrophy with abnormal Bruch’s membrane can present with reticular drusen. PubMed

10. Late-onset retinal degeneration (C1QTNF5/CTRP5). This inherited disorder frequently shows reticular drusen, often spreading to the periphery. PubMed Central

11. Co-existence with cuticular drusen. Some AMD eyes show both cuticular drusen and reticular drusen, pointing to shared pathways. Nature

12. Acquired vitelliform lesions (association reports). Areas with abnormal photoreceptor–RPE interaction can be linked to reticular patterns. EyeWiki

13. Vitamin A deficiency and retinoid pathway problems. Rod photoreceptors rely on vitamin A; deficiency and related disorders can coexist with reticular patterns. PubMed Central

14. Fundus albipunctatus (night-blindness disorder). Some rod-pathway dystrophies are listed among associations. EyeWiki

15. Retinitis punctata albescens. Another rod-photoreceptor dystrophy occasionally reported with reticular-like patterns. EyeWiki

16. Complement pathway activity in AMD. Systemic complement dysregulation shows up in AMD and may relate to deposit biology. PubMed Central

17. General AMD lipid biology (e.g., HDL/triglycerides patterns). Population studies link certain lipid profiles to AMD and drusen biology, which may extend to reticular drusen. Ophthalmology ScienceScienceDirect

18. Chronic oxidative stress at the RPE–Bruch’s membrane. Oxidative injury can drive deposit formation and remodeling. JAMA Network

19. Genetic–environment interaction (AREDS2). Reticular drusen prevalence tracks with AMD severity and genetics together. PubMed Central

20. “Reticular drusen” as part of AMD natural history. They can appear, evolve, and sometimes regress while overall AMD risk persists. BMJ Open

Note: Many items above are associations, not direct one-to-one causes; in individuals, several factors often act together.

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Symptoms

1. Often no early symptoms. Many people feel fine while deposits are found on imaging.

2. Trouble in dim light. People say “I can see, but I struggle in restaurants or at dusk.” This reflects rod dysfunction. JAMA Network

3. Slower dark adaptation. After bright light, vision takes longer to recover than it used to. AAO Journal

4. Night-driving difficulty. Headlights and low-contrast signs are hard to manage. JAMA Network

5. Glare sensitivity. Bright lights feel harsher and more disabling. JAMA Network

6. Reduced contrast sensitivity. Fine gray-on-gray details are harder to see. JAMA Network

7. Reading trouble in low light. Words blur or fade unless lighting is strong. ScienceDirect

8. Small “dim” spots near the center. Some notice paracentral scotomas on careful testing. IOVS

9. Eyes feel more easily “washed out” after flash or sun. This is photostress intolerance. AAO Journal

10. Mild blur that seems worse in poor lighting. Function drops more in mesopic/scotopic conditions. ScienceDirect

11. Color seems a bit dull in dim rooms. Rod dysfunction affects color cues in low light indirectly. JAMA Network

12. If geographic atrophy develops: blank or missing patches creep into the visual field. PubMed Central

13. If type 3 neovascularization develops: wavy lines or distortion (metamorphopsia). PubMed Central

14. Reading speed fluctuates with lighting quality. People often read better under brighter, even illumination. ScienceDirect

15. Symptoms vary day to day. Small changes in lighting or glare can change function noticeably. JAMA Network

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Diagnostic Tests

A) Physical Exam

1. Dilated slit-lamp fundus examination.
   The doctor examines the retina through a dilated pupil. Reticular drusen can be subtle and may be easiest to suspect when a net-like pattern is seen superotemporally, but exam alone can miss them, so imaging is usually added. EyeWiki

2. Standard color fundus photography.
   High-quality photos document lesions over time. The typical reticular pattern can be faint on color images, so photos are often paired with other modalities for confirmation. EyeWiki

3. Blue-channel–enhanced color photography.
   Bright blue light makes the pattern stand out more in some eyes, improving visibility compared with standard white-light photos. Sensitivity is still limited compared with OCT/IR. PubMed

4. Red-free (green) photography.
   Green light suppresses red choroidal background, so pale subretinal dots and networks are easier to see than on full-spectrum color images. EyeWiki

B) Manual (chair-side) Functional Tests

5. Amsler grid at usual and low luminance.
   A simple square grid helps people notice wavy lines or missing spots near the center, especially if neovascular change or atrophy begins.

6. Low-luminance visual acuity (LLVA).
   Reading letters through a neutral density filter simulates dim lighting; a larger gap between best-corrected VA and LLVA suggests low-light vulnerability, which is common in reticular drusen phenotypes. ScienceDirect

7. Contrast sensitivity (e.g., Pelli-Robson).
   This test measures how well you see faint gray letters; many patients with reticular drusen show reduced contrast, especially under mesopic conditions. JAMA Network

8. Photostress recovery.
   After a bright light exposure, recovery time is measured; delayed recovery is consistent with outer-retinal stress seen in AMD phenotypes with reticular drusen. AAO Journal

C) Lab & Pathological

9. Serum vitamin A and nutrition work-up (when history suggests).
   Because rod function depends on vitamin A, deficiency can mimic or compound low-light symptoms that also occur with reticular drusen. Testing is useful if diet, surgery, or malabsorption raise suspicion. PubMed Central

10. Genetic testing (selected cases).
    Panels can look for TIMP3 (Sorsby), ABCC6 (PXE), C1QTNF5/CTRP5 (L-ORD) when the family history or exam suggests these conditions; research or clinical genotyping may also include AMD-risk loci (ARMS2/HTRA1, CFH) to inform risk discussions. PubMed+2PubMed+2PubMed Central

11. Lipid profile and cardiometabolic markers.
    AMD biology intersects with systemic lipid handling (e.g., HDL patterns), so general lipid checks may be considered in comprehensive care. Ophthalmology Science

12. Research/advanced biomarkers (complement activity).
    Complement system activity is tied to AMD pathogenesis and to drusen biochemistry; while not routine, such markers help in studies exploring why deposits form. PubMed Central

D) Electrodiagnostic & Functional

13. Dark adaptation testing (e.g., dark-adapted chromatic perimeter / AdaptDx).
    This directly measures how quickly rod vision recovers in the dark; delayed recovery is common when reticular drusen are present. PubMed CentralAAO Journal

14. Microperimetry (mesopic and scotopic).
    Light sensitivity is mapped point-by-point across the macula; reticular drusen areas often show depressed sensitivity even when central acuity looks normal. JAMA NetworkIOVS

15. Multifocal ERG.
    This test samples electrical responses from many small retinal regions; reduced signals over reticular drusen zones support the idea of localized outer-retinal dysfunction. IOVS

16. Full-field ERG (rod-weighted protocols).
    Global rod responses can be mildly reduced in some patients, complementing dark-adaptation and microperimetry findings. IOVS

E) Imaging (structural & vascular)

17. Spectral-domain OCT (cross-sectional).
    This is the key structural test. It shows reticular drusen as reflective material above the RPE and lets clinicians stage the deposits and monitor nearby photoreceptors. PubMed Central

18. En face / widefield swept-source OCT.
    Layer-by-layer “top-down” views map the reticular network and track its area over time, often more comprehensively than small scans. Healio JournalsScienceDirect

19. Near-infrared reflectance (IR-SLO).
    IR imaging is very sensitive for reticular drusen and pairs well with OCT; the lesions appear as dark spots against a bright background. PubMed

20. Fundus autofluorescence (FAF) and confirmatory angiography.
    On FAF, reticular drusen appear as many small dark spots with bright lines between them; late-phase indocyanine green angiography (ICGA) can show corresponding hypofluorescent dots and has high specificity for confirmation when needed. EyeWikiLippincott Journals

Non-pharmacological treatments (therapies & others)

Each item includes: What it is, Purpose, How it helps (mechanism)—all in simple language.

1. Quit smoking completely
   Purpose: cut the strongest modifiable risk for AMD progression.
   How it helps: smoking drives oxidative stress and blood-vessel damage in the retina; stopping reduces this damage over time. PubMed Central

2. Mediterranean-style eating pattern
   Purpose: support retinal cells with antioxidant-rich foods.
   How it helps: more leafy greens, colorful vegetables, legumes, whole grains, nuts, olive oil, and fish provide carotenoids (lutein/zeaxanthin) and healthy fats that correlate with lower AMD risk and slower worsening. AAO-HNS

3. Regular fish intake (2–3 times/week)
   Purpose: give the retina DHA/EPA from natural foods.
   How it helps: dietary omega-3s in fish are linked with lower risk of developing AMD; supplements don’t show the same benefit in trials, so focus on food. JAMA Network+1

4. Low-glycemic eating (choose slow-release carbs)
   Purpose: reduce sugar spikes that stress retinal metabolism.
   How it helps: higher dietary glycemic index has been associated with greater AMD risk and progression; swapping to low-GI carbs can help protect macular function. American Journal of Clinical Nutrition

5. AREDS2 eye vitamins (when your eye doctor says you qualify)
   Purpose: slow progression from intermediate to advanced AMD.
   How it helps: specific antioxidant/mineral doses (see “supplements” section) lower the risk of worsening; these do not treat reticular drusen directly and are not for prevention in healthy eyes. Age Related Eye Diseases

6. Blood-pressure control
   Purpose: keep choroidal/retinal circulation steady.
   How it helps: blood-vessel stability supports nutrient delivery to the macula; long-term BP variability may relate to advanced AMD risk. Ophthalmology Science

7. Regular physical activity
   Purpose: reduce systemic inflammation and improve vascular health.
   How it helps: exercise supports good circulation and metabolic balance, indirectly helping retinal resilience (a general recommendation in AMD care).

8. Healthy weight and lipid management
   Purpose: decrease oxidative and inflammatory stress.
   How it helps: better metabolic health may lower the stress load on the retina and RPE, supporting slower degeneration (part of global AMD risk reduction). PubMed Central

9. UV/bright-light protection (quality sunglasses, hats)
   Purpose: reduce light-induced oxidative stress.
   How it helps: less high-energy light reaching the macula means less cumulative stress on retinal cells (a common, low-risk protective step).

10. Amsler grid self-monitoring at home
    Purpose: catch sudden wavy or missing spots early.
    How it helps: simple weekly checks can reveal new distortion suggesting conversion to wet AMD so treatment starts sooner. Astellas Pharma

11. Home electronic monitoring (e.g., ForeseeHome® for eligible eyes)
    Purpose: detect very early changes toward wet AMD.
    How it helps: device-based monitoring detected conversion earlier than standard care in a randomized study, enabling earlier anti-VEGF treatment. FDA Access Data

12. Scheduled dilated retinal exams and OCT
    Purpose: track reticular drusen, macular structure, and signs of GA/CNV.
    How it helps: regular imaging finds subtle changes before vision drops.

13. Low-vision rehabilitation (when central vision declines)
    Purpose: keep reading, working, and navigating safely.
    How it helps: training + tools (magnifiers, electronic readers, contrast/lighting optimization) improve daily function even if the disease progresses. National Eye Institute

14. Optimize home/work lighting and contrast
    Purpose: reduce glare and eye strain.
    How it helps: brighter, even lighting and high-contrast print/icons make tasks easier with macular changes.

15. Falls-prevention and mobility strategies
    Purpose: stay safe as central vision dims.
    How it helps: clutter reduction, high-contrast stair edges, and orientation training reduce accident risk.

16. Medication review with your doctors
    Purpose: avoid unnecessary agents that might dry the eye severely or worsen glare; coordinate supplements with other drugs.
    How it helps: safer combinations reduce side-effects that can make vision tasks harder.

17. Manage diabetes and blood sugar well (if present)
    Purpose: lower vascular stress on the retina.
    How it helps: stable glucose supports retinal energy use and may reduce risk of wet AMD in those with poor glycemic status. PubMed

18. Adequate sleep and treat sleep apnea
    Purpose: keep oxygen delivery steady overnight.
    How it helps: better oxygenation reduces oxidative stress on photoreceptors and RPE.

19. Stop or avoid beta-carotene supplements if you smoke
    Purpose: avoid extra lung-cancer risk.
    How it helps: in smokers, beta-carotene supplements increase lung-cancer risk; AREDS2 removed beta-carotene and used lutein/zeaxanthin instead. Age Related Eye Diseases

20. Patient education & support
    Purpose: understand your condition and respond quickly to changes.
    How it helps: knowing warning signs and healthy habits improves outcomes; AAO patient resources explain risks and steps that help. AAO-HNS

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Drug treatments

Important note: there is no medicine that “clears” reticular drusen themselves. Medicines are used for complications of AMD that people with reticular drusen are at higher risk of—mainly wet AMD and geographic atrophy (GA). Dosing below reflects current labeling or consensus and must be individualized by your retina specialist.

1. Ranibizumab (Lucentis®) — anti-VEGF
   Dose & time: 0.5 mg intravitreal, typically monthly at start, then “treat-and-extend” as guided by your doctor.
   Purpose: stop and dry up abnormal leaking vessels in wet AMD.
   Mechanism: blocks VEGF-A to reduce leakage and new vessel growth.
   Key side effects: injection-related risks (endophthalmitis, IOP rise), rare arterial thromboembolic events. FDA Access Data

2. Aflibercept 8 mg (Eylea HD®) — VEGF-A/PlGF trap
   Dose & time: 8 mg monthly for 3 doses, then every 8–16 weeks as directed.
   Purpose: maintain drying of wet AMD with fewer injections.
   Mechanism: binds VEGF-A/B and PlGF to suppress leakage and neovascular growth.
   Key side effects: similar intravitreal injection risks. Regeneron

3. Aflibercept 2 mg (Eylea®) — VEGF-A/PlGF trap
   Dose & time: 2 mg monthly for 3 doses, then every 8 weeks (many adopt treat-and-extend).
   Purpose/Mechanism/Side effects: as above. Regeneron

4. Faricimab (Vabysmo®) — dual Ang-2 & VEGF-A inhibitor
   Dose & time: 6 mg; after loading, many patients maintain on q8–16 weeks depending on response.
   Purpose: control wet AMD with longer intervals between injections in suitable eyes.
   Mechanism: blocks VEGF-A and Ang-2 to stabilize vessels more durably.
   Key side effects: injection-related risks. GeneFDA Access Data

5. Bevacizumab (Avastin®; off-label for eye use) — anti-VEGF
   Dose & time: commonly 1.25 mg monthly then treat-and-extend (off-label practice).
   Purpose/Mechanism: similar to other anti-VEGF agents; widely used based on strong clinical experience and guideline acceptance.
   Key side effects: injection risks; systemic effects appear low at ocular doses. AAO-HNS

6. Brolucizumab (Beovu®) — anti-VEGF
   Dose & time: label-guided loading then up-to-q12w in selected responders.
   Purpose: dry the retina with fewer injections in some patients.
   Mechanism: small anti-VEGF molecule for high tissue penetration.
   Key caution: rare retinal vasculitis/occlusion has been reported; careful selection and monitoring needed (not suitable for everyone). AAO-HNS

7. Pegcetacoplan (SYFOVRE®) — complement C3 inhibitor
   For: geographic atrophy (GA) secondary to AMD.
   Dose & time: 15 mg (0.1 mL) intravitreal every 25–60 days (monthly or every-other-month, per label).
   Purpose: slow GA lesion growth; it does not restore lost retina.
   Mechanism: dampens overactive complement (immune) cascade that damages retinal cells.
   Key side effects: injection risks; rare retinal vasculitis/occlusion; slightly increased risk of conversion to wet AMD in some patients—eyes are monitored closely. FDA Access Data

8. Avacincaptad pegol (IZERVAY®) — complement C5 inhibitor
   For: GA secondary to AMD.
   Dose & time: label-directed intravitreal dosing (monthly in clinical practice early on; see PI).
   Purpose: slow GA enlargement.
   Mechanism: inhibits complement C5 to reduce immune-mediated tissue injury.
   Key side effects: injection risks, potential for exudation; careful monitoring. Astellas PharmaFDA Access Data

9. Verteporfin photodynamic therapy (PDT) — photosensitizer drug + laser procedure
   For: selected, non-typical neovascular patterns where PDT can help (your retina specialist decides).
   Purpose/Mechanism: verteporfin accumulates in abnormal vessels; a low-energy laser activates it to close those vessels without major damage to surrounding tissue (used far less since anti-VEGF era). AAO-HNS

10. Combination strategies (anti-VEGF + treat-and-extend protocols)
    For: practical control of wet AMD over years.
    Purpose/Mechanism: same drug, optimized scheduling to keep the macula dry with the fewest injections while protecting vision, tailored per patient. AAO-HNS

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Dietary molecular supplements

Always review supplements with your eye doctor and primary care physician. Some interact with medicines; smokers should avoid beta-carotene.

1. AREDS2 core formula — Vitamin C 500 mg, Vitamin E 400 IU, Zinc 80 mg (or 25 mg alternative) + Copper 2 mg, Lutein 10 mg, Zeaxanthin 2 mg daily.
   Function: slows progression from intermediate to advanced AMD.
   Mechanism: antioxidant + zinc support reduce oxidative/immune injury in the macula; lutein/zeaxanthin bolster macular pigment. No beta-carotene in AREDS2 (safer in smokers). Age Related Eye Diseasesmkuh.nhs.uk

2. Lutein 10 mg (if not already in your AREDS2)
   Function: enrich macular pigment for blue-light filtering and antioxidant action.
   Mechanism: concentrates in the macula to neutralize free radicals. JAMA Network

3. Zeaxanthin 2 mg (if not already in your AREDS2)
   Function/Mechanism: works with lutein to strengthen macular pigment. JAMA Network

4. Zinc (25–80 mg as zinc oxide) + Copper 2 mg
   Function: supports retinal enzymes; copper prevents copper-deficiency anemia caused by high-dose zinc.
   Mechanism: co-factor roles in antioxidant defenses. mkuh.nhs.uk

5. Omega-3 DHA/EPA from food; supplements not proven
   Function: support retinal cell membranes and anti-inflammatory balance.
   Mechanism: dietary DHA/EPA correlate with lower AMD risk, but large trials did not show benefit from adding fish-oil pills to AREDS2. Prefer fish over capsules. JAMA NetworkAge Related Eye Diseases

6. Saffron 20 mg/day
   Function: small trials reported improvements in some visual functions in early/intermediate AMD.
   Mechanism: carotenoid spice with antioxidant actions; evidence is promising but limited. PubMed Central

7. Meso-zeaxanthin (varies; often 10–17 mg in studies)
   Function: may further increase macular pigment (not in AREDS2).
   Mechanism: central macular carotenoid; evidence mixed; discuss with your doctor.

8. Astaxanthin 4–12 mg/day
   Function: potent antioxidant carotenoid found in seafood; exploratory support for retinal oxidative stress.
   Mechanism: quenches reactive oxygen species; clinical AMD data limited.

9. Resveratrol 150–500 mg/day
   Function: antioxidant/polyphenol with anti-inflammatory signaling; human AMD evidence limited and mostly preliminary.
   Mechanism: modulates oxidative and inflammatory pathways. PubMed

10. Curcumin 500–1000 mg/day (often with piperine for absorption)
    Function: systemic antioxidant/anti-inflammatory; ocular evidence is early; use as adjunct only.
    Mechanism: down-regulates inflammatory signals and oxidative stress.

Safety pearls: high-dose Vitamin E may interact with anticoagulants; zinc 80 mg can upset stomach and lower copper—use the matched copper; smokers/former smokers should avoid beta-carotene and use AREDS2 instead. Age Related Eye Diseases

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Regenerative / stem-cell” therapies

These options do not erase reticular drusen. They either modulate the immune complement system in GA or aim for long-lasting anti-VEGF or cell replacement. Several are investigational.

1. Pegcetacoplan (SYFOVRE®) — approved for GA
   Dose: 15 mg intravitreal every 25–60 days.
   Function: slows GA growth.
   Mechanism: Complement C3 inhibition reduces immune attack on retinal cells.
   Key notes: requires continued injections and close monitoring for conversion to wet AMD. FDA Access Data

2. Avacincaptad pegol (IZERVAY®) — approved for GA
   Dose: label-directed monthly intravitreal dosing initially (specialist adjusts).
   Function: slows GA enlargement.
   Mechanism: Complement C5 inhibition to reduce downstream inflammatory damage. Astellas Pharma

3. RGX-314 gene therapy (subretinal or suprachoroidal) — investigational
   Dose: one-time surgical (subretinal) or in-office (suprachoroidal) vector delivery.
   Function: long-term expression of an anti-VEGF protein to control wet AMD with far fewer injections.
   Mechanism: AAV8 vector delivers DNA so your eye makes its own anti-VEGF locally. Early studies suggest durable VEGF suppression. ClinicalTrials.govPubMed

4. Ixoberogene soroparvovec (Ixo-vec/ADVM-022) — investigational
   Dose: generally a single intravitreal gene-therapy injection in trials.
   Function: sustained aflibercept production to reduce injection burden in wet AMD.
   Mechanism: AAV vector programs retinal cells to secrete anti-VEGF. Phase 1/2 data show maintained anatomy with fewer rescue shots; Phase 3 is underway. The LancetAdverum Biotechnologies

5. RPE patch transplantation (hESC-RPE on parylene scaffold) — investigational
   Dose: one-time surgical implant beneath the macula.
   Function: replace diseased RPE to support overlying photoreceptors.
   Mechanism: a living RPE monolayer on a synthetic Bruch’s-membrane-like film is placed under the atrophic area; early trials show feasibility and safety signals. PubMedTVST

6. iPSC-RPE or other stem-cell–derived RPE strategies — investigational
   Dose: surgical sheet or cell suspension under the retina, as per study design.
   Function: restore the RPE layer to slow further photoreceptor loss.
   Mechanism: cell replacement aims to re-establish nutrient recycling and waste handling for photoreceptors. Multiple approaches are in early clinical stages. PubMed CentralFrontiers

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Surgeries

1. Subretinal RPE patch implantation (clinical trials)
   Why: for selected patients with advanced GA, replacing the support layer (RPE) may help the surviving photoreceptors. Research setting only. PubMed

2. Vitrectomy for tractional problems (when present)
   Why: if an epiretinal membrane or vitreomacular traction is pulling on the macula and blurring vision, surgery can relieve the traction and improve quality of vision for tasks.

3. Cataract surgery (when cataract—not AMD—limits clarity)
   Why: clearing a cloudy lens can improve light and contrast reaching the retina; it doesn’t treat drusen but can improve everyday seeing.

4. Photodynamic therapy (PDT) with verteporfin (drug-laser procedure)
   Why: in selected, non-typical neovascular patterns, PDT can help shut down abnormal vessels, sometimes combined with anti-VEGF. AAO-HNS

5. Low-vision device fitting (procedural rehab)
   Why: a structured, multi-visit program to test and customize optical/electronic devices helps you read, recognize faces, and navigate more safely. National Eye Institute

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Preventions

1. Don’t smoke—ever. PubMed Central

2. Eat Mediterranean-style, rich in leafy greens and fish. AAO-HNS

3. Choose low-glycemic carbs (oats, legumes, whole grains). American Journal of Clinical Nutrition

4. Keep blood pressure well-controlled. Ophthalmology Science

5. Stay active most days of the week.

6. Maintain a healthy weight and manage cholesterol. PubMed Central

7. Wear quality sunglasses and a brimmed hat outdoors.

8. Have regular dilated eye exams and OCT checks.

9. Use an Amsler grid weekly and report changes fast. Astellas Pharma

10. If your doctor says you qualify, take AREDS2 vitamins exactly as directed (no beta-carotene if you smoke). Age Related Eye Diseases

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When to see a doctor

• Right away (urgent): sudden new wavy lines, a dark/blank spot in the center, a quick drop in reading vision, new distortion of faces or print, flashes/floaters with a curtain effect, or eye pain after an injection. These can signal conversion to wet AMD or other emergencies that need fast treatment. Astellas Pharma

• Soon (within days): a steady, noticeable change in central clarity or contrast, or a new Amsler grid change that doesn’t go away.

• Routine (as advised): scheduled exams with OCT imaging to track reticular drusen, macular health, and risk markers.

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What to eat” and “what to avoid”

Eat more of:

1. Dark leafy greens (spinach, kale) for lutein/zeaxanthin.

2. Oily fish (salmon, sardines, mackerel) 2–3x/week. JAMA Network

3. Colorful vegetables & fruits (peppers, oranges, berries) for antioxidants.

4. Legumes & whole grains (lentils, oats, barley) for low-GI carbs. American Journal of Clinical Nutrition

5. Nuts & olive oil for healthy fats (Mediterranean pattern). AAO-HNS

Limit/avoid:

1. Smoking (including exposure)—the top avoidable harm. PubMed Central

2. High-GI refined carbs (sugary drinks, white bread) that spike glucose. American Journal of Clinical Nutrition

3. Trans/saturated fats heavy diets (processed snacks, fatty red meats). AAO-HNS

4. Excess alcohol (can worsen nutrition and overall eye health).

5. Beta-carotene supplements if you smoke (use AREDS2 instead). Age Related Eye Diseases

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Frequently asked questions (FAQs)

1. Do reticular drusen always mean I’ll go blind?
   No. They are a risk marker for later AMD complications, so close follow-up and healthy-vision habits are vital to protect sight. PubMed Central

2. Can reticular drusen go away?
   They typically don’t “melt” with treatment. The goal is to slow or prevent progression to GA or wet AMD and protect usable vision.

3. What tests pick up reticular drusen best?
   Doctors use near-infrared reflectance, fundus autofluorescence, and OCT to see them clearly and to check their position above the RPE. PubMed

4. Are AREDS2 vitamins for everyone?
   No. They’re recommended for intermediate AMD or certain higher-risk features. They don’t prevent AMD in healthy eyes. Ask your eye doctor. Age Related Eye Diseases

5. Should I take fish-oil capsules?
   Large trials found no added benefit from omega-3 supplements in AREDS2; instead, eat fish regularly if your diet allows. Age Related Eye Diseases

6. If my eye becomes wet AMD, what happens?
   You’ll likely start anti-VEGF injections (e.g., ranibizumab, aflibercept, faricimab) to dry leakage and protect vision; intervals extend once stable. FDA Access DataRegeneronGene

7. If I develop geographic atrophy, are there treatments?
   Yes, pegcetacoplan and avacincaptad pegol can slow GA growth; they don’t restore lost retina, so earlier detection and ongoing monitoring matter. FDA Access DataAstellas Pharma

8. How often are injections needed?
   It varies. Many need monthly injections at first, then move to every 8–16 weeks depending on the drug and response (your doctor tailors this). RegeneronGene

9. Are there long-lasting options to reduce injection burden?
   Gene therapies like RGX-314 or Ixo-vec are being studied to provide sustained anti-VEGF after a single procedure; they’re not yet standard of care. PubMedThe Lancet

10. Do blue-light–blocking glasses stop AMD?
    Evidence is mixed; blue-light filters may reduce glare/eye strain but haven’t proven to prevent AMD. Sunglasses outdoors are still wise.

11. Can light therapy help?
    Photobiomodulation shows early signals in studies, but it’s not established care for AMD yet. Consider only in research-guided settings.

12. Is PDT still used?
    Occasionally, for selected lesion types or in combination strategies; anti-VEGF remains first-line for most wet AMD. AAO-HNS

13. What if I notice new waviness or a dark spot?
    Call your retina clinic immediately—early wet AMD treatment saves vision. Use your Amsler grid weekly to catch changes. Astellas Pharma

14. Do cataract surgeries help AMD?
    They don’t treat AMD itself but can improve clarity and brightness if a cataract is limiting vision, making daily tasks easier.

15. What’s the single most powerful habit?
    Don’t smoke—and if you do, quit now. Pair that with Mediterranean-style eating and regular eye checks. PubMed CentralAAO-HNS

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The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: August 23, 2025.