What is age-related macular degeneration?

AMD is progressive damage to the macula — the small central part of the retina responsible for sharp, detailed and colour vision. It causes loss of CENTRAL vision while peripheral vision is preserved, so people with advanced AMD can usually still walk around independently but cannot read, recognise faces, drive or do fine work. There are two forms. Dry (non-neovascular) AMD, around 85-90% of cases, progresses slowly over years through accumulation of deposits called drusen to geographic atrophy. Wet (neovascular) AMD, 10-15% of cases, occurs when abnormal new blood vessels grow beneath the retina and leak fluid and blood — it can destroy central vision within weeks and is the form responsible for most severe, rapid loss.

What symptoms should prompt urgent attention?

Any sudden change: straight lines appearing bent, wavy or distorted (metamorphopsia — door frames, window frames, tiles, lines of text); a new grey, dark or blank patch in the centre of vision; a sudden drop in central vision or in reading ability; objects appearing smaller or a different size in one eye. These suggest conversion to wet AMD and need ophthalmology assessment within days, not weeks — because anti-VEGF treatment given before scarring develops preserves far more vision than the same treatment given later. Anyone with AMD in one or both eyes should be given an Amsler grid to check each eye separately every day (with reading glasses on, covering the other eye) and told explicitly to seek urgent review rather than wait for their next routine appointment.

How is wet AMD treated?

With intravitreal anti-VEGF injections — a drug injected into the vitreous cavity through the white of the eye under topical anaesthesia, taking a few minutes. The drugs (ranibizumab, aflibercept, bevacizumab, brolucizumab, faricimab) block vascular endothelial growth factor, the signal driving the abnormal vessels. Treatment usually starts with three or four loading injections at monthly intervals, then continues on a treat-and-extend schedule guided by OCT scans — treating at each visit while gradually lengthening the interval if the retina stays dry. Treatment is generally long-term. Before anti-VEGF became available, wet AMD meant near-certain loss of central vision; now the majority of treated eyes maintain their vision and a substantial minority improve — provided treatment begins promptly and is not interrupted.

Do vitamin supplements help?

Only for a specific group. The AREDS2 formulation reduces the risk of progression to ADVANCED AMD by around 25% over five years — but only in people who already have intermediate AMD (large drusen and/or pigment changes), or advanced AMD in one eye. It does NOT prevent AMD in people with healthy eyes or only early changes, and taking it in that situation is of no benefit. Two safety points matter. First, the original AREDS formulation contained beta-carotene, which increased lung cancer risk in current and former smokers; AREDS2 replaced it with lutein and zeaxanthin, and any smoker or ex-smoker on a beta-carotene-containing eye supplement should be switched. Second, many commercial "eye health" products do not match the AREDS2 formulation and doses — check the composition rather than the marketing.

Can anything be done for dry AMD?

Historically nothing, and this is changing slowly. For intermediate dry AMD, AREDS2 supplements reduce progression risk by around 25%, and smoking cessation, blood pressure control and a diet rich in leafy green vegetables and oily fish all matter. For geographic atrophy — advanced dry AMD — complement inhibitors (pegcetacoplan and avacincaptad pegol) were approved by the FDA in 2023 and slow the growth of atrophy by roughly 14-20%. However, they do not restore or improve vision, do not halt progression, require repeated intravitreal injections indefinitely, and increase the risk of conversion to wet AMD; the EMA declined approval for pegcetacoplan. Alongside this, low vision rehabilitation — magnifiers, task lighting, eccentric viewing training, screen readers — is consistently the most under-used and most immediately useful intervention for people already living with central vision loss.

How does GMJ News cover AMD?

GMJ News covers AMD epidemiology and projections, dry vs wet classification and drusen staging, metamorphopsia as an urgent referral symptom and Amsler grid self-monitoring, anti-VEGF agents and treat-and-extend regimens, the CATT/IVAN bevacizumab equivalence and its global access implications, geographic atrophy and the 2023 complement inhibitors with their limitations, AREDS2 supplement indications and the beta-carotene smoking hazard, OCT and OCTA imaging, low vision rehabilitation, Charles Bonnet syndrome, and smoking as the dominant modifiable risk factor. Relevant to PHIG's eye health, ageing and rehabilitation programmes.

Home › Topics › Age-Related Macular Degeneration

Age-Related Macular Degeneration

GMJ News knowledge hub · last reviewed September 2026 · Georgian Medical Journal

Summary Statistics Glossary GMJ news FAQ Documents Organizations Research

Age-related macular degeneration (AMD) — progressive degeneration of the macula, the central retina responsible for detailed and colour vision — is the leading cause of irreversible blindness in high-income countries, affecting an estimated 200 million people globally with projections approaching 288 million by 2040, and is divided into dry AMD (approximately 85-90%, slowly progressive, culminating in geographic atrophy) and neovascular or wet AMD (10-15%, driven by choroidal neovascularisation, capable of destroying central vision within weeks) (WHO). The therapeutic transformation came with intravitreal anti-VEGF therapy (ranibizumab, aflibercept, bevacizumab off-label, brolucizumab, and the longer-acting faricimab), which converted wet AMD from a condition of near-certain central vision loss into one where the majority of treated eyes maintain or improve vision — provided treatment begins early, which is why any patient reporting sudden distortion of straight lines (metamorphopsia) requires urgent, not routine, ophthalmological assessment.

Key messages

Leading cause of irreversible blindness in high-income countries — ~200 million affected

AMD affects an estimated 200 million people globally, projected to approach 288 million by 2040 as populations age. It causes loss of CENTRAL vision — reading, faces, driving, fine detail — while peripheral vision is preserved, so patients are rarely totally blind but lose functional independence. Dry (non-neovascular) AMD accounts for approximately 85-90%; wet (neovascular) AMD for 10-15% but a disproportionate share of severe vision loss.

Metamorphopsia is an emergency symptom — same-week referral

Sudden distortion of straight lines (door frames, tiles, window frames appearing bent or wavy), a new central grey or blank patch (scotoma), or abrupt reduction in central vision, suggests conversion to neovascular AMD. This requires URGENT ophthalmological assessment — ideally within days — because anti-VEGF treatment started before subfoveal fibrosis develops preserves far more vision than treatment started weeks later. Patients with dry AMD in one or both eyes should be taught Amsler grid self-monitoring and given explicit instructions to present urgently, not to wait for a routine appointment.

Anti-VEGF therapy transformed wet AMD outcomes

Intravitreal anti-VEGF injections (ranibizumab, aflibercept, bevacizumab used off-label, brolucizumab, faricimab) block vascular endothelial growth factor driving choroidal neovascularisation. Before anti-VEGF, wet AMD meant near-certain loss of central vision; with treatment, the majority of eyes maintain vision and a substantial minority improve. Regimens: fixed monthly/bimonthly; pro re nata (PRN) with monthly monitoring; or treat-and-extend (the most widely used — treating at every visit while progressively lengthening intervals). Faricimab (bispecific anti-VEGF-A/anti-Ang-2) and the ranibizumab port delivery system aim to extend treatment intervals and reduce injection burden.

Bevacizumab is as effective as ranibizumab — and central to global access

The CATT (NEJM 2011) and IVAN trials established that bevacizumab (a cancer drug, compounded into intravitreal doses) is clinically equivalent to ranibizumab for wet AMD at a fraction of the cost. Because it is unlicensed for intraocular use, its availability depends on regulatory tolerance and safe compounding pharmacy practice, and it has been the subject of repeated litigation and lobbying. WHO includes bevacizumab in the Model List of Essential Medicines for this indication. For most of the world, the difference between treatable and untreatable wet AMD is a compounding and regulatory question, not a scientific one.

Geographic atrophy — the advanced dry AMD frontier

Geographic atrophy (GA) — progressive, well-demarcated loss of retinal pigment epithelium, photoreceptors and choriocapillaris — is the advanced form of dry AMD and had no treatment for decades. Complement pathway inhibitors targeting the underlying dysregulated complement activation (pegcetacoplan, avacincaptad pegol) were approved by the FDA in 2023 and slow the rate of GA lesion growth by approximately 14-20% — but they do NOT restore vision, do not stop progression, require ongoing intravitreal injections, and are associated with an increased risk of conversion to neovascular AMD. Their clinical value remains actively debated; EMA declined approval for pegcetacoplan.

AREDS2 supplements — for intermediate AMD only, and smokers must avoid beta-carotene

The AREDS2 formulation (vitamin C 500mg, vitamin E 400 IU, zinc 80mg or 25mg, copper 2mg, lutein 10mg, zeaxanthin 2mg) reduces progression to ADVANCED AMD by approximately 25% over five years. Critical qualifications: it benefits only patients with INTERMEDIATE AMD or advanced AMD in one eye — it does NOT prevent AMD in people with no or early AMD; and the original AREDS formulation contained beta-carotene, which INCREASED lung cancer risk in current and former smokers — AREDS2 replaced it with lutein and zeaxanthin for exactly this reason. Any smoker or ex-smoker taking a beta-carotene-containing eye supplement should be switched.

Key statistics

~200M

people affected by AMD globally; projected ~288 million by 2040

Lancet Glob Health/WHO

85-90%

of AMD is dry (non-neovascular); 10-15% wet but causes most severe vision loss

AAO/RCOphth

CATT 2011

bevacizumab clinically equivalent to ranibizumab at a fraction of the cost (NEJM)

NEJM 2011

~25%

reduction in progression to advanced AMD with AREDS2 — intermediate AMD only

AREDS2/JAMA

Smoking

the strongest modifiable risk factor for AMD — roughly doubles to quadruples risk

AAO/RCOphth

FDA 2023

complement inhibitors for geographic atrophy slow lesion growth ~14-20% but do not restore vision

FDA 2023

AMD — intervention impact on visual outcomes

Source: AAO/RCOphth. Anti-VEGF for wet AMD is the single most effective intervention; supplements act only on intermediate dry AMD.

Glossary of key terms

AMD classification
OphthalmologyEarly AMD: medium drusen (63-125μm), no pigmentary abnormality. Intermediate AMD: large drusen (>125μm) and/or AMD pigmentary abnormalities — this is the group in whom AREDS2 supplements are indicated. Late AMD: either geographic atrophy (advanced dry) or neovascular/exudative AMD (wet). Drusen: extracellular deposits of lipid and protein between the retinal pigment epithelium and Bruch's membrane — the pathological hallmark. Reticular pseudodrusen (subretinal drusenoid deposits): a distinct and higher-risk phenotype associated with faster progression to both GA and neovascular AMD. Beyond this, subtypes of neovascular AMD (type 1 occult, type 2 classic, type 3 retinal angiomatous proliferation, polypoidal choroidal vasculopathy) differ in treatment response.

OCT and OCT angiography
ImagingOptical coherence tomography (OCT) is the central investigation in AMD — a non-invasive, few-second scan producing cross-sectional retinal images at near-histological resolution. It detects the signs of activity that drive treatment decisions: intraretinal fluid, subretinal fluid, pigment epithelial detachment, and subretinal hyperreflective material. Treat-and-extend regimens are driven almost entirely by OCT findings. OCT angiography (OCTA) visualises retinal and choroidal blood flow without dye injection, allowing detection of choroidal neovascular membranes non-invasively. Fluorescein angiography remains useful for classifying lesion type and detecting leakage; indocyanine green angiography is used particularly for polypoidal choroidal vasculopathy.

Treat-and-extend regimen
Ophthalmology/PracticeThe dominant contemporary anti-VEGF strategy, designed to balance disease control against injection burden and clinic capacity. The patient is treated at EVERY visit (unlike PRN, where they may attend and not be treated), while the interval between visits is progressively extended by typically two weeks at a time as long as OCT shows the macula remains dry, and shortened if fluid recurs. Advantages over PRN: fewer total clinic visits; less undertreatment; better real-world visual outcomes. Advantages over fixed monthly: fewer injections. It also reduces the "monitoring visit" burden, which in real-world health systems is often the limiting resource, and is the reason real-world outcomes historically fell short of the pivotal trials.

Low vision rehabilitation
RehabilitationThe most under-referred intervention in AMD. Because peripheral vision is retained, patients with even advanced AMD can usually be helped substantially: magnifiers (hand, stand, electronic video magnifiers); high-power reading additions; task lighting (often the single most effective and cheapest intervention); high-contrast and large-print materials; screen readers, text-to-speech and smartphone accessibility features; eccentric viewing training (learning to use a preferred retinal locus outside the scotoma); and home hazard assessment for falls. Registration as sight-impaired or severely sight-impaired unlocks benefits and services. Depression is common and substantially under-recognised in AMD — screening and treating it improves functional outcomes as much as optical aids.

Charles Bonnet syndrome
Neuro-ophthalmologyComplex visual hallucinations occurring in people with significant vision loss who have intact cognition and insight — a release phenomenon of deafferented visual cortex, not a psychiatric disorder. Reported by a substantial proportion of patients with AMD (estimates range widely, 10-40%). Hallucinations are typically formed and detailed: patterned geometric shapes, faces, figures in period costume, animals, landscapes. Patients very frequently do NOT report them, fearing a diagnosis of dementia or psychosis. Proactive explanation is therapeutic in itself and is a simple, high-value clinical act: telling a patient before it happens that this is a known consequence of vision loss, not a sign of losing their mind, substantially reduces distress. No routine drug treatment is indicated.

Modifiable risk factors
PreventionSmoking is by far the strongest modifiable risk factor, roughly doubling to quadrupling risk and bringing forward onset by several years; risk declines after cessation but remains elevated for years — making AMD a powerful and under-used argument in smoking cessation consultations. Other associations: hypertension and cardiovascular disease; obesity; low dietary intake of leafy green vegetables and oily fish; and, more weakly, cumulative light exposure. Genetics contribute substantially (CFH and ARMS2/HTRA1 polymorphisms), but genetic testing is not currently recommended in routine practice because it does not change management. Cataract surgery does not cause AMD progression — an important reassurance, as the belief persists.