الفهرس 
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Abstract
Age-related macular degeneration (AMD) is a leading cause of irreversible blindness in the world. Although the etiology and pathogenesis of AMD remain largely unclear, a complex interaction of genetic and environmental factors is
thought to exist. AMD pathology is characterized by degeneration involving the retinal photoreceptors, retinal pigment epithelium, and Bruch’s membrane, as well as, in some cases, alterations in choroidal capillaries.
Patients with AMD are classified as having early disease,in which visual function is well preserved, or late disease, in which central vision is lost. Until recently, there was no therapy available by which the course of the disorder could be modified. Now, the most common form of late-stage AMD —
choroidal neovascularization — responds to treatment with anti-VEGF therapies; although visual loss is modified in a portion of these cases, no therapeutic approach exists that alters
the evolution from early to late disease.
Manipulation of micro-environmental variables (eg,antioxidant levels, anti-inflammatory, immune-modulation) provides an opportunity for early therapeutic intervention. Gene and/or cellular therapy provide an opportunity for later, sightrestoring treatment.
The use of external low vision aids, and experimental implantable intraocular telescopes still play an important role in these dry AMD patients as well as wet AMD patients who have
failed current treatments.
In the last few decades, the mainstay of treatment for CNV due to AMD has been thermal laser photocoagulation. In the last decade, photodynamic therapy with verteporfin extended
treatment for more patients. While both of these treatments have prevented further vision loss in a subset of patients,improvement in visual acuity is rare.
The management of SMH due to CNV has evolved greatly.
A variety of therapeutic approaches including intravitreal gas injection; pars plana vitrectomy and submacular surgery, both with and without the assistance of intravitreal recombinant
tissue plasminogen activator; also new neovascular AMD radiation therapy are being investigated.
Anti-vascular endothelial growth factor (VEGF) therapy has revolutionized the treatment of AMD-related CNV.
Pegaptanib, an anti-VEGF aptamer prevents vision loss in CNV, although the performance is similar to that of photodynamic therapy. Ranibizumab, an antibody fragment and
bevacizumab, a full-length humanized monoclonal antibody against VEGF have both shown promising results with improvements in visual acuity with either agent. VEGF trap, a
modified soluble VEGF receptor analogue, binds VEGF more tightly than all other anti-VEGF agents and has also shown promising results in early trials.
Other treatment strategies to decrease the effect of VEGF have used small interfering ribonucleic acid (RNA) to inhibit VEGF production and VEGF receptor production. Steroids,including anecortave acetate in the treatment and prevention of CNV, have shown promise in controlled trials. Receptor tyrosine kinase inhibitors, such as vatalanib, inhibit downstream
effects of VEGF, and have been effective in the treatment of CNV in early studie. Other growth factors, including pigment epithelium-derived growth factor that has been administered via
an adenoviral vector has shown promising initial results.
The inflammatory process exacerbates AMD pathogenesis.
Anti-inflammatory agents such as corticosteroid
(Triamcinolone acetonide (TA), dexamethazone) ,Nonsteroidal anti-inflammatory drugs (NSAIDs), Immunosuppressants.