More than 90% of the information that humans obtain from the outside world comes from the visual system, and the loss of sight is as terrifying and devastating as having cancer. Age-related macular degeneration (AMD), also known as age-related macular degeneration, is a multifactorial blindness disease that develops with age. AMD occurs in people over 50 years of age, with both eyes developing successively or simultaneously. ARMD is currently one of the most prevalent diseases worldwide, with a prevalence of 1.7-7% between the ages of 55 and 65, 14.4-24% between the ages of 65 and 74, and up to 40-44.4% above the age of 75. According to the epidemiological survey in China, it is 10.59% in Tibet and Guangdong, and 15.5% in Shanghai for people over 50 years old. The number of patients worldwide exceeds 30 million. The National Eye Institute (NIH) recently published the results of the Age-Related Eye Disease Study, stating that AMD is the leading cause of vision loss and blindness, and that as the average human lifespan increases, blindness from ARMD will become a public health problem that cannot be ignored. The epidemiological report released by the International Council of Ophthalmology also shows that ARMD has become the first of the four major blindness-causing eye diseases in humans. Therefore, this disease is not only the primary cause of low vision and blindness in western countries for people over 50 years old, but also the main blinding eye disease facing China in the future. 1.The anatomical basis of macula The human eye can see the object because the reflected light shining on the object, after refracted by the refractive medium of the cornea, crystal and vitreous humor of the eye, is imaged on the retina. In this way, the human eye is like a camera. The retina is equivalent to the camera’s photoreceptor plate, which is composed of many well-defined nerve cells. In the inner surface of the retina directly opposite to the visual axis, there is an oval depression area called macula, is a very important part of the retina, when a person soon after death, the tissue is turned yellow, so the name macula. The macula is only 1~3mm in diameter, don’t see it is a bullet, but more than 90% in charge of the visual and color vision function of the visual cone cells are concentrated here, the macula nerve fibers accounted for about half of all the fibers contained in the optic nerve. The central macula has a diameter of only 0.2 mm called the central recess, the retina in this area is the thinnest, the high density of photoreceptor cells up to 147,300 per square millimeter. This very fine structure ensures that visual information is transmitted to the brain center in the fastest and direct way. Therefore, the macula is the golden zone of the visual system where the senses of form, color and light are most acute, and is responsible for the very important function of perception and processing of visual information. Damage to its structure and function is an important cause of serious damage to human visual health today. 2, the pathogenesis of AMD From a large number of epidemiological surveys, clinical case analysis and a variety of animal experiments, its onset may be related to race, genetics, congenital defects, chronic exposure to light, poisoning, drug effects, immune abnormalities, malnutrition and other factors, it is currently believed that it may be the result of the compound effect of a variety of causes. It is generally believed that Caucasians have higher RPE than Blacks, which may be related to the fact that Caucasians have less retinal pigment epithelium (RPE) and poorer absorption of light, resulting in damage caused by large amounts of light exposure to the retina. Long-term repeated exposure to light can lead to increased susceptibility of the macula to light damage. There are reports of macular pigment changes in sailors who work under outdoor sunlight for a long time in the United States are more common than sailors who go to sea part of the time. In particular, blue light at wavelengths of 400-500 microns is a risk factor for the disease based on its possible phototoxic effects. Harvard University reported a close genetic relationship between this disease and maternal or sibling history of the disease. The pathogenesis is related to the following: 1. degeneration of photoreceptor cells: retinal pigment epithelial cells are the primary site of the disease, and their molecular degeneration may be caused by ageing, and pigment epithelial cell degeneration causes apoptosis of photoreceptor cells. 2, metabolic dysregulation: the retinal pigment epithelium has reduced phagocytosis and digestion of the outer segmental disc membrane of the optic cells, and the residual material forms lipofuscin accumulates between the pigment epithelium and the vitreous membrane to form vitreous membrane warts, causing thickening of the collagen fiber layer and fracture of the elastic fiber layer, which hinders fluid and metabolite exchange and weakens the adhesion between the two, which in turn stimulates the choroidal neovascular membrane to invade into the subretina. 3.Circulatory disorders: due to sclerosis or obstruction of choroidal capillaries in the central part of macula, causing choroidal circulation disorders, resulting in vitreous membrane degeneration, pigment epithelium and photoreceptor disc membrane damage. 4.Immune reaction: it is related to retinal antibodies and autoimmune factors. Antibodies positive for normal retinal biphasic proteins can be detected in the serum of patients, which can pass through and destroy the blood-retinal barrier, causing an increase in retinal vascular permeability and degeneration of pigment epithelium and photoreceptor cells. AMD is divided into two categories: atrophic and exudative according to different clinical manifestations and pathological changes: atrophic, also known as dry or non-exudative, is symmetrical in both eyes, with no discomfort other than a slow, progressive decrease in visual acuity. The macular area has a large number of yellowish-white vitreous warts of different sizes and poorly defined borders, and pigment disorders or map-like atrophy and choroidal capillary atrophy can be seen. If atrophic AMD is not effectively treated and controlled, the disease may develop into exudative AMD, which can seriously affect vision. Exudative AMD, also known as wet or discoid degeneration, develops at an older age and often presents with sudden visual impairment in one eye, while the other eye takes a longer time to develop the same lesion. The main cause is the destruction of the vitreous membrane, the choroidal capillaries invade the subretinal formation of choroidal neovascularization in the macular area, and the plasmacytic or hemorrhagic disciform detachment occurs under the retinal pigment epithelium or under the neuroepithelium, which eventually becomes a mechanized scar. A clear distinction between dry or wet age-related macular degeneration can be made by the typical features of fundus fluorescence angiography. Progressive loss of central vision may occur due to severe involvement of macular function. Hemorrhage, edema and exudation in the macula will lead to blurred vision, visual distortion and even loss of central vision. 4, the status of macular disease treatment Although the progress of science and technology has made it possible to prevent most of the blinding eye diseases in the world today, the effective treatment of AMD has not yet been truly solved, resulting in the increasing number of blind people with AMD, and the loss of patients’ ability to work and live brings a heavy burden to families and the whole society. Governments and the medical community are taking AMD prevention and treatment very seriously today. The British Prime Minister Tony Blair, on November 3, 2006, said that the number of blind people with AMD is increasing. In a speech at the King’s Centre at Oxford University on November 3, 2006, Tony Blair stressed the importance of AMD treatment and stated, “The economic benefits of innovation in the treatment of AMD will be unprecedented. This is evident. In atrophic AMD the progression of the disease is mainly controlled or alleviated by zinc or antioxidant supplementation. The National Eye Institute hosted a clinical study of 3640 ARMD cases with at least 5 years of follow-up from 1992 to 1998. The trace element zinc, which plays an important role in the metabolism of the retina and others as a variety of metalloenzymes, is used to treat patients with varying degrees of vision loss due to vitreous warts and can delay visual impairment. Since the occurrence of this disease is related to the chronic photoaccumulation poisoning of retinal tissues, the results of simulated light damage in animals have revealed the fact that a large amount of reduced ascorbic acid is oxidized and plays an important role in this pathological damage process, therefore, the administration of vitamins E and C with antioxidant properties, as hydroxyl scavengers, can prevent cell damage by free radicals, protect the retinal cells and play a role as retinal tissue The vitamin E and C, as hydroxyl scavengers, can prevent cell damage by free radicals, protect retinal cells, and act as retinal tissue nutrients. For exudative AMD the main treatment is to target choroidal neovascularization (CNV). Argon or krypton lasers can be used for photocoagulation to destroy CNV beyond 200 m of the macular sulcus. photodynamic therapy (PDT) is a selective treatment modality for CNV below the macular sulcus. Vizudar, a photosensitizing drug, has been awarded the PrixGalien Prize, which is known as the Nobel Prize in the pharmaceutical industry, and is administered intravenously to accumulate dye in CNV tissue cells. thrombus formation and closure. Anti-vascular endothelial growth factor (VEGF) is one of the latest therapeutic approaches that can effectively inhibit CNV production. One of the biologics, Ranibizumab (trade name Lucenti), has achieved an unprecedented high response rate in therapeutic applications: approximately 95% of patients’ vision is maintained. It was named one of the top ten scientific advances of 2006 by the American journal Science, and was described as “giving hope to patients with macular degeneration”. However, Ranibizumab is expensive, and its long-term effects and side effects need to be further investigated. In addition, there are also surgical procedures to remove CNV or macular transposition, but surgical treatment requires a high level of skill and is risky, and is not yet widely available. From the above, further emphasis on immediate interventional treatment of macular hemorrhage, edema, exudation, and other pathological metabolites is important, given that the technical approaches currently employed are mainly focused on the treatment of CNV. More effective treatment modalities will be pinned on PDT combined with anti-vascular endothelial growth factor and other drugs. Only through rational and personalized treatment with both specimens can we achieve the goal of both CNV closure and restoration of macular visual function. Our hospital is the first to apply PDT combined with Chinese and Western drugs, which actively promotes the absorption of hemorrhage and edema on the basis of effective destruction of CNV, and achieves better efficacy for the recovery of visual function, opening up a new way for the treatment of AMD.