Key risk factors are age, smoking, and family history. Advanced age is the strongest predictor of AMD, particularly over 50. Environment and lifestyle *Smoking: Smoking tobacco increases the risk of AMD by two to three times that of someone who has never smoked, and may be the most important modifiable factor in its prevention. A review of previous studies found "a strong association between current smoking and AMD. ... Cigarette smoking is likely to have toxic effects on the retina." *Hypertension (high blood pressure): In the ALIENOR study 2013, early and late AMD were not significantly associated with systolic or diastolic blood pressure (BP), hypertension, or use of antihypertensive medications, but elevated pulse pressure (PP) systolic BP minus diastolic BP was significantly associated with an increased risk of late AMD. *Atherosclerosis *High cholesterol: Elevated cholesterol may increase the risk of AMD *Obesity: Abdominal obesity is a risk factor, especially among men *Fat intake: Consuming high amounts of certain fats, including saturated fats, trans fats, and omega-6 fatty acids, likely contributes to AMD, while monounsaturated fats are potentially protective. In particular, omega-3 fatty acids may decrease the risk of AMD. *Exposure to UV light from sunlight is maybe associated with an increased risk of developing AMD, although evidence is weaker than other causes. *Digital screen does not radiate harmful energy against human eyes, but staring at the screen for a long time without pauses does increase eye strain. There is no evidence to support the claim that exposure to digital screen contributes to the risk of<unk> . Genetics AMD is a highly heritable condition. Recurrence ratios for siblings of an affected individual are three- to six-fold higher than in the general population. Genetic linkage analysis has identified 5 sets of gene variants at three locations on different chromosomes (1, 6 and 10) as explaining at least 50% of the risk. These genes have roles regulating the immune response, inflammatory processes and homeostasis of the retina. Variants of these genes give rise to different kinds of dysfunction in these processes. Over time, this results in accumulation of intracellular and extracellular metabolic debris. This can cause scarring of the retina or breakdown of its vascularization. The list of genetic variations association with AMD include complement factors, apolipoprotein E, fibroblast growth factor 2, DNA excision repair protein, and age-related maculopathy susceptibility protein 2. Although genetic testing can lead to the identification of genetic variation which can predispose to AMD, the complex pathogenesis of the condition prevents the use of these tests in routine practice. Nevertheless, they can be useful in selecting patients for clinical trials and analysing their response to treatment. The three loci where identified gene variants are found are designated: * Complement Factor H (CFH) on chromosome 1 at location 1q31.3 * HTRA serine peptidase 1/Age Related Maculopathy Susceptibility 2 (HTRA1/ARMS2) on chromosome 10 at location 10q26 * Complement Factor B/Complement Component 2 (CFB/CC2) on chromosome 6 at 6p21.3 Specific genes * Polymorphisms in genes for complement system proteins: Variation in the genes for the complement system proteins factor H (CFH), factor B (CFB) and factor 3 (C3), among others, are strongly associated with a person's risk for developing AMD. CFH is involved in inhibiting the inflammatory response. The mutation in CFH (Y402H) results in reduced ability of the protein to localise to and protect tissues such as the retina from complement overactivation. Absence of the complement factor H-related genes R3 and R1 protects against AMD. Two independent studies in 2007 showed a certain common mutation Arg80Gly in the C3 gene, which is a central protein of the complement system, is strongly associated with the occurrence of AMD. The authors of both papers consider their study to underscore the influence of the complement pathway in the pathogenesis of this disease. * In two 2006 studies, another gene that has implications for the disease, called HTRA1 (encoding a secreted serine protease), was identified. * Six mutations of the gene SERPING1 (Serpin Peptidase Inhibitor, Clade G (C1 Inhibitor), Member 1) are associated with AMD. Mutations in this gene can also cause hereditary angioedema. * Fibulin-5 mutation: Rare forms of the disease are caused by genetic defects in fibulin-5, in an autosomal dominant manner. In 2004, Stone et al. performed a screen on 402 AMD patients and revealed a statistically significant correlation between mutations in fibulin-5 and incidence of the disease. *Mitochondrial-related gene polymorphisms such as that in the MT-ND2 molecule, predicts wet AMD.
Macular degeneration
Optic disc drusen
Macular scarring
Retinal degeneration 
Retinal vasculitis
Macular corneal dystrophy
Autoimmune optic neuropathy
Corneal neovascularization