Introduction of Age-Related Macular Degeneration
Age-related macular degeneration (AMD) is a major cause of blindness worldwide and it is also the leading cause of visual impairment among older adults, particularly in the developed world. With aging populations in many countries, approximately 20% might catch the disorder. Advanced AMD, including neovascular age-related macular degeneration (wet) and geographic atrophy (late dry), is associated with substantial, progressive visual impairment.
AMD affects the macula. It exerts negative effects on the central vision we use to look straight ahead. Central vision is necessary for daily activities such as recognizing faces, reading or navigating the stairs. If the macula is damaged, people can see something but the fine points of the picture reflected in the eyes are not clear.
Fig. 1 Age-related macular degeneration. There are irregular pale dots at the macula, which are called drusen.1
Pathophysiology
The pathophysiology of AMD includes diffuse thickening of the inner aspect of Bruch’s membrane associated with soft drusen and may be accompanied by abnormalities of the retinal pigment epithelium with focal hyperpigmentation.
Risk Factor
There are a number of risk factors associated with AMD progression, which may be addressed by disease reduction strategies. These risk factors include:
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Age
Getting old is the major risk factor for age-related macular degeneration. Approximately 10% of the people who are older than 80 years of age have late age-related macular degeneration.
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Genetic risk factor
Several genetic variants that influence susceptibility to AMD have recently been identified. Individuals who’s already had one or more of these genetic variations are at particularly high risk of developing AMD if they also smoke. The gene related to AMD is shown below.
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Complement factor H
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ATP-binding cassette transporter
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Collagen type 8 alpha 1 subunit
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Vascular endothelial growth factor A
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Complement factor B
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Fyn-related kinase/alpha chain of type X collagen
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HtrA-serinepeptidase1
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Hepatic lipase
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Cholesterylester transfer protein
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Complement factor 1
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Apolipoprotein E
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Tissue inhibitor of metalloproteinase 3
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Complement component 3
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Complement component 2
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Tumour necrosis factor receptor superfamily 10a
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Environmental and behavioral factors
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Cigarette smoking - the association between AMD and smoking has been consistently demonstrated in a number of studies in the last decades. Cross-sectional studies and prospective cohort studies have unraveled the natural history of AMD and its association with risk factors. Smoking has been the most consistent factor linked to geographic atrophy and neovascular AMD.
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Obesity - the relationship between obesity and AMD has been the subject of cross-sectional, case-control studies and longitudinal studies. For most studies, obesity is defined by the BMI (Body Mass Index). The BMI is significantly associated with AMD.
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Low dietary intake of antioxidants - Studies revealed that dietary intake of both vitamin E and zinc was inversely associated with incident AMD.
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Reference
1. From Wikipedia: https://commons.wikimedia.org/wiki/File:Intermediate_age_related_macular_degeneration.jpg
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Questions & Answer
A: AMD is a progressive retinal disease and a major cause of irreversible vision loss in the elderly. Numerous studies have identified common and rare genetic variants in the complement pathway that play a role in the pathogenesis of AMD. Through genetic studies, complement factor I (CFI), complement component 3 (C3), complement component 2 (C2), complement component 9 (C9), complement factor B (CFB), and bilirubin (VTN) have been found to be associated with the disease as disease-associated variants have been identified across multiple biological systems.
A: Rare coding variants in CFH, CFI, C3, and C9 were identified in AMD patients, including Arg1210Cys variant in CFH, Gly119Arg variant in CFI, Lys155Gln variant in C3, and Pro167Ser variant in C9.
A: Because of the central role of the complement system in AMD, complement inhibition is considered a potential therapeutic option. Several clinical trials have been conducted to investigate this possibility. Examples include humanized IgG antibodies that inhibit C5 and antibodies against complement factor D, which may have a beneficial role in slowing AMD progression.
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