Ординатура / Офтальмология / Английские материалы / Retinal Degenerations biology, diagnostics, and therapeutics_Tombran-Tink, Barnstable_2007
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Fig. 5. (A) Prior cataract surgery and the risk of subsequent development of late AMD. *Salisbury Eye Evaluation (SEE), Baltimore Eye Survey (BES), and Proyecto VER (PVER) pooled cross-sectional data (59): prior cataract surgery and late AMD detected at the surveys; **SEE and BES pooled cross-sectional data (59): cataract surgery ≥5 yr ago and late AMD detected at the surveys; †Beaver Dam Eye Study (BDES) and Blue Mountains Eye Study (BMES) pooled incidence data (306): cataract surgery prior to baseline and 5-yr incidence of late AMD.
(B) Cataract surgery prior to baseline and risk of 10-yr incidence of AMD, the BDES (304).
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obvious. Many studies have shown that visual impairment decreases the ability of older people to perform usual activities of daily living (58,319–328). Visual impairment, a direct consequence of AMD, also links with other conditions and disabilities in older people including falls (329,330), fractures (331,332), depression (333–335), hearing loss (336), Alzheimer’s disease (337), cognitive function decline (338), and low self-rated health (339). A possible contribution from visual impairment to subsequent premature admission to nursing homes (340) and to reduced survival (276,277,319,341–345) have also been reported.
The Burden From AMD
It was estimated that 3.5% of the UK population aged 75 yr or older in 2003 (214,000 persons) were visually impaired as a result of AMD (346). The number of persons with geographic atrophy and neovascular AMD in the United Kingdom was estimated at 172,000 and 245,000, respectively (346). In the United States, the estimated proportion and number of persons aged 40 yr or older with AMD using the 2000 US Census population data was 1.5% and 1.75 million, respectively (44). The projected numbers with AMD 10 to 20 yr in the future will be higher, owing to population aging (44,346). The economic impact of visual impairment from AMD and the cost utility of screening and treatment of early AMD with antioxidants has been explored recently (347–349), but remains under-researched.
SUMMARY
Early in the 21st century, our knowledge of the epidemiology of AMD has grown substantially. Reliable data on prevalence and incidence is available for projecting the magnitude of this disease (44) and to estimate the societal burden it causes (44,346). Investigations of etiological factors for AMD have led to the identification of a number of definite or probable risk factors—particularly age, susceptibility genes, and smok- ing—and a number of possible risk factors such as light exposure, antioxidant status, inflammatory processes, cataract surgery or aphakic/pseudophakic status, and cardio- vascular-related pathogenesis including atherosclerosis and hypertension. At present, our understanding of AMD etiology can be summarized thus: it appears that AMD is caused by environmental factors triggering disease in genetically susceptible individuals (106). If AMD-related genes are identified as susceptibility factors that interact with environmental factors during the aging process, then multiple genes and environmental factors, together with all possible combinations for the possible interactions between each of these genes and environmental factors will result in a much more complex picture of the pathogenesis of AMD (350). Research in animal models has already shed some light on the complexity of possible interactions (219). A speculative etiology model proposed by the authors is that interactions of susceptibility genes with various environmental factors result in multiple pathogenetic pathways leading to the same disease. An example supporting this possible model is that elevated blood pressure, high serum cholesterol, elevated blood glucose, and high BMI can all lead to coronary heart disease (CHD). It is also possible that multiple pathogenetic pathways overlap between different diseases and so the same pathogenetic pathway can lead to different diseases.
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An example supporting the latter is that high BMI can lead to a number of chronic conditions like diabetes, hypertension, and CHD. This hypothetical AMD etiology model may mirror etiologies of other diseases, such as cardiovascular disease and cancer. The birth cohort effect on AMD prevalence observed in the BDES population (262) also suggests that unmeasured risk factors and/or unknown interactions between susceptibility genes and environmental factors may exist. The elucidation of the genetic basis of AMD and the gene–environmental interactions responsible for the development of AMD in some but not all aged individuals (19), is one of the challenges of ophthalmic research within the next decade or two (143). With the collaboration between epidemiology and genetics research teams, and use of currently advancing genetic (46,108,138,147) and statistical techniques, together with basic scientists’ experiments in vivo and in vitro, this goal is apparently achievable (350). Preventive and therapeutic strategies should follow.
ACKNOWLEDGMENTS
The authors would like to thank Ms. Kirsten Jakobsen and Ms. Bronwen Taylor for editing and proof reading, and Ms. Ava Tan for preparing Figs. 3, 4, and 5.
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