Age-related Macular Degeneration by L. Ho, R. van Leeuwen, P. T. V. M. de Jong, J. R.

By L. Ho, R. van Leeuwen, P. T. V. M. de Jong, J. R. Vingerling, C. C. W. Klaver (auth.), Frank G. Holz, Daniel Pauleikhoff, Richard F. Spaide, Alan C. Bird (eds.)

Age-related macular degeneration is the most typical reason for the lack of critical imaginative and prescient past the age of fifty in commercial international locations. Triplication of the variety of affected sufferers is predicted over the subsequent 25 years. specifically during the last years the normal of information concerning etiology, chance elements, diagnostics and treatment of this retina affliction has considerably grown – this may be lined during this up to date multi-authored paintings. except epidemiologically and genetically pointed out danger components either many of the pathophysiological features together with the function of the supplement process and scientific manifestations together with OCT and angiographic features are basically represented. in addition, the several healing methods are provided and mentioned, together with confirmed strategies similar to intravitreal anti-VEGF remedy and seeing-aid structures, as well as the most recent and upcoming equipment within the region of pharmacology. the amount is well-illustrated and tables and summaries whole the presentation.

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Moreover, they proposed that not the in/del but A69S confers AMD risk because of the strong LD between these variants. The precise function of ARMS2 in AMD remains to be elucidated. Earlier findings of disorganized mitochondrial membranes, as well as decreased number of mitochondria, in retinal pigment epithelium cells of AMD donors have provided evidence of mitochondrial dysfunction in AMD [157, 158]. This suggests that ARMS2 may jeopardize mitochondrial function, and consequently lead to the formation of reactive oxygen species, apoptosis, and AMD [144, 157–161].

It is a RPE signature gene [216], which is mutated in Sorby’s fundus dystrophy [217]. 1 × 10−11). 6 × 10−3) [135]. It should be noted that only variants near TIMP3 reached genome-wide significance (P < 5 × 10−8). In a parallel GWAS, only associations between variants at LIPC and AMD reached genome-wide significance [220]. 34 × 10−8). However, confirmation was achieved after targeted examination of the suggestive markers of the other GWAS. CETP and LPL play important roles in the production and degradation of HDL-c, whereas LIPC and ABCA1 are involved in mediating the uptake of HDL-c at the cell surface [221].

37. 38. 39. 40. maculopathy: follow-up at 6 1/2 years in the Rotterdam study. Arch Ophthalmol 121(4):519–526 Klein R, Klein BE, Tomany SC, Meuer SM, Huang GH (2002) Ten-year incidence and progression of age-related maculopathy: the Beaver Dam eye study. Ophthalmology 109(10):1767–1779 Mitchell P, Wang JJ, Foran S, Smith W (2002) Five-year incidence of age-related maculopathy lesions: the Blue Mountains Eye Study. Ophthalmology 109(6): 1092–1097 Klaver CC, Assink JJ, van Leeuwen R et al (2001) Incidence and progression rates of age-related maculopathy: the Rotterdam Study.

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