Original Article
Complement C3 Variant and the Risk of Age-Related Macular Degeneration
N Engl J Med 2007; 357:553-561August 9, 2007
- Abstract
Background
Age-related macular degeneration is the most common cause of blindness in Western populations. Susceptibility is influenced by age and by genetic and environmental factors. Complement activation is implicated in the pathogenesis.
Methods
We tested for an association between age-related macular degeneration and 13 single-nucleotide polymorphisms (SNPs) spanning the complement genes C3 and C5 in case subjects and control subjects from the southeastern region of England. All subjects were examined by an ophthalmologist and had independent grading of fundus photographs to confirm their disease status. To test for replication of the most significant findings, we genotyped a set of Scottish cases and controls.
Results
The common functional polymorphism rs2230199 (Arg80Gly) in the C3 gene, corresponding to the electrophoretic variants C3S (slow) and C3F (fast), was strongly associated with age-related macular degeneration in both the English group (603 cases and 350 controls, P=5.9×10–5) and the Scottish group (244 cases and 351 controls, P=5.0×10–5). The odds ratio for age-related macular degeneration in C3 S/F heterozygotes as compared with S/S homozygotes was 1.7 (95% confidence interval [CI], 1.3 to 2.1); for F/F homozygotes, the odds ratio was 2.6 (95% CI, 1.6 to 4.1). The estimated population attributable risk for C3F was 22%.
Conclusions
Complement C3 is important in the pathogenesis of age-related macular degeneration. This finding further underscores the influence of the complement pathway in the pathogenesis of this disease.
Media in This Article
Figure 1
Structure of Complement C3b, Showing the Location of Arg80.Table 1
Disease Status, Sex, Age, and Smoking History of Subjects.Article Activity
- Article
Age-related macular degeneration is the leading cause of visual impairment in the elderly and the most common cause of blindness in Western countries.1 It affects the macular region of the retina. The macula has a high density of photoreceptors and provides detailed central vision. In the early stages of the disease (referred to as age-related maculopathy), deposits called drusen develop between the retinal pigment epithelium and underlying choroid.1 Later, the disease is manifested as either extensive atrophy of the retinal pigment epithelium and overlying photoreceptor cells (geographic atrophy) or aberrant choroidal angiogenesis (choroidal neovascularization).1 Both of these conditions can lead to a loss of central vision. The pathogenesis of age-related macular degeneration is poorly understood. As with other late-onset chronic diseases, susceptibility is influenced by age, ethnic background, and a combination of environmental and genetic factors.1,2 Smoking status and family history are well-established determinants of risk.1,2
Recently, polymorphisms in the genes coding for complement factor H (CFH) and complement factor B (CFB) have been shown to be predictors of risk for age-related macular degeneration.3-11 Another susceptibility locus has been mapped to chromosome 10q26; the causative variation probably lies in a hypothetical gene called LOC387715 or in the promoter of the neighboring gene HTRA1.11-14 The population attributable risk associated with variants in CFH, CFB, and LOC387715/HTRA1 is at least 50%.11
CFH and CFB are key components of the alternative complement pathway. Their involvement in age-related macular degeneration, together with the finding that drusen contain proteins associated with inflammation and immune-mediated processes,15 supports the hypothesis that inflammation and complement activation influence the pathogenesis of age-related macular degeneration. To test whether variants in other genes encoding proteins in the complement pathway influence susceptibility to age-related macular degeneration, we genotyped single-nucleotide polymorphisms (SNPs) spanning the complement genes C3 and C5, encoding central proteins in the complement cascade, in subjects with age-related macular degeneration and in control subjects.
Methods
Cases and Controls
We studied three case–control groups, two in England and one in Scotland. English group 1 comprised 446 case subjects with end-stage age-related macular degeneration (geographic atrophy or choroidal neovascularization) and 267 control subjects, who were spouses of the index patients. All subjects were recruited from ophthalmic clinics in eight hospitals in southeastern England from 2002 to 2004.7 English group 2 comprised 157 case subjects with end-stage age-related macular degeneration and 83 controls (67 spouses and 16 friends of index patients) recruited from 2003 to 2005, the majority from Moorfields Eye Hospital in London and the remainder from southeastern England. All subjects described themselves as “white” rather than “other” on a recruitment questionnaire.
The Scottish group comprised 505 case subjects with age-related maculopathy or end-stage age-related macular degeneration and 351 control subjects. A total of 337 case subjects from the Lothian region were recruited from ophthalmic clinics in Edinburgh and 46 case subjects from hospitals in Dundee and Inverness from 2004 to 2006. Control subjects, who were recruited from the same sources in similar proportions, comprised 32 spouses and 174 subjects who had undergone cataract surgery. Another 122 case subjects and 145 controls came from the 1921 Lothian birth cohort.16
Written informed consent was obtained from all subjects. The research protocol was in keeping with the provisions of the Declaration of Helsinki, and approval was obtained from a multicenter research ethics committee and from research ethics committees for each institution. Subjects were examined by an ophthalmologist, and data were collected regarding medical history, lifestyle, and smoking history. Color, stereoscopic fundus photography of the macular region was performed in all subjects. For English subjects, the images were graded at the Reading Centre, Moorfields Eye Hospital, with the use of the International Classification of Age-Related Maculopathy and Macular Degeneration.17 For Scottish subjects, a study investigator graded images; for validation, images from 100 case subjects and controls were independently graded at the Moorfields Reading Centre (kappa statistic, 0.84). Eight prospective English controls with age-related macular degeneration and 60 prospective Scottish controls with age-related maculopathy were reclassified as case subjects. Data on disease status, sex, age, and smoking history of subjects are provided in Table 1Table 1
Disease Status, Sex, Age, and Smoking History of Subjects..Genotyping
We extracted genomic DNA from peripheral-blood leukocytes. We selected SNPs spanning the C3 and C5 genes from the International HapMap Project18 data (release 19) for the Centre d'Étude du Polymorphisme Humain (CEPH) population (Utah residents with ancestry from northern and western Europe). Criteria for the selection of SNPs were high heterozygosity with a minor allele frequency of at least 10%, tagging of the most common haplotypes, and coverage of the main blocks of linkage disequilibrium. The C3 SNP rs2230199 — which is predicted to result in a substitution of a glycine residue for arginine at position 80 (Arg80Gly) — generates the “fast” electrophoretic allotype of C3 (called C3F); the alternative allotype is “slow” (C3S).19,20 We included this SNP in the analysis to provide extra coverage and because of evidence of a functional difference between the two alleles. On the basis of our initial analysis, we included rs1047286 (Pro292Leu), which has a known association with rs2230199.20,21 Initial genotyping was carried out in English group 1. Markers of interest were genotyped in group 2 when samples became available. Data from the Scottish group were used for replication.
We performed genotyping in English subjects with the use of a single-nucleotide primer extension assay (ABI Prism SNaPshot Multiplex Kit, Applied Biosystems) and a genetic analyzer (ABI Prism 3100, Applied Biosystems) and in Scottish subjects — for rs2230199 and rs1047286 — with the use of competitive allele-specific polymerase-chain-reaction assays (Taqman SNP Genotyping Assay, Applied Biosystems and KASPar SNP Genotyping System, KBiosciences, respectively). Manufacturers' protocols were followed.
Statistical Analysis
We used the chi-square test for comparisons of categorical variables and allele and genotype frequencies and to check for Hardy–Weinberg equilibrium. All P values were calculated with two-sided tests, and no correction was made for multiple testing. The Mann–Whitney U test was used to compare the ages of case subjects and controls. Logistic-regression analysis was used to investigate interactions between genotype and other variables and to estimate odds ratios and 95% confidence intervals. The covariables of age and smoking history were included in the logistic model if univariate analysis had shown a significant difference. Odds ratios for categorical variables were estimated in relation to a reference category. Data were analyzed with the use of the SPSS statistical software package, version 11.0.
The population attributable risk was calculated from the formula 100D÷(1+D), in which D was equal to P1(RR1–1) + P2(RR2–1), where P1 and P2 are the frequencies of the at-risk genotypes, and RR1 and RR2 their associated relative risks, as compared with the low-risk genotype. For the purposes of estimation, odds ratios were equated to relative risks, since the disease prevalence is low.
Results
In the initial screening, 12 SNPs spanning C3 and C5 (those listed in Table 2Table 2
Genotyping Results for English Subjects., excluding rs1047286) were genotyped in 446 case subjects with late-stage age-related macular degeneration and 267 control subjects (English group 1). No evidence of an association was found with variants in C5 (Table 2). In C3, the expressed SNP rs2230199 showed strong evidence of an association (P<0.001) and was genotyped in an additional 157 case subjects and 83 controls (English group 2). The enlarged sample also provided strong evidence of an association (P=5.9×10–5) (Table 2).To test for replication of this finding, rs2230199 was genotyped by a different laboratory in 244 case subjects with late-stage age-related macular degeneration, 261 case subjects with age-related maculopathy, and 351 controls (Scottish group). Again, there was a highly significant association between the minor allele and age-related macular degeneration (P=5.0×10–5) (Table 3Table 3
Genotyping Results for Scottish Replication Group.). International HapMap Project18 data for the CEPH population showed that rs2230199 had an r2 value of 0.75 with rs2230203 but a low r2 value with other C3 SNPs in our marker panel and with other C3 SNPs in the HapMap data set. SNP rs2230203 did not show a significant association with age-related macular degeneration in group 1 alone, but there was weak evidence of an association in groups 1 and 2 combined (Table 2).Because of the known association between the allotypes of rs2230199 and the expressed C3 SNP rs1047286, the English and Scottish subjects were genotyped for this marker (Table 2 and Table 3). The minor allele frequency was significantly higher in case subjects than in controls in both groups, but the association was not as strong as for rs2230199. Stepwise logistic-regression analysis confirmed that rs2230199 is a significantly better predictor of risk for age-related macular degeneration. With this SNP in the model, adding rs1047286 made no contribution (P=0.90). With rs1047286 in the model, adding rs2230199 produced a significant improvement in fit (P=0.02).
Odds ratios for age-related macular degeneration as a function of rs2230199 genotype are given in Table 4Table 4
Complement C3 rs2230199 Genotype (C3 S/F Allotype) and Odds Ratios for Age-Related Macular Degeneration.. Results for the English and Scottish groups were similar. In the combined data set, with the common CC genotype as the reference, the odds ratio was 1.7 for CG heterozygotes and 2.6 for GG homozygotes. The estimated population attributable risk for this variant was 22%.Subgroup analysis that was confined to case subjects with only choroidal neovascularization showed a highly significant association in both case–control groups. For case subjects with only geographic atrophy, the association was significant in the English group (P=4.6×10–4) but not in the Scottish group, which had fewer subjects with geographic atrophy. The Scottish group included case subjects with age-related maculopathy, and in this subgroup the association fell just short of significance (Table 3).
Data on other susceptibility loci for age-related macular degeneration were available for English group 1. Results for CFH Y402H have been published previously and are in agreement with other reports.7 Odds ratios and population attributable risks for LOC387715 (rs10490924) and CFB (rs641153) are given in Table 5Table 5
Odds Ratios for Age-Related Macular Degeneration and Population Attributable Risk for Variants at the Susceptibility Loci CFH, CFB, and LOC387715 in English Group 1.. The results are similar to those of other studies, except that we found a lower odds ratio for rs10490924 homozygotes. When these variables were included in the stepwise logistic model, C3 rs2230199 remained significant, with an odds ratio of 1.4 for CG heterozygotes and 3.3 for GG homozygotes (with CC genotype as the reference), confirming that these susceptibility loci are independent risk factors.Discussion
Our study showed a strong association between the complement C3 S/F (Arg80Gly) polymorphism and age-related macular degeneration, with similar findings for geographic atrophy and choroidal neovascularization. The C3F allele frequency is approximately 20% in white populations but lower in other ethnic groups. For age-related maculopathy, the association fell just short of significance, raising the possibility that this polymorphism has less influence on the earlier stages of the disease.
The complement system comprises more than 30 plasma and cell-surface proteins. It mediates the host defense against pathogens and the elimination of immune complexes and apoptotic cells; it also facilitates adaptive immune responses.22 C3 is the most abundant complement component, synthesized predominantly in the liver but to a lesser extent in other cells and tissues. Significant C3 messenger RNA is detectable in the neural retina, choroid, retinal pigment epithelium, and cultured retinal-pigment-epithelium cells.15
Cleavage of C3 into C3a and C3b is the central step in complement activation and can be initiated by the classic antibody-mediated pathway, the lectin pathway, or the alternative complement pathway.22 C3b attaches to pathogens or other target surfaces and binds factor B, which is then cleaved. The resulting C3bBb complex has C3 convertase activity, which amplifies the response by further cleavage of C3 and leads to the formation of C3b2Bb complexes with C5 convertase activity. This brings about cleavage of component C5 and recruitment by C5b of components C6 through C9 to form a large molecular pore on target membranes (the membrane attack complex), resulting in cell lysis.22
Drusen contain C3 and its activation products, as well as C5, membrane attack complex, and CFH,6,15 supporting the hypothesis that local inflammation and activation of the complement cascade contribute to the pathogenesis of age-related macular degeneration. Further support for this hypothesis comes from conclusive evidence that variants in CFH influence susceptibility to age-related macular degeneration.3-9 CFH is a key regulator of the alternative complement pathway and prevents uncontrolled complement activation. Variants in factor B also appear to influence susceptibility to age-related macular degeneration.10,11 In mice, activation of complement and formation of the membrane attack complex are essential for the development of laser-induced choroidal neovascularization. Indeed, the finding that choroidal neovascularization cannot be induced by laser coagulation in C3−/− mice demonstrates the key role of C3 in this process.23
As a result of cleavage of C3 to form C3b, the molecule undergoes conformational changes that expose several binding sites, including the thioester moiety, which is essential for C3b binding to target surfaces.24 Exposure of this activated acyl-imidazole intermediate requires a substantial relocation of the thioester-containing domain to a position adjacent to the first macroglobulin domain.24 Arg80 together with Arg72 and Lys82 forms a positively charged patch on the surface of this domain, which, in C3b, is brought into close proximity with the negatively charged carboxyl groups of several amino acids on the surface of the thioester-containing domain (Figure 1Figure 1
Structure of Complement C3b, Showing the Location of Arg80.). Substitution of an uncharged glycine for the positively charged Arg80 is predicted to weaken the interaction between these oppositely charged surfaces and could potentially influence thioester activity or other binding interactions of the thioester-containing domain, including a probable C3b/C3d binding site with CFH.25 It follows that there could well be functional differences between the C3 S/F variants.Direct experimental evidence of functional differences in vitro between the C3 S/F allotypes is not conclusive. Arvilommi26 reported that erythrocytes coated with C3F showed greater rosetting with peripheral-blood mononuclear cells than those coated with C3S. Welch et al.27 studied uptake on sheep erythrocytes, hemolytic activity, conversion to inactive C3b, and capacity to solubilize preformed immune complexes. The only significant difference was that C3F had lower activity than C3S in a hemolytic assay using sensitized sheep erythrocytes as a result of a small difference in cell-surface binding. Bartók and Walport28 found no differences between binding of C3S and C3F and the major complement receptor types 1, 2, and 3.
On the other hand, there is compelling indirect evidence of a functional difference between C3S and C3F. A recent study has shown that the C3 S/F genotype is an important determinant of the long-term outcome of renal transplantation.29 In recipients who were C3S homozygotes, graft survival was substantially prolonged and renal function significantly better with C3 F/F and C3 F/S donor kidneys than with C3 S/S kidneys.
Several associations of disease with C3F have been reported, including IgA nephropathy,30 systemic vasculitis,31 partial lipodystrophy, and membranoproliferative glomerulonephritis type II (MPGNII).32,33 The association with MPGNII is particularly relevant. This is a rare disease characterized by complement-containing dense deposits in the glomerular basement membrane of the kidney.34 The condition is caused by uncontrolled activation of the alternative complement pathway. In the majority of patients, the condition is associated with serum C3 nephritic factor,34 an autoantibody directed against the C3bBb complex, but rare cases associated with mutations in CFH have been reported.35 A similar form of glomerulonephritis develops in CFH-deficient pigs36 and CFH knockout mice.37 The interface of the capillary tuft, the glomerular basement membrane, and the glomerular epithelial cells in the kidney is similar in structure to the interface involving choriocapillaris, Bruch's membrane, and retinal pigment epithelium in the eye, and macular drusen similar to those in age-related macular degeneration develop in patients with MPGNII, but at a much younger age.38 These lesions are structurally and compositionally identical to those in patients with age-related macular degeneration and show immunoreactivity to complement C5 and C5b-9 complexes.39 Drusen have also been reported in patients with partial lipodystrophy.40 The association of MPGNII and partial lipodystrophy with C3F fits well with our current findings.
In summary, our study shows a strong association between the C3F variant and age-related macular degeneration, and there is evidence of functional differences between the C3 S/F allotypes. It follows that C3F is likely to have a causal role in the disorder. The estimated population attributable risk in the white population is 22%. These findings add to our growing understanding of the genetics of age-related macular degeneration and provide conclusive evidence that the complement pathway has a key role in the pathogenesis of this common and debilitating condition.
Supported by grants from the Medical Research Council, United Kingdom (to Drs. Yates, Clayton, Bird, and Moore), the Chief Scientist Office, Scotland (to Dr. Dhillon), the Macular Vision Research Foundation (to Dr. Wright), and the Wellcome Trust and the Juvenile Diabetes Research Foundation (to Dr. Clayton). The Lothian Birth Cohort collection was supported by the Biotechnology and Biological Sciences Research Council. Dr. Deary is the recipient of a Royal Society–Wolfson Research Merit Award.
Dr. Dhillon reports receiving consulting fees from Novartis and Pfizer. No other potential conflict of interest relevant to this article was reported.
Drs. Yates and Sepp contributed equally to this article.
This article (10.1056/NEJMoa072618) was published at www.nejm.org on July 18, 2007.
We thank members of the Scottish Macula Society Study Group (M. Gavin, F. Imrie, N. Lois, R. Murray, A. Purdie, A. Pyott, S. Roxburgh, C. Styles, M. Virdi, and W. Wykes) for their help in the recruitment of patients for our study; clinic staff and medical photographers at the participating clinics for their help; Tunde Peto and colleagues at the Reading Centre, Moorfields Eye Hospital, London, for grading the fundus photographs; the staff at Tepnel Life Sciences for performing the DNA extractions; Roger Williams for his helpful discussion about C3b protein structure; the International HapMap Consortium for the use of data; and all the patients and their families who participated in the study.
Source Information
From the Cambridge Institute for Medical Research, University of Cambridge, Cambridge (J.R.W.Y., T.S., B.K.M., J.C.K., D.A.T., H.S., D.G.C.); the Medical Research Council Human Genetics Unit, Edinburgh (C.H., J.M., A.F.W.); the Princess Alexandra Eye Pavilion, Edinburgh (A.M.A., B.D.); the University of Edinburgh, Edinburgh (I.J.D.); the Institute of Ophthalmology, University College London (E.R., A.C.B., A.T.M.); and Moorfields Eye Hospital, London (A.C.B., A.T.M.) — all in the United Kingdom.
Address reprint requests to Dr. Yates at the Department of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, Wellcome Trust/MRC Bldg., Box 139, Addenbrooke's Hospital, Cambridge CB2 0XY, United Kingdom, or at jrwy1@cam.ac.uk.
Other members of the Genetic Factors in Age-Related Macular Degeneration (AMD) Study Group are listed in the Appendix.
Appendix
The following investigators are members of the Genetic Factors in Age-Related Macular Degeneration Study Group: S.S. Bhattacharya, P. Bishop, P. Black, Z. Butt, V. Chong, N.E. Day, C. Edelsten, A. Fitt, D.W. Flanagan, A. Glenn, S. Harding, C. Jakeman, C. Jones, R.J. Lamb, A. Lotery, V. Moffatt, C.M. Moorman, T. Peto, R.J. Pushpanathan, and T. Rimmer.
- References
References
1
de Jong PTMV . Age-related macular degeneration. N Engl J Med 2006;355:1474-1485
Full Text | Web of Science | Medline2
Haddad S ,Chen CA ,Santangelo SL ,Seddon JM . The genetics of age-related macular degeneration: a review of progress to date. Surv Ophthalmol 2006;51:316-363
CrossRef | Web of Science | Medline3
Klein RJ ,Zeiss C ,Chew EY , et al. Complement factor H polymorphism in age-related macular degeneration. Science 2005;308:385-389
CrossRef | Web of Science | Medline4
Haines JL ,Hauser MA ,Schmidt S , et al. Complement factor H variant increases the risk of age-related macular degeneration. Science 2005;308:419-421
CrossRef | Web of Science | Medline5
Edwards AO ,Ritter R III ,Abel KJ ,Manning A ,Panhuysen C ,Farrer LA . Complement factor H polymorphism and age-related macular degeneration. Science 2005;308:421-424
CrossRef | Web of Science | Medline6
Hageman GS ,Anderson DH ,Johnson LV , et al. A common haplotype in the complement regulatory gene factor H (HF1/CFH) predisposes individuals to age-related macular degeneration. Proc Natl Acad Sci U S A 2005;102:7227-7232
CrossRef | Web of Science | Medline7
Sepp T ,Khan JC ,Thurlby DA , et al. Complement factor H variant Y402H is a major risk determinant for geographic atrophy and choroidal neovascularization in smokers and nonsmokers. Invest Ophthalmol Vis Sci 2006;47:536-540
CrossRef | Web of Science | Medline8
Li M ,Atmaca-Sonmez P ,Othman M , et al. CFH haplotypes without the Y402H coding variant show strong association with susceptibility to age-related macular degeneration. Nat Genet 2006;38:1049-1054
CrossRef | Web of Science | Medline9
Hughes AE ,Orr N ,Esfandiary H ,Diaz-Torres M ,Goodship T ,Chakravarthy U . A common CFH haplotype, with deletion of CFHR1 and CFHR3, is associated with lower risk of age-related macular degeneration. Nat Genet 2006;38:1173-1177[Erratum, Nat Genet 2007;39:567.]
CrossRef | Web of Science | Medline10
Gold B ,Merriam JE ,Zernant J , et al. Variation in factor B (BF) and complement component 2 (C2) genes is associated with age-related macular degeneration. Nat Genet 2006;38:458-462
CrossRef | Web of Science | Medline11
Maller J ,George S ,Purcell S , et al. Common variation in three genes, including a noncoding variant in CFH, strongly influences risk of age-related macular degeneration. Nat Genet 2006;38:1055-1059
CrossRef | Web of Science | Medline12
Jakobsdottir J ,Conley YP ,Weeks DE ,Mah TS ,Ferrell RE ,Gorin MB . Susceptibility genes for age-related maculopathy on chromosome 10q26. Am J Hum Genet 2005;77:389-407
CrossRef | Web of Science | Medline13
Dewan A ,Liu M ,Hartman S , et al. HTRA1 promoter polymorphism in wet age-related macular degeneration. Science 2006;314:989-992
CrossRef | Web of Science | Medline14
Yang Z ,Camp NJ ,Sun H , et al. A variant of the HTRA1 gene increases susceptibility to age-related macular degeneration. Science 2006;314:992-993
CrossRef | Web of Science | Medline15
Mullins RF ,Russell SR ,Anderson DH ,Hageman GS . Drusen associated with aging and age-related macular degeneration contain proteins common to extracellular deposits associated with atherosclerosis, elastosis, amyloidosis, and dense deposit disease. FASEB J 2000;14:835-846
Web of Science | Medline16
Deary IJ ,Whiteman MC ,Starr JM ,Whalley LJ ,Fox HC . The impact of childhood intelligence on later life: following up the Scottish mental surveys of 1932 and 1947. J Pers Soc Psychol 2004;86:130-147
CrossRef | Web of Science | Medline17
Bird AC ,Bressler NM ,Bressler SB , et al. An international classification and grading system for age-related maculopathy and age-related macular degeneration. Surv Ophthalmol 1995;39:367-374
CrossRef | Web of Science | Medline18
The International HapMap Consortium
CrossRef | Web of Science | Medline19
Azen EA ,Smithies O . Genetic polymorphism of C'3(beta1C-globulin) in human serum. Science 1968;162:905-907
CrossRef | Web of Science | Medline20
Botto M ,Fong KY ,So AK ,Koch C ,Walport MJ . Molecular basis of polymorphisms of human complement component C3. J Exp Med 1990;172:1011-1017
CrossRef | Web of Science | Medline21
Koch C ,Behrendt N . A novel polymorphism of human complement component C3 detected by means of a monoclonal antibody. Immunogenetics 1986;23:322-325
CrossRef | Web of Science | Medline22
Walport MJ . Complement (first of two parts). N Engl J Med 2001;344:1058-1066
Full Text | Web of Science | Medline23
Bora PS ,Hu Z ,Tezel TH , et al. Immunotherapy for choroidal neovascularization in a laser-induced mouse model simulating exudative (wet) macular degeneration. Proc Natl Acad Sci U S A 2003;100:2679-2684
CrossRef | Web of Science | Medline24
Janssen BJ ,Christodoulidou A ,McCarthy A ,Lambris JD ,Gros P . Structure of C3b reveals conformational changes that underlie complement activity. Nature 2006;444:213-216
CrossRef | Web of Science | Medline25
Jokiranta TS ,Jaakola VP ,Lehtinen MJ ,Parepalo M ,Meri S ,Goldman A . Structure of complement factor H carboxyl-terminus reveals molecular basis of atypical haemolytic uremic syndrome. EMBO J 2006;25:1784-1794
CrossRef | Web of Science | Medline26
Arvilommi H . Capacity of complement c3 phenotypes to bind on to mononuclear cells in man. Nature 1974;251:740-741
CrossRef | Web of Science | Medline27
Welch TR ,Beischel L ,Kleesattel A . Functional consequences of the genetic polymorphism of the third component of complement. J Pediatr 1990;116:S92-S97
CrossRef | Web of Science | Medline28
Bartok I ,Walport MJ . Comparison of the binding of C3S and C3F to complement receptors types 1, 2, and 3. J Immunol 1995;154:5367-5375
Web of Science | Medline29
Brown KM ,Kondeatis E ,Vaughan RW , et al. Influence of donor C3 allotype on late renal-transplantation outcome. N Engl J Med 2006;354:2014-2023
Full Text | Web of Science | Medline30
Rambausek M ,van den Wall Bake AW ,Schumacher-Ach R , et al. Genetic polymorphism of C3 and Bf in IgA nephropathy. Nephrol Dial Transplant 1987;2:208-211
Medline31
Finn JE ,Zhang L ,Agrawal S ,Jayne DR ,Oliveira DB ,Mathieson PW . Molecular analysis of C3 allotypes in patients with systemic vasculitis. Nephrol Dial Transplant 1994;9:1564-1567
Web of Science | Medline32
Finn JE ,Mathieson PW . Molecular analysis of C3 allotypes in patients with nephritic factor. Clin Exp Immunol 1993;91:410-414
CrossRef | Web of Science | Medline33
McLean RH ,Winkelstein JA . Genetically determined variation in the complement system: relationship to disease. J Pediatr 1984;105:179-188
CrossRef | Web of Science | Medline34
Appel GB ,Cook HT ,Hageman G , et al. Membranoproliferative glomerulonephritis type II (dense deposit disease): an update. J Am Soc Nephrol 2005;16:1392-1403
CrossRef | Web of Science | Medline35
Abrera-Abeleda MA ,Nishimura C ,Smith JL , et al. Variations in the complement regulatory genes factor H (CFH) and factor H related 5 (CFHR5) are associated with membranoproliferative glomerulonephritis type II (dense deposit disease). J Med Genet 2006;43:582-589
CrossRef | Web of Science | Medline36
Hogasen K ,Jansen JH ,Mollnes TE ,Hovdenes J ,Harboe M . Hereditary porcine membranoproliferative glomerulonephritis type II is caused by factor H deficiency. J Clin Invest 1995;95:1054-1061
CrossRef | Web of Science | Medline37
Pickering MC ,Cook HT ,Warren J , et al. Uncontrolled C3 activation causes membranoproliferative glomerulonephritis in mice deficient in complement factor H. Nat Genet 2002;31:424-428
Web of Science | Medline38
Colville D ,Guymer R ,Sinclair RA ,Savige J . Visual impairment caused by retinal abnormalities in mesangiocapillary (membranoproliferative) glomerulonephritis type II (“dense deposit disease”). Am J Kidney Dis 2003;42:E2-E5
CrossRef | Web of Science | Medline39
Mullins RF ,Aptsiauri N ,Hageman GS . Structure and composition of drusen associated with glomerulonephritis: implications for the role of complement activation in drusen biogenesis. Eye 2001;15:390-395
CrossRef | Web of Science | Medline40
Patel D ,Page B . Ocular complications in acquired partial lipodystrophy. Postgrad Med J 2006;82:774-774
CrossRef | Web of Science | Medline
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Mohammed Aiyaz, Michelle K. Lupton, Petroula Proitsi, John F. Powell, Simon Lovestone. (2012) Complement activation as a biomarker for Alzheimer's disease. Immunobiology 217:2, 204-215
CrossRef6
Petroula Proitsi, Michelle K. Lupton, Frank Dudbridge, Magda Tsolaki, Gillian Hamilton, Makrina Daniilidou, Megan Pritchard, Kathryn Lord, Belinda M. Martin, David Craig, Stephen Todd, Bernadette McGuinness, Paul Hollingworth, Denise Harold, Iwona Kloszewska, Hilkka Soininen, Patrizia Mecocci, Bruno Velas, Michael Gill, Brian Lawlor, David C. Rubinsztein, Carol Brayne, Peter A. Passmore, Julie Williams, Simon Lovestone, John F. Powell. (2012) Alzheimer's disease and age-related macular degeneration have different genetic models for complement gene variation. Neurobiology of Aging
CrossRef7
Robyn Troutbeck, Salmaan Al-Qureshi, Robyn H Guymer. (2012) Therapeutic targeting of the complement system in age-related macular degeneration: a review. Clinical & Experimental Ophthalmology 40:1, 18-26
CrossRef8
Evy De Witte, Marijn M. Speeckaert, Lot Van De Moortel, Elke Lecocq, Joris R. Delanghe. (2012) Human complement factor 3 polymorphism determination by capillary electrophoresis of serum. ELECTROPHORESISn/a-n/a
CrossRef9
Valentina Cipriani, Baljinder K Matharu, Jane C Khan, Humma Shahid, Caroline Hayward, Alan F Wright, Ana Maria Armbrecht, Baljean Dhillon, Simon P Harding, Paul N Bishop, Catey Bunce, David G Clayton, Anthony T Moore, John RW Yates. (2012) No evidence of association between complement factor I genetic variant rs10033900 and age-related macular degeneration. European Journal of Human Genetics 20:1, 1-2
CrossRef10
Suk Jin Kim, Soo Jeong Lee, Na Rae Kim, Hee Seung Chin. (2012) Association of polymorphisms in C2, CFB and C3 with exudative age-related macular degeneration in a Korean population. Experimental Eye Research
CrossRef11
Inga Peter, Gordon S. Huggins, Jose M. Ordovas, Mary Haan, Johanna M. Seddon. (2011) Evaluation of New and Established Age-Related Macular Degeneration Susceptibility Genes in the Women's Health Initiative Sight Exam (WHI-SE) Study. American Journal of Ophthalmology 152:6, 1005-1013.e1
CrossRef12
Jaekyung Choi, Jun Woong Moon, Hyun Jin Shin. (2011) Chronic Kidney Disease, Early Age-related Macular Degeneration, and Peripheral Retinal Drusen. Ophthalmic Epidemiology 18:6, 259-263
CrossRef13
L. A. Trouw, S. Böhringer, N. A. Daha, E. A. Stahl, S. Raychaudhuri, F. A. Kurreeman, G. Stoeken-Rijsbergen, J. J. Houwing-Duistermaat, T. W. Huizinga, R. E. Toes. (2011) The major risk alleles of age-related macular degeneration (AMD) in CFH do not play a major role in rheumatoid arthritis (RA). Clinical & Experimental Immunology 166:3, 333-337
CrossRef14
Gareth J. McKay, Chris C. Patterson, Usha Chakravarthy, Shilpa Dasari, Caroline C. Klaver, Johannes R. Vingerling, Lintje Ho, Paulus T.V.M. de Jong, Astrid E. Fletcher, Ian S. Young, Johan H. Seland, Mati Rahu, Gisele Soubrane, Laura Tomazzoli, Fotis Topouzis, Jesus Vioque, Aroon D. Hingorani, Reecha Sofat, Michael Dean, Julie Sawitzke, Johanna M. Seddon, Inga Peter, Andrew R. Webster, Anthony T. Moore, John R.W. Yates, Valentina Cipriani, Lars G. Fritsche, Bernhard H.F. Weber, Claudia N. Keilhauer, Andrew J. Lotery, Sarah Ennis, Michael L. Klein, Peter J. Francis, Dwight Stambolian, Anton Orlin, Michael B. Gorin, Daniel E. Weeks, Chia-Ling Kuo, Anand Swaroop, Mohammad Othman, Atsuhiro Kanda, Wei Chen, Goncalo R. Abecasis, Alan F. Wright, Caroline Hayward, Paul N. Baird, Robyn H. Guymer, John Attia, Ammarin Thakkinstian, Giuliana Silvestri. (2011) Evidence of association of APOE with age-related macular degeneration - a pooled analysis of 15 studies. Human Mutation 32:12, 1407-1416
CrossRef15
Robert G. Salomon, Li Hong, Joe G. Hollyfield. (2011) Discovery of Carboxyethylpyrroles (CEPs): Critical Insights into AMD, Autism, Cancer, and Wound Healing from Basic Research on the Chemistry of Oxidized Phospholipids. Chemical Research in Toxicology 24:11, 1803-1816
CrossRef16
Claudia N. Keilhauer, Lars G. Fritsche, Bernhard H. F. Weber. (2011) Age-related macular degeneration with discordant late stage phenotypes in monozygotic twins. Ophthalmic Genetics 32:4, 237-244
CrossRef17
Edward Loane, John M. Nolan, Gareth J. McKay, Stephen Beatty. (2011) The association between macular pigment optical density and CFH, ARMS2, C2/BF, and C3 genotype. Experimental Eye Research 93:5, 592-598
CrossRef18
Anna Machalińska, Miłosz P. Kawa, Wojciech Marlicz, Bogusław Machaliński. (2011) Complement system activation and endothelial dysfunction in patients with age-related macular degeneration (AMD): possible relationship between AMD and atherosclerosis. Acta Ophthalmologicano-no
CrossRef19
Johanna M. Seddon, Robyn Reynolds, Yi Yu, Mark J. Daly, Bernard Rosner. (2011) Risk Models for Progression to Advanced Age-Related Macular Degeneration Using Demographic, Environmental, Genetic, and Ocular Factors. Ophthalmology 118:11, 2203-2211
CrossRef20
Dzenita Smailhodzic, Caroline C.W. Klaver, B. Jeroen Klevering, Camiel J.F. Boon, Joannes M.M. Groenewoud, Bernd Kirchhof, Mohamed R. Daha, Anneke I. den Hollander, Carel B. Hoyng. (2011) Risk Alleles in CFH and ARMS2 Are Independently Associated with Systemic Complement Activation in Age-related Macular Degeneration. Ophthalmology
CrossRef21
Milam A. Brantley, Melissa P. Osborn, Barton J. Sanders, Kasra A. Rezaei, Pengcheng Lu, Chun LI, Ginger L. Milne, Jiyang Cai, Paul Sternberg. (2011) Plasma Biomarkers of Oxidative Stress and Genetic Variants in Age-Related Macular Degeneration. American Journal of Ophthalmology
CrossRef22
Robert F. Mullins, Aaron D. Dewald, Luan M. Streb, Kai Wang, Markus H. Kuehn, Edwin M. Stone. (2011) Elevated membrane attack complex in human choroid with high risk complement factor H genotypes. Experimental Eye Research 93:4, 565-567
CrossRef23
Jennyfer Zerbib, Nathalie Puche, Florence Richard, Nicolas Leveziel, Salomon Y. Cohen, Jean-François Korobelnik, José Sahel, Arnold Munnich, Josseline Kaplan, Jean-Michel Rozet, Eric H. Souied. (2011) No association between the T280M polymorphism of the CX3CR1 gene and exudative AMD. Experimental Eye Research 93:4, 382-386
CrossRef24
D. E. Weiner, H. Tighiouart, R. Reynolds, J. M. Seddon. (2011) Kidney function, albuminuria and age-related macular degeneration in NHANES III. Nephrology Dialysis Transplantation 26:10, 3159-3165
CrossRef25
Michael Goldberg, Véronique Fremeaux-Bacchi, Penina Koch, Zvi Fishelson, Yitzhak Katz. (2011) A novel mutation in the C3 gene and recurrent invasive pneumococcal infection: A clue for vaccine development. Molecular Immunology 48:15-16, 1926-1931
CrossRef26
Marisol Cano, Natalia Fijalkowski, Naoshi Kondo, Sonny Dike, James Handa. (2011) Advanced Glycation Endproduct Changes to Bruch's Membrane Promotes Lipoprotein Retention by Lipoprotein Lipase. The American Journal of Pathology 179:2, 850-859
CrossRef27
J.-D. Ding, L. V. Johnson, R. Herrmann, S. Farsiu, S. G. Smith, M. Groelle, B. E. Mace, P. Sullivan, J. A. Jamison, U. Kelly, O. Harrabi, S. S. Bollini, J. Dilley, D. Kobayashi, B. Kuang, W. Li, J. Pons, J. C. Lin, C. B. Rickman. (2011) PNAS Plus: Anti-amyloid therapy protects against retinal pigmented epithelium damage and vision loss in a model of age-related macular degeneration. Proceedings of the National Academy of Sciences 108:28, E279-E287
CrossRef28
Marc Biarnés, Jordi Monés, Jordi Alonso, Luis Arias. (2011) Update on Geographic Atrophy in Age-Related Macular Degeneration. Optometry and Vision Science 88:7, 881-889
CrossRef29
Kyoko Ohno-Matsui. (2011) Parallel findings in age-related macular degeneration and Alzheimer’s disease. Progress in Retinal and Eye Research 30:4, 217-238
CrossRef30
MengMeng Xu, Odell D. Jones, Shangen Zheng, Li Yanfei, Guifang Yan, Yuexing Pan, Harry G. Davis, Donald D. Anthony, Yi Xu, Joseph L. Bryant, Xuehong Xu. (2011) Cytoplasmic Accumulation of Liquid-Crystal Like Droplets in Post-Infection Sputum Generated by Gram-Positive Bacteria. Molecular Crystals and Liquid Crystals 547:1, 173/[1863]-180/[1870]
CrossRef31
A. Thakkinstian, G. J. McKay, M. McEvoy, U. Chakravarthy, S. Chakrabarti, G. Silvestri, I. Kaur, X. Li, J. Attia. (2011) Systematic Review and Meta-Analysis of the Association Between Complement Component 3 and Age-related Macular Degeneration: A HuGE Review and Meta-Analysis. American Journal of Epidemiology 173:12, 1365-1379
CrossRef32
G. J. McKay, G. Silvestri, U. Chakravarthy, S. Dasari, L. G. Fritsche, B. H. Weber, C. N. Keilhauer, M. L. Klein, P. J. Francis, C. C. Klaver, J. R. Vingerling, L. Ho, P. T. D. V. De Jong, M. Dean, J. Sawitzke, P. N. Baird, R. H. Guymer, D. Stambolian, A. Orlin, J. M. Seddon, I. Peter, A. F. Wright, C. Hayward, A. J. Lotery, S. Ennis, M. B. Gorin, D. E. Weeks, C.-L. Kuo, A. D. Hingorani, R. Sofat, V. Cipriani, A. Swaroop, M. Othman, A. Kanda, W. Chen, G. R. Abecasis, J. R. Yates, A. R. Webster, A. T. Moore, J. H. Seland, M. Rahu, G. Soubrane, L. Tomazzoli, F. Topouzis, J. Vioque, I. S. Young, A. E. Fletcher, C. C. Patterson. (2011) Variations in Apolipoprotein E Frequency With Age in a Pooled Analysis of a Large Group of Older People. American Journal of Epidemiology 173:12, 1357-1364
CrossRef33
Søren E. Degn, Jens C. Jensenius, Steffen Thiel. (2011) Disease-Causing Mutations in Genes of the Complement System. The American Journal of Human Genetics 88:6, 689-705
CrossRef34
D T Bradley, P F Zipfel, A E Hughes. (2011) Complement in age-related macular degeneration: a focus on function. Eye 25:6, 683-693
CrossRef35
Salvatore Grisanti, Julia Lueke, Matthias Lueke, Martin Rudolf, Swaantje Peters. (2011) Current and future strategies for nonexudative age-related macular degeneration. Expert Review of Ophthalmology 6:3, 315-322
CrossRef36
M. Heurich, R. Martinez-Barricarte, N. J. Francis, D. L. Roberts, S. Rodriguez de Cordoba, B. P. Morgan, C. L. Harris. (2011) Common polymorphisms in C3, factor B, and factor H collaborate to determine systemic complement activity and disease risk. Proceedings of the National Academy of Sciences 108:21, 8761-8766
CrossRef37
Johanna M. Seddon, Robyn Reynolds, Heeral R. Shah, Bernard Rosner. (2011) Smoking, Dietary Betaine, Methionine, and Vitamin D in Monozygotic Twins with Discordant Macular Degeneration: Epigenetic Implications. Ophthalmology
CrossRef38
Zohar Yehoshua, Philip J. Rosenfeld, Thomas A. Albini. (2011) Current Clinical Trials in Dry AMD and the Definition of Appropriate Clinical Outcome Measures. Seminars in Ophthalmology 26:3, 167-180
CrossRef39
Margaret M. DeAngelis, Alexandra C. Silveira, Elizabeth A. Carr, Ivana K. Kim. (2011) Genetics of Age-Related Macular Degeneration: Current Concepts, Future Directions. Seminars in Ophthalmology 26:3, 77-93
CrossRef40
V. Frémeaux-Bacchi, F. Fakhouri, L. Roumenina, M.-A. Dragon–Durey, C. Loirat. (2011) Syndrome hémolytique et urémique lié à des anomalies du complément. La Revue de Médecine Interne 32:4, 232-240
CrossRef41
Haris Kokotas, Maria Grigoriadou, Michael B. Petersen. (2011) Age-related macular degeneration: genetic and clinical findings. Clinical Chemistry and Laboratory Medicine 49:4, 601-616
CrossRef42
An Truong, Tien Y. Wong, Levon M. Khachigian. (2011) Emerging therapeutic approaches in the management of retinal angiogenesis and edema. Journal of Molecular Medicine 89:4, 343-361
CrossRef43
U. Friedrich, C. A. Myers, L. G. Fritsche, A. Milenkovich, A. Wolf, J. C. Corbo, B. H. F. Weber. (2011) Risk- and non-risk-associated variants at the 10q26 AMD locus influence ARMS2 mRNA expression but exclude pathogenic effects due to protein deficiency. Human Molecular Genetics 20:7, 1387-1399
CrossRef44
María Brión, Manuel Sanchez-Salorio, Marta Cortón, Maria de la Fuente, Belen Pazos, Mohammad Othman, Anand Swaroop, Goncalo Abecasis, Beatriz Sobrino, Angel Carracedo, . (2011) Genetic association study of age-related macular degeneration in the Spanish population. Acta Ophthalmologica 89:1, e12-e22
CrossRef45
Gui-shuang Ying, Maureen G. Maguire. (2011) Development of a Risk Score for Geographic Atrophy in Complications of the Age-related Macular Degeneration Prevention Trial. Ophthalmology 118:2, 332-338
CrossRef46
Naoshi Kondo, Hiroaki Bessho, Shigeru Honda, Akira Negi. (2011) Complement Factor H Y402H Variant and Risk of Age-Related Macular Degeneration in Asians: A Systematic Review and Meta-Analysis. Ophthalmology 118:2, 339-344
CrossRef47
Lucia Sobrin, Robyn Reynolds, Yi Yu, Jesen Fagerness, Nicolas Leveziel, Paul S. Bernstein, Eric H. Souied, Mark J. Daly, Johanna M. Seddon. (2011) ARMS2/HTRA1 Locus Can Confer Differential Susceptibility to the Advanced Subtypes of Age-Related Macular Degeneration. American Journal of Ophthalmology 151:2, 345-352.e3
CrossRef48
Peter Charbel Issa, N. Victor Chong, Hendrik P. N. Scholl. (2011) The significance of the complement system for the pathogenesis of age-related macular degeneration — current evidence and translation into clinical application. Graefe's Archive for Clinical and Experimental Ophthalmology 249:2, 163-174
CrossRef49
Katayoon B. Ebrahimi, James T. Handa. (2011) Lipids, Lipoproteins, and Age-Related Macular Degeneration. Journal of Lipids 2011, 1-14
CrossRef50
Nicolas Leveziel, Julien Tilleul, Nathalie Puche, Jennyfer Zerbib, Franck Laloum, Giuseppe Querques, Eric H. Souied. (2011) Genetic Factors Associated with Age-Related Macular Degeneration. Ophthalmologica 226:3, 87-102
CrossRef51
Stephen G. Schwartz, Milam A. Brantley. (2011) Pharmacogenetics and Age-Related Macular Degeneration. Journal of Ophthalmology 2011, 1-8
CrossRef52
Baoying Liu, Lai Wei, Catherine Meyerle, Jingsheng Tuo, H Nida Sen, Zhiyu Li, Sagarika Chakrabarty, Elvira Agron, Chi-Chao Chan, Michael L Klein, Emily Chew, Frederick Ferris, Robert B Nussenblatt. (2011) Complement component C5a Promotes Expression of IL-22 and IL-17 from Human T cells and its Implication in Age-related Macular Degeneration. Journal of Translational Medicine 9:1, 111
CrossRef53
Kacie J. Meyer, Lea K. Davis, Emily I. Schindler, John S. Beck, Danielle S. Rudd, A. Jason Grundstad, Todd E. Scheetz, Terry A. Braun, John H. Fingert, Wallace L. Alward, Young H. Kwon, James C. Folk, Stephen R. Russell, Thomas H. Wassink, Edwin M. Stone, Val C. Sheffield. (2011) Genome-wide analysis of copy number variants in age-related macular degeneration. Human Genetics 129:1, 91-100
CrossRef54
Marian M Humphries, Paul F Kenna, Matthew Campbell, Lawrence C S Tam, Anh T H Nguyen, G Jane Farrar, Marina Botto, Anna Sophia Kiang, Peter Humphries. (2011) C1q enhances cone photoreceptor survival in a mouse model of autosomal recessive retinitis pigmentosa. European Journal of Human Genetics
CrossRef55
Poul Suadicani, Hans Ole Hein, Finn Gyntelberg. (2011) Complement C3 Genotype Variants and Risk of Lung Cancer Mortality. ISRN Pulmonology 2011, 1-4
CrossRef56
Cécile Delcourt, J. -F. Korobelnik, P. Barberger-Gateau, M. -N. Delyfer, M. -B. Rougier, M. Goff, F. Malet, J. Colin, J. -F. Dartigues. (2010) Nutrition and age-related eye diseases: The Alienor (Antioxydants, lipides essentiels, nutrition et maladies oculaires) study. The journal of nutrition, health & aging 14:10, 854-861
CrossRef57
Benedetta Peruzzi, Martina Serra, Chiara Pescucci, Michela Sica, Sonia Lastraioli, Tommaso Rondelli, Simona Pedemonte, Antonio Maria Risitano, Maria De Angioletti, Patrizia Piccioli, Rosario Notaro. (2010) Easy genotyping of complement C3 ‘slow’ and ‘fast’ allotypes by tetra-primer amplification refractory mutation system PCR. Molecular and Cellular Probes 24:6, 401-402
CrossRef58
A. Lommatzsch. (2010) Pigmentepithelabhebung bei exsudativer Makuladegeneration. Der Ophthalmologe 107:12, 1115-1122
CrossRef59
L J Kopplin, R P Igo, Y Wang, T A Sivakumaran, S A Hagstrom, N S Peachey, P J Francis, M L Klein, J P SanGiovanni, E Y Chew, G J T Pauer, G M Sturgill, T Joshi, L Tian, Q Xi, A K Henning, K E Lee, R Klein, B E K Klein, S K Iyengar. (2010) Genome-wide association identifies SKIV2L and MYRIP as protective factors for age-related macular degeneration. Genes and Immunity 11:8, 609-621
CrossRef60
Reecha Sofat, Juan P. Casas, Meena Kumari, Philippa J. Talmud, Helen Ireland, Mika Kivimaki, Michael Marmot, Alun D. Hughes, Simon Thom, Shah Ebrahim, John C. Whittaker, Liam Smeeth, Debbie A. Lawlor, Steve E. Humphries, Aroon D. Hingorani. (2010) Genetic variation in complement factor H and risk of coronary heart disease: Eight new studies and a meta-analysis of around 48,000 individuals. Atherosclerosis 213:1, 184-190
CrossRef61
J.-L. Liao, J. Yu, K. Huang, J. Hu, T. Diemer, Z. Ma, T. Dvash, X.-J. Yang, G. H. Travis, D. S. Williams, D. Bok, G. Fan. (2010) Molecular signature of primary retinal pigment epithelium and stem-cell-derived RPE cells. Human Molecular Genetics 19:21, 4229-4238
CrossRef62
Norimoto Gotoh, Kenji Yamashiro, Hideo Nakanishi, Masaaki Saito, Tomohiro Iida, Nagahisa Yoshimura. (2010) Haplotype analysis of the ARMS2/HTRA1 region in Japanese patients with typical neovascular age-related macular degeneration or polypoidal choroidal vasculopathy. Japanese Journal of Ophthalmology 54:6, 609-614
CrossRef63
Robyn Reynolds, Bernard Rosner, Johanna M. Seddon. (2010) Serum Lipid Biomarkers and Hepatic Lipase Gene Associations with Age-Related Macular Degeneration. Ophthalmology 117:10, 1989-1995
CrossRef64
Sam Khandhadia, Andrew Lotery. (2010) Oxidation and age-related macular degeneration: insights from molecular biology. Expert Reviews in Molecular Medicine 12,
CrossRef65
Marco A Zarbin, Philip J Rosenfeld. (2010) PATHWAY-BASED THERAPIES FOR AGE-RELATED MACULAR DEGENERATION. Retina 30:9, 1350-1367
CrossRef66
Inga Peter, Johanna M. Seddon. (2010) Genetic Epidemiology: Successes and Challenges of Genome-Wide Association Studies Using the Example of Age-Related Macular Degeneration. American Journal of Ophthalmology 150:4, 450-452.e2
CrossRef67
Peter J Francis. 2010. Genetics of Retinal Disease. .
CrossRef68
Alan C. Bird. (2010) Therapeutic targets in age-related macular disease. Journal of Clinical Investigation 120:9, 3033-3041
CrossRef69
Gwen M. Sturgill, Elisa Bala, Stacia S. Yaniglos, Neal S. Peachey, Stephanie A. Hagstrom. (2010) Mutation screen of β-crystallin genes in 274 patients with age-related macular degeneration. Ophthalmic Genetics 31:3, 129-134
CrossRef70
Xiaoqi Liu, Peiquan Zhao, Shibo Tang, Fang Lu, Jianbin Hu, Chuntao Lei, Xian Yang, Ying Lin, Shi Ma, Jiyun Yang, Dingding Zhang, Yi Shi, Tao Li, Yiye Chen, Yinchuan Fan, Zhenglin Yang. (2010) ASSOCIATION STUDY OF COMPLEMENT FACTOR H, C2, CFB, AND C3 AND AGE-RELATED MACULAR DEGENERATION IN A HAN CHINESE POPULATION. Retina 30:8, 1177-1184
CrossRef71
Michael L. Klein, Frederick L. Ferris, Peter J. Francis, Anne S. Lindblad, Emily Y. Chew, Sara C. Hamon, Jurg Ott. (2010) Progression of Geographic Atrophy and Genotype in Age-Related Macular Degeneration. Ophthalmology 117:8, 1554-1559.e1
CrossRef72
Johanna M. Seddon, Gary Gensler, Bernard Rosner. (2010) C-Reactive Protein and CFH, ARMS2/HTRA1 Gene Variants Are Independently Associated with Risk of Macular Degeneration. Ophthalmology 117:8, 1560-1566
CrossRef73
Timothy YY Lai, Li Jia Chen, Gary HF Yam, Clement CY Tham, Chi Pui Pang. (2010) Development of novel drugs for ocular diseases: possibilities for individualized therapy. Personalized Medicine 7:4, 371-386
CrossRef74
Alexa N. Bramall, Alan F. Wright, Samuel G. Jacobson, Roderick R. McInnes. (2010) The Genomic, Biochemical, and Cellular Responses of the Retina in Inherited Photoreceptor Degenerations and Prospects for the Treatment of These Disorders. Annual Review of Neuroscience 33:1, 441-472
CrossRef75
Nathan L Mata, Roger Vogel. (2010) Pharmacologic treatment of atrophic age-related macular degeneration. Current Opinion in Ophthalmology 21:3, 190-196
CrossRef76
Vidyullatha Vasireddy, Paul Wong, Radha Ayyagari. (2010) Genetics and molecular pathology of Stargardt-like macular degeneration. Progress in Retinal and Eye Research 29:3, 191-207
CrossRef77
W. Chen, D. Stambolian, A. O. Edwards, K. E. Branham, M. Othman, J. Jakobsdottir, N. Tosakulwong, M. A. Pericak-Vance, P. A. Campochiaro, M. L. Klein, P. L. Tan, Y. P. Conley, A. Kanda, L. Kopplin, Y. Li, K. J. Augustaitis, A. J. Karoukis, W. K. Scott, A. Agarwal, J. L. Kovach, S. G. Schwartz, E. A. Postel, M. Brooks, K. H. Baratz, W. L. Brown, , A. J. Brucker, A. Orlin, G. Brown, A. Ho, C. Regillo, L. Donoso, L. Tian, B. Kaderli, D. Hadley, S. A. Hagstrom, N. S. Peachey, R. Klein, B. E. K. Klein, N. Gotoh, K. Yamashiro, F. Ferris, J. A. Fagerness, R. Reynolds, L. A. Farrer, I. K. Kim, J. W. Miller, M. Corton, A. Carracedo, M. Sanchez-Salorio, E. W. Pugh, K. F. Doheny, M. Brion, M. M. DeAngelis, D. E. Weeks, D. J. Zack, E. Y. Chew, J. R. Heckenlively, N. Yoshimura, S. K. Iyengar, P. J. Francis, N. Katsanis, J. M. Seddon, J. L. Haines, M. B. Gorin, G. R. Abecasis, A. Swaroop, R. N. Johnson, E. Ai, H. R. McDonald, M. Stolarczuk, P. R. Pavan, K. K. Billiris, M. Iyer, M. M. Menosky, S. E. Pautler, S. M. Millard, B. Hubbard, T. Aaberg, L. DuBois, A. Lyon, S. Anderson-Nelson, L. M. Jampol, D. V. Weinberg, A. Munana, Z. Rozenbajgier, D. Orth, J. Cohen, M. MacCumber, M. MacCumber, C. Figliulo, L. Porcz, J. Folk, H. C. Boldt, S. R. Russell, R. Ivins, C. J. Hinz, C. C. Barr, S. Bloom, K. Jaegers, B. Kritchman, G. Whittington, J. Heier, A. R. Frederick, M. G. Morley, T. Topping, H. L. Davis, S. B. Bressler, N. M. Bressler, W. Doll, M. Trese, A. Capone, B. R. Garretson, T. S. Hassan, A. J. Ruby, T. Osentoski, C. A. McCannel, M. J. Ruszczyk, G. Grand, K. Blinder, N. M. Holekamp, D. P. Joseph, G. Shah, G. S. Nobel, A. N. Antoszyk, D. J. Browning, A. H. Stallings, L. J. Singerman, D. Miller, M. Novak, S. Pendergast, H. Zegarra, S. A. Schura, S. Smith-Brewer, F. H. Davidorf, R. Chambers, L. Chorich, J. Salerno, R. F. Dreyer, C. Ma, M. R. Kopfer, M. L. Klein, D. J. Wilson, S. K. Nolte, J. E. Grunwald, A. J. Brucker, J. Dunaief, S. L. Fine, A. M. Maguire, R. A. Stoltz, M. N. McRay, G. E. Fish, R. Anand, R. Spencer, J. Arnwine, S. R. Chandra, M. Altaweel, B. Blodi, J. Gottlieb, M. Ip, T. M. Nork, J. Perry-Raymond, S. L. Fine, M. G. Maguire, M. Brightwell-Arnold, S. Harkins, E. Peskin, G.-S. Ying, N. Kurinij. (2010) Genetic variants near TIMP3 and high-density lipoprotein-associated loci influence susceptibility to age-related macular degeneration. Proceedings of the National Academy of Sciences 107:16, 7401-7406
CrossRef78
B. M. Neale, J. Fagerness, R. Reynolds, L. Sobrin, M. Parker, S. Raychaudhuri, P. L. Tan, E. C. Oh, J. E. Merriam, E. Souied, P. S. Bernstein, B. Li, J. M. Frederick, K. Zhang, M. A. Brantley, A. Y. Lee, D. J. Zack, B. Campochiaro, P. Campochiaro, S. Ripke, R. T. Smith, G. R. Barile, N. Katsanis, R. Allikmets, M. J. Daly, J. M. Seddon. (2010) Genome-wide association study of advanced age-related macular degeneration identifies a role of the hepatic lipase gene (LIPC). Proceedings of the National Academy of Sciences 107:16, 7395-7400
CrossRef79
Y. Wu, E. Yanase, X. Feng, M. M. Siegel, J. R. Sparrow. (2010) Structural characterization of bisretinoid A2E photocleavage products and implications for age-related macular degeneration. Proceedings of the National Academy of Sciences 107:16, 7275-7280
CrossRef80
Norann A. Zaghloul, Nicholas Katsanis. (2010) Functional modules, mutational load and human genetic disease. Trends in Genetics 26:4, 168-176
CrossRef81
Alan F. Wright, Christina F. Chakarova, Mai M. Abd El-Aziz, Shomi S. Bhattacharya. (2010) Photoreceptor degeneration: genetic and mechanistic dissection of a complex trait. Nature Reviews Genetics 11:4, 273-284
CrossRef82
Sanna Seitsonen, Päivi Onkamo, Suvi Torniainen, Milla Ihalainen, Ilkka Immonen, Seppo Meri, Irma Järvelä. (2010) Screening of DNA-variants in the properdin gene (CFP) in age-related macular degeneration (AMD). Molecular Immunology 47:6, 1334-1336
CrossRef83
Amir Ghorbanihaghjo, Alireza Javadzadeh, Nadereh Rashtchizadeh, Hassan Argani, Sima Masoodnia, Nariman Nezami. (2010) High-sensitivity C-reactive protein and endothelin-1 in age-related macular degeneration. Journal of Men's Health 7:1, 85-91
CrossRef84
Dominique C. Baas, Lintje Ho, Sarah Ennis, Joanna E. Merriam, Michael W.T. Tanck, André G. Uitterlinden, Paulus T.V.M. de Jong, Angela J. Cree, Helen L. Griffiths, Fernando Rivadeneira, Albert Hofman, Cornelia van Duijn, R. Theodore Smith, Gaetano R. Barile, Theo G.M.F. Gorgels, Johannes R. Vingerling, Caroline C.W. Klaver, Andrew J. Lotery, Rando Allikmets, Arthur A.B. Bergen. (2010) The Complement Component 5 Gene and Age-Related Macular Degeneration. Ophthalmology 117:3, 500-511
CrossRef85
Don H. Anderson, Monte J. Radeke, Natasha B. Gallo, Ethan A. Chapin, Patrick T. Johnson, Christy R. Curletti, Lisa S. Hancox, Jane Hu, Jessica N. Ebright, Goldis Malek, Michael A. Hauser, Catherine Bowes Rickman, Dean Bok, Gregory S. Hageman, Lincoln V. Johnson. (2010) The pivotal role of the complement system in aging and age-related macular degeneration: Hypothesis re-visited. Progress in Retinal and Eye Research 29:2, 95-112
CrossRef86
Gayle J.T. Pauer, Gwen M. Sturgill, Neal S. Peachey, Stephanie A. Hagstrom. (2010) Protective Effect of Paraoxonase 1 Gene Variant Gln192Arg in Age-Related Macular Degeneration. American Journal of Ophthalmology 149:3, 513-522
CrossRef87
Navdeep Dhillon, Liron Walsh, Bernd Krüger, Anita Mehrotra, Stephen C. Ward, Jim Godbold, Mohamed Radwan, Thomas Schiano, Barbara Murphy, Bernd Schröppel. (2010) Complement component C3 allotypes and outcomes in liver transplantation. Liver Transplantation 16:2, 198-203
CrossRef88
L. A. Hecker, A. O. Edwards, E. Ryu, N. Tosakulwong, K. H. Baratz, W. L. Brown, P. C. Issa, H. P. Scholl, B. Pollok-Kopp, K. E. Schmid-Kubista, K. R. Bailey, M. Oppermann. (2010) Genetic control of the alternative pathway of complement in humans and age-related macular degeneration. Human Molecular Genetics 19:1, 209-215
CrossRef89
Marco Zarbin, Janet S Sunness. 2010. Dry age-related macular degeneration and age-related macular degeneration pathogenesis. , 527-535.
CrossRef90
Saritha Katta, Inderjeet Kaur, Subhabrata Chakrabarti. (2009) The molecular genetic basis of age-related macular degeneration: an overview. Journal of Genetics 88:4, 425-449
CrossRef91
Asako Goto, Masakazu Akahori, Haru Okamoto, Masayoshi Minami, Naoki Terauchi, Yuji Haruhata, Minoru Obazawa, Toru Noda, Miki Honda, Atsushi Mizota, Minoru Tanaka, Takaaki Hayashi, Masaki Tanito, Naoko Ogata, Takeshi Iwata. (2009) Genetic analysis of typical wet-type age-related macular degeneration and polypoidal choroidal vasculopathy in Japanese population. Journal of Ocular Biology, Diseases, and Informatics 2:4, 164-175
CrossRef92
Yureeda Qazi, Surekha Maddula, Balamurali K. Ambati. (2009) Mediators of ocular angiogenesis. Journal of Genetics 88:4, 495-515
CrossRef93
Robert F. Mullins, Elizabeth A. Faidley, Heather T. Daggett, Catherine Jomary, Andrew J. Lotery, Edwin M. Stone. (2009) Localization of complement 1 inhibitor (C1INH/SERPING1) in human eyes with age-related macular degeneration. Experimental Eye Research 89:5, 767-773
CrossRef94
Christine A. Curcio, Mark Johnson, Jiahn-Dar Huang, Martin Rudolf. (2009) Aging, age-related macular degeneration, and the response-to-retention of apolipoprotein B-containing lipoproteins. Progress in Retinal and Eye Research 28:6, 393-422
CrossRef95
I. Steinbrugger, A. Haas, W. Renner, M. Mayer, A. Wedrich, Y. El-Shabrawi, C. Werner, O. Schmut, M. Weger. (2009) Die Bedeutung des C3 Arg102Gly Genpolymorphismus als Risikofaktor für die exsudative altersabhängige Makuladegeneration. Spektrum der Augenheilkunde 23:5, 353-357
CrossRef96
Paul N Baird, Gregory S Hageman, Robyn H Guymer. (2009) New era for personalized medicine: the diagnosis and management of age-related macular degeneration. Clinical & Experimental Ophthalmology 37:8, 814-821
CrossRef97
Andrew F. Ducruet, Brad E. Zacharia, Zachary L. Hickman, Bartosz T. Grobelny, Mason L. Yeh, Sergey A. Sosunov, E. Sander Connolly. (2009) The complement cascade as a therapeutic target in intracerebral hemorrhage. Experimental Neurology 219:2, 398-403
CrossRef98
Olli Arjamaa, Mikko Nikinmaa, Antero Salminen, Kai Kaarniranta. (2009) Regulatory role of HIF-1α in the pathogenesis of age-related macular degeneration (AMD). Ageing Research Reviews 8:4, 349-358
CrossRef99
Andrew YC Ting, Thomas KM Lee, Ian M MacDonald. (2009) Genetics of age-related macular degeneration. Current Opinion in Ophthalmology 20:5, 369-376
CrossRef100
Anand Swaroop, Emily Y. Chew, Catherine Bowes Rickman, Gonçalo R. Abecasis. (2009) Unraveling a Multifactorial Late-Onset Disease: From Genetic Susceptibility to Disease Mechanisms for Age-Related Macular Degeneration. Annual Review of Genomics and Human Genetics 10:1, 19-43
CrossRef101
Rando Allikmets, Michael Dean, Gregory S Hageman, Paul N Baird, Caroline C Klaver, Arthur A Bergen, Bernhard H Weber. (2009) The SERPING1 gene and age-related macular degeneration. The Lancet 374:9693, 875-876
CrossRef102
Marina Botto, Michael Kirschfink, Paolo Macor, Matthew C. Pickering, Reinhard Würzner, Francesco Tedesco. (2009) Complement in human diseases: Lessons from complement deficiencies. Molecular Immunology 46:14, 2774-2783
CrossRef103
Lars G. Fritsche, Sandra Freitag-Wolf, Thomas Bettecken, Thomas Meitinger, Claudia N. Keilhauer, Michael Krawczak, Bernhard H.F. Weber. (2009) Age-related macular degeneration and functional promoter and coding variants of the apolipoprotein E gene. Human Mutation 30:7, 1048-1053
CrossRef104
Fiona M. Cuthbertson, Stuart N. Peirson, Katharina Wulff, Russell G. Foster, Susan M. Downes. (2009) Blue light–filtering intraocular lenses: Review of potential benefits and side effects. Journal of Cataract & Refractive Surgery 35:7, 1281-1297
CrossRef105
O. M. Woodward, A. Kottgen, J. Coresh, E. Boerwinkle, W. B. Guggino, M. Kottgen. (2009) Cozzarelli Prize Winner@;DELIM@;From the Cover: Identification of a urate transporter, ABCG2, with a common functional polymorphism causing gout. Proceedings of the National Academy of Sciences 106:25, 10338-10342
CrossRef106
P. J. Lachmann, R. A. G. Smith. (2009) Taking Complement to the Clinic - has the Time Finally Come?. Scandinavian Journal of Immunology 69:6, 471-478
CrossRef107
Camiel J.F. Boon, Nicole C. van de Kar, B. Jeroen Klevering, Jan E.E. Keunen, Frans P.M. Cremers, Caroline C.W. Klaver, Carel B. Hoyng, Mohamed R. Daha, Anneke I. den Hollander. (2009) The spectrum of phenotypes caused by variants in the CFH gene. Molecular Immunology 46:8-9, 1573-1594
CrossRef108
Tsutomu Yasukawa. (2009) Inflammation in age-related macular degeneration: pathological or physiological?. Expert Review of Ophthalmology 4:2, 107-112
CrossRef109
T. Montes, A. Tortajada, B. P. Morgan, S. Rodriguez de Cordoba, C. L. Harris. (2009) Functional basis of protection against age-related macular degeneration conferred by a common polymorphism in complement factor B. Proceedings of the National Academy of Sciences 106:11, 4366-4371
CrossRef110
Dominiek D.G. Despriet, Cornelia M. van Duijn, Ben A. Oostra, Andre G. Uitterlinden, Albert Hofman, Alan F. Wright, Jacoline B. ten Brink, Arne Bakker, Paulus T.V.M. de Jong, Johannes R. Vingerling, Arthur A.B. Bergen, Caroline C.W. Klaver. (2009) Complement Component C3 and Risk of Age-Related Macular Degeneration. Ophthalmology 116:3, 474-480.e2
CrossRef111
Varagunam, Mira, Yaqoob, Muhammad M., Döhler, Bernd, Opelz, Gerhard, . (2009) C3 Polymorphisms and Allograft Outcome in Renal Transplantation. New England Journal of Medicine 360:9, 874-880
Full Text112
Xiaoyan Ding, Mrinali Patel, Chi-Chao Chan. (2009) Molecular pathology of age-related macular degeneration. Progress in Retinal and Eye Research 28:1, 1-18
CrossRef113
Brooke L. Fridley. (2009) Bayesian variable and model selection methods for genetic association studies. Genetic Epidemiology 33:1, 27-37
CrossRef114
V. Fremeaux-Bacchi, E. C. Miller, M. K. Liszewski, L. Strain, J. Blouin, A. L. Brown, N. Moghal, B. S. Kaplan, R. A. Weiss, K. Lhotta, G. Kapur, T. Mattoo, H. Nivet, W. Wong, S. Gie, B. H. de Ligny, M. Fischbach, R. Gupta, R. Hauhart, V. Meunier, C. Loirat, M.-A. Dragon-Durey, W. H. Fridman, B. J. C. Janssen, T. H. J. Goodship, J. P. Atkinson. (2008) Mutations in complement C3 predispose to development of atypical hemolytic uremic syndrome. Blood 112:13, 4948-4952
CrossRef115
Peter F. Zipfel, Teresia Hallström, Sven Hammerschmidt, Christine Skerka. (2008) The complement fitness Factor H: Role in human diseases and for immune escape of pathogens, like pneumococci. Vaccine 26, I67-I74
CrossRef116
Sarah Ennis, Catherine Jomary, Robert Mullins, Angela Cree, Xiaoli Chen, Alex MacLeod, Stephen Jones, Andrew Collins, Edwin Stone, Andrew Lotery. (2008) Association between the SERPING1 gene and age-related macular degeneration: a two-stage case–control study. The Lancet 372:9652, 1828-1834
CrossRef117
Hanna R Coleman, Chi-Chao Chan, Frederick L Ferris, Emily Y Chew. (2008) Age-related macular degeneration. The Lancet 372:9652, 1835-1845
CrossRef118
Celia J. Fang, Anna Richards, M. Kathryn Liszewski, David Kavanagh, John P. Atkinson. (2008) Advances in understanding of pathogenesis of aHUS and HELLP. British Journal of Haematology 143:3, 336-348
CrossRef119
Caroline CW Klaver, Arthur AB Bergen. (2008) The SERPING1 gene and age-related macular degeneration. The Lancet 372:9652, 1788-1789
CrossRef120
Yang, Zhenglin, Stratton, Charity, Francis, Peter J., Kleinman, Mark E., Tan, Perciliz L., Gibbs, Daniel, Tong, Zongzhong, Chen, Haoyu, Constantine, Ryan, Yang, Xian, Chen, Yuhong, Zeng, Jiexi, Davey, Lisa, Ma, Xiang, Hau, Vincent S., Wang, Chi, Harmon, JenniferBuehler, Jeanette, Pearson, Erik, Patel, Shrena, Kaminoh, Yuuki, Watkins, Scott, Luo, Ling, Zabriskie, Norman A., Bernstein, Paul S., Cho, Wongil, Schwager, Andrea, Hinton, David R., Klein, Michael L., Hamon, Sara C., Simmons, Emily, Yu, Beifeng, Campochiaro, Betsy, Sunness, Janet S., Campochiaro, Peter, Jorde, Lynn, Parmigiani, Giovanni, Zack, Donald J., Katsanis, Nicholas, Ambati, Jayakrishna, Zhang, Kang, . (2008) Toll-like Receptor 3 and Geographic Atrophy in Age-Related Macular Degeneration. New England Journal of Medicine 359:14, 1456-1463
Full Text121
Mihály Józsi, Peter F. Zipfel. (2008) Factor H family proteins and human diseases. Trends in Immunology 29:8, 380-387
CrossRef122
E C Fletcher, N V Chong. (2008) Looking beyond Lucentis on the management of macular degeneration. Eye 22:6, 742-750
CrossRef123
A Lotery. (2008) Progress in understanding and treating age-related macular degeneration. Eye 22:6, 739-741
CrossRef124
F. Fajnkuchen, S.Y. Cohen. (2008) Dégénérescence maculaire liée à l’âge et génétique : données actuelles. Journal Français d'Ophtalmologie 31:6, 630-637
CrossRef125
Mrinali Patel, Chi-Chao Chan. (2008) Immunopathological aspects of age-related macular degeneration. Seminars in Immunopathology 30:2, 97-110
CrossRef126
Thomas A. Ferguson, Rajendra S. Apte. (2008) Angiogenesis in eye disease: immunity gained or immunity lost?. Seminars in Immunopathology 30:2, 111-119
CrossRef127
Nalini S. Bora, Purushottam Jha, Puran S. Bora. (2008) The role of complement in ocular pathology. Seminars in Immunopathology 30:2, 85-95
CrossRef128
STEFFEN SCHMITZ-VALCKENBERG, FRANK G. HOLZ, ALAN C. BIRD, RICHARD F. SPAIDE. (2008) FUNDUS AUTOFLUORESCENCE IMAGING. Retina 28:3, 385-409
CrossRef129
Stephen F. Kingsmore, Ingrid E. Lindquist, Joann Mudge, Damian D. Gessler, William D. Beavis. (2008) Genome-wide association studies: progress and potential for drug discovery and development. Nature Reviews Drug Discovery 7:3, 221-230
CrossRef130
Joe G Hollyfield, Vera L Bonilha, Mary E Rayborn, Xiaoping Yang, Karen G Shadrach, Liang Lu, Rafael L Ufret, Robert G Salomon, Victor L Perez. (2008) Oxidative damage–induced inflammation initiates age-related macular degeneration. Nature Medicine 14:2, 194-198
CrossRef131
Mi In Roh, Ji Hyun Kim, Suk Ho Byeon, Hyoung Jun Koh, Sung Chul Lee, Oh Woong Kwon. (2008) Estimated Prevalence and Risk Factor for Age-related Maculopathy. Yonsei Medical Journal 49:6, 931
CrossRef132
Hans C Fischer, Warren CW Chan. (2007) Nanotoxicity: the growing need for in vivo study. Current Opinion in Biotechnology 18:6, 565-571
CrossRef133
Herbert W 'Skip' Virgin. (2007) In vivo veritas: pathogenesis of infection as it actually happens. Nature Immunology 8:11, 1143-1147
CrossRef134
J. L. Haines, K. M. Spencer, M. A. Pericak-Vance. (2007) Bringing the genetics of macular degeneration into focus. Proceedings of the National Academy of Sciences 104:43, 16725-16726
CrossRef135
P. J. Coffey, C. Gias, C. J. McDermott, P. Lundh, M. C. Pickering, C. Sethi, A. Bird, F. W. Fitzke, A. Maass, L. L. Chen, G. E. Holder, P. J. Luthert, T. E. Salt, S. E. Moss, J. Greenwood. (2007) Complement factor H deficiency in aged mice causes retinal abnormalities and visual dysfunction. Proceedings of the National Academy of Sciences 104:42, 16651-16656
CrossRef136
Wendy K. Chung. (2007) Implementation of Genetics to Personalize Medicine. Gender Medicine 4:3, 248-265
CrossRef
