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Purpose: To measure and contrast 2 biomarkers of cardiovascular disease, C-reactive protein (CRP) and plasma homocysteine, in individuals with age-related macular degeneration (AMD) and control individuals without AMD. Design: Case–control study. Participants: Seventy-nine affected individuals and 77 unaffected individuals from the AMD Genetic Study Group returned to obtain CRP and homocysteine levels. Methods: Both affected and unaffected individuals underwent testing for CRP and homocysteine. A detailed cardiovascular history was taken. Main Outcome Measures: Mean CRP and homocysteine levels in affected and unaffected individuals. Results: Mean CRP levels for affected and unaffected individuals were 3.42 and 2.30 mg/l, respectively (P = 0.03). Mean homocysteine levels for affected and unaffected individuals were 11.72 and 8.88 μmol/l, respectively (P<0.0001). In logistic regression models, older age, higher CRP, and higher homocysteine were risk factors for AMD. There were no significant differences between cases and controls in terms of gender, diabetes, hypertension, use of statin drugs, and smoking. The control group was significantly younger and had a lower rate of vitamin usage than the affected group. Conclusions: Elevated CRP and homocysteine levels are associated with AMD and implicate the role of chronic inflammation and atherosclerosis. [Copyright &y& Elsevier]

Age-related macular degeneration (AMD) is a complex multifactorial disease that affects the central region of the retina. AMD is clinically heterogeneous, leading to geographic atrophy (GA) and/or choroidal neovascularization (CNV) at advanced stages. Considerable data exists in support of a genetic predisposition for AMD. Recent linkage studies have provided evidence in favor of several AMD susceptibility loci. We have performed a high-resolution (5-cM) genome scan of 412 affected relative pairs that were enriched for late-stage disease (GA and/or CNV). Nonparametric linkage analysis was performed using two different diagnostic criteria and also by dividing the affected individuals according to GA or CNV phenotype. Our results demonstrate evidence of linkage in regions that were suggested in at least one previous study at chromosomes 1q (236--240 cM in the Marshfield genetic map), 5p (40--50 cM), and 9q (111 cM). Multipoint analysis of affected relatives with CNV provided evidence of additional susceptibility loci on chromosomes 2p (10 cM) and 22q (25 cM). A recently identified Gln5345Arg change in HEMICENTIN-1 on chromosome 1q25 was not detected in 274 affected members in the restricted group with AMD, 346 additional patients with AMD, and 237 unaffected controls. Our results consolidate the chromosomal locations of several AMD susceptibility loci and, together with previous reports, should facilitate the search for disease-associated sequence variants. [ABSTRACT FROM AUTHOR]