Clinical risk factors for age-related macular degeneration: a systematic review and meta-analysis

Background: Age-related macular degeneration (AMD) is the leading cause of blindness in Western countries. Numerous risk factors have been reported but the evidence and strength of association is variable. We aimed to identify those risk factors with strong levels of evidence which could be easily assessed by physicians or ophthalmologists to implement preventive interventions or address current behaviours.

The association between macular pigment optical density and CFH, ARMS2, C2/BF, and C3 genotype.

Age-related macular degeneration (AMD) is the most common cause of blindness in older people in developed countries, and risk for this condition may be classified as genetic or environmental, with an interaction between such factors predisposing to this disease. This study investigated the relationship between AMD risk genes, macular pigment optical density (MPOD), which may protect against AMD, and serum concentrations of the macular carotenoids, lutein (L) and zeaxanthin (Z). This was a cross-sectional study of 302 healthy adult subjects. Dietary intake of L and Z was assessed by food frequency questionnaire, and MPOD was measured by customized heterochromatic flicker photometry. We also calculated MPOD Area as the area of MP under the spatial profile curve, to reflect MP across the macula. Serum L and Z were measured by HPLC. Genotyping of tag SNPs in the genes CFH, ARMS2, C3, C2 and BF was undertaken with multiplex polymerase chain reaction (PCR) and primer extension methodology (ABI Snapshot, ABI Warrington UK) on DNA extracted from peripheral blood. The mean ± SD (range) age of the subjects in this study was 48 ± 11 (21-66) years. There was a statistically significant association between CFH genotype and family history of AMD, with subjects having two non-risk CFH haplotypes (n =35), or one non-risk and one protective CFH haplotype (n = 33), being significantly more likely to have a negative family history of AMD (Pearson Chi square: p = 0.001). There was no significant association between the AMD risk genes investigated and either MPOD (One way ANOVA: p > 0.05) or serum concentrations of L or Z (One way ANOVA: p > 0.05, for both). Subjects who were homozygous for risk alleles of both CFH and ARMS2 (n = 4) had significantly lower MPOD at 0.5_ and 1_ retinal eccentricity (Independent samples t test: p

Evaluation of leukocyte dynamic in mouse retinal circulation with scanning laser ophthalmoloscopy (Video report)

http://bjo.bmj.com/content/suppl/2001/06/20/85.7.DC1 Leukocyte-endothelial cell interactions play an important role in the pathogenesis of various types of retinal vascular diseases, including diabetes, uveitis, and ischemic lesions. Over the last few years, several methods have been devised in which the scanning laser ophthalmoscope (SLO) is used to study leukocyte-endothelial interactions in vivo [1,2]. Previously we reported a noninvasive in vivo leukocyte tracking method using the SLO in rat. In this method, a nontoxic fluorescent agent (6-carboxyfluorescein diacetate, CFDA) was used to label leukocytes in vitro. Leukocyte velocities within the retinal and choroidal circulations were be quantified simultaneously [3]. None of the previous methods has been developed for imaging the murine fundus, mainly due to problems arising from the small size of the mouse eye. However, there are many advantages of using a murine model to study retinal vascular diseases such as enhanced genetic definition, increased range of reagents available for immunological studies and cost reduction. We have developed our SLO method such that we can track leukocytes in the mouse retinal and choroidal circulations.