Abstract
PurposeThe complement factor H (CFH) tyrosine 402 histidine (Y402H, rs1061170) variant is known to be significantly associated with age-related macular degeneration (AMD). Whether this genetic variant may impact retinal blood flow regulation is largely unknown. This study investigated whether flicker-induced vasodilation, an indicator for the coupling between neural activity and blood flow, is altered in subjects carrying the rs1061170 risk allele.MethodsOne hundred healthy subjects (aged between 18 and 45 years) were included in this study. Retinal blood flow regulation was tested by assessing retinal vessel calibres in response to stimulation with diffuse flicker light. Retinal vascular flicker responses were determined with a Dynamic Vessel Analyzer (DVA). In addition, genotyping for rs1061170 was performed.ResultsEighteen subjects were homozygous for the risk allele C, 50 were homozygous for the ancestral allele T, and 31 subjects were heterozygous (CT). One subject had to be excluded from data evaluation, as no genetic analysis could be performed due to technical difficulties. Baseline diameters of retinal arteries (p = 0.39) and veins (p = 0.64) were comparable between the three groups. Flicker-induced vasodilation in both retinal arteries (p = 0.38) and retinal veins (p = 0.62) was also comparable between the three studied groups.ConclusionsOur data indicate that homozygous healthy young carriers of the C risk allele at rs1061170 do not show abnormal flicker-induced vasodilation in the retina. This suggests that the high-risk genetic variant of CFH polymorphism does not impact neuro-vascular coupling in healthy subjects.
Highlights
Alterations of the ocular circulation have been implicated in the pathogenesis of several ocular diseases, including age-related macular degeneration (AMD) (Feigl 2009), diabetic retinopathy (Pemp & Schmetterer 2008) and glaucoma (Grieshaber et al 2007; Cherecheanu et al 2013)
We have recently shown that healthy carriers of the complement factor H polymorphism (CFH, rs1061170, Y402H) have altered choroidal blood flow autoregulation, even below 45 years (Told et al 2013)
Retinal vascular dysregulation has been observed in a variety of ocular diseases such as diabetic retinopathy or glaucoma (Pemp & Schmetterer 2008; Pournaras et al 2008; Venkataraman et al 2010; Kur et al 2012; Pournaras & Riva 2013)
Summary
Alterations of the ocular circulation have been implicated in the pathogenesis of several ocular diseases, including age-related macular degeneration (AMD) (Feigl 2009), diabetic retinopathy (Pemp & Schmetterer 2008) and glaucoma (Grieshaber et al 2007; Cherecheanu et al 2013). It has been reported that lower choroidal perfusion is a risk factor for the development of choroidal neovascularization (CNV) in the fellow eye (Metelitsina et al 2008; Boltz et al 2010a,b). Whereas the latter studies indicate that choroidal blood flow regulation is impaired in patients with AMD, less evidence is available concerning retinal blood flow regulation. It has been shown that flickering light-induced vasodilation of retinal vessels is altered in patients with advanced AMD (Lanzl e540 et al 2011). One might hypothesize that retinal blood flow regulation may be compromised in patients with AMD
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