Purchase this article with an account.
Rami Gabriel, Mitul C. Mehta, Cristina M Kenney; A Prospective Study on Hereditary Proclivity of Age-Related Macular Degeneration. Invest. Ophthalmol. Vis. Sci. 2018;59(9):1419.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Recent research shows that Age-related Macular Degeneration (AMD) has a cellular etiology with significant contributions from the patient’s mitochondria. Following this logic, the hereditary pattern of AMD should have a proclivity of maternal passage. This study employed a prospective survey to evaluate whether maternal family history or paternal family history is more likely to be found in patients with AMD.
We conducted surveys of 215 patients who were confirmed by an ophthalmologist to have AMD. Family history was self-reported, however, proper education was given on AMD and other eye diseases. Proportions of probands with paternal and maternal history of AMD were compared by McNemar's and chi-square tests. Probands with parents deceased before the age of 60 were excluded from the study results. Baseline characteristics between probands and between parental characteristics disease were compared using logistic regression.
Of the 215 surveys conducted, 20 patients had parental history of AMD and both parents living beyond age 60. There were 4 probands that had paternal history, 14 that had maternal history and 1 proband that had both. This shows a significantly larger proportion of patients with maternal rather than paternal history (p=0.0339) with an odds ratio of 3.500 (95% confidence interval extending from 1.099 to 14.603). Average age of proband fathers and mothers was calculated (78.2 and 84.6, respectively, p=0.0962) and was not statistically different.
Our results show that individuals with parental history of AMD may be at a significantly increased risk for developing AMD if their mother had the disease rather than if their father had the disease. This correlates with literature describing a mitochondrial component in the disease process and supports further exploration into mitochondrial etiology as well as similar hereditary studies with larger sample sizes.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.
This PDF is available to Subscribers Only