Original ArticleApolipoprotein E Gene and Early Age-Related Maculopathy: The Atherosclerosis Risk in Communities Study
Section snippets
Study Population
The Atherosclerosis Risk in Communities (ARIC) study is a population-based cohort study that included 15 792 women and men 45 to 64 years of age at recruitment in 1987 through 1989.18 The study population was selected by probability sampling from 4 U.S. communities: Forsyth County, NC; Jackson, MS; the suburbs of Minneapolis, MN; and Washington County, MD. The Jackson sample included black persons only; in the other field centers, samples were representative of the populations in these
Results
Characteristics between persons with (n = 531) and without (n = 9608) any ARM are presented in Table 1. In general, persons with any ARM were significantly older, less likely to be black, to have hypertension, and to have higher systolic blood pressure than persons without ARM. Other characteristics were not associated with any ARM status. Because of the small number of persons with late ARM in this middle-aged population (n = 15), subsequent analysis was confined to early ARM signs only.
The
Discussion
The APOE gene has been shown to influence lipoprotein metabolism and has been linked to a variety of neurodegenerative disorders, most notably Alzheimer’s disease.4, 5, 6 Previous studies that have examined a possible relationship between APOE and ARM have focused on late stages of ARM (exudative macular degeneration and geographic atrophy) and on elderly populations.9, 10, 11, 12, 13, 14, 15, 16, 17 Few have been population based.9 In general, most of these studies suggest that ϵ4 is
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Cited by (32)
Macular xanthophylls, lipoprotein-related genes, and age-related macular degeneration
2014, American Journal of Clinical NutritionParallel findings in age-related macular degeneration and Alzheimer's disease
2011, Progress in Retinal and Eye ResearchCitation Excerpt :Earlier studies reported that the presence of the ε4 allele of APOE was inversely associated with late AMD, whereas the ε2 allele may be associated with an increased risk of AMD. Wong et al. (2006) examined the association between the APOE gene and early AMD in the participants of the Atherosclerosis Risk Communities Study and showed that the prevalence of early AMD was not significantly different in participants with different APOE genotypes. So far, it appears that the results of earlier studies using GWAS have not identified genetic loci common to AD and AMD.
Molecular pathology of age-related macular degeneration
2009, Progress in Retinal and Eye ResearchCitation Excerpt :Based on the role of ApoE in recycling of cholesterol and lipids for cell-membrane biosynthesis after neuronal injury, these polymorphisms have been speculated to impact retinal membrane renewal and affect macular integrity. Several studies later confirmed a role for ApoE SNP in AMD (Baird et al., 2006; Jun et al., 2005; Kovacs et al., 2007; Schmidt et al., 2002; Souied et al., 1998; Zareparsi et al., 2004), while others found no effect (Kaur et al., 2006; Schmidt et al., 2005; Schultz et al., 2003; Wong et al., 2006). We have also found the association between ApoE112R (E4) and a decreased risk of AMD development, and the underlying mechanisms might involve differential regulation of both CCL2 and VEGF by the ApoE isoforms (Bojanowski et al., 2006).
Apolipoprotein E ε4 offers protection against age-related macular degeneration
2007, Medical HypothesesSphingolipids and physical function in the Atherosclerosis Risk in Communities (ARIC) study
2021, Scientific ReportsPlasma metabolites associated with brain MRI measures of neurodegeneration in older adults in the atherosclerosis risk in communities– neurocognitive study (ARIC-NCS)
2019, International Journal of Molecular Sciences
Manuscript no. 2005-449.
The authors have no proprietary interests.
Carried out as a collaborative study supported by the National Heart, Lung, and Blood Institute, Bethesda, Maryland (contract nos.: N01-HC-55015, N01-HC-55016, N01-HC-55018, N01-HC-55019, N01-HC-55020, N01-HC-55021, N01-HC-55022); National Institutes of Health, Bethesda, Maryland (grant nos.: HL073366, UR6/CCU617218 [MSB], EYO13939 [TYW, RK]); and Sylvia and Charles Viertel Clinical Investigator Award (TYW).