SynthesisEnvironmental and molecular mutagenesis2006
An apolipoprotein E variant may protect against age-related macular degeneration through cytokine regulation.
Synthesis in Environmental and molecular mutagenesis, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 62 citations in OpenAlex.
- Changes in ApoE and TIMP-1 expression correlate with outer blood-retinal barrier disruption in an in vitro model of retinal aging.GeroScience · 2026Article
- Immunogenetic and Environmental Factors in Age-Related Macular Disease.International journal of molecular sciences · 2024Review
- Alzheimer's disease: a comprehensive review of epidemiology, risk factors, symptoms diagnosis, management, caregiving, advanced treatments and associated challenges.Frontiers in medicine · 2024Review
- Apolipoprotein ε in Brain and Retinal Neurodegenerative Diseases.Aging and disease · 2023Review
- Orthogonal analysis of variants in APOE gene usingFrontiers in bioinformatics · 2023Article
- Biomarkers as Predictive Factors of Anti-VEGF Response.Biomedicines · 2022Review
- Evaluation ofExperimental biology and medicine (Maywood, N.J.) · 2021Article
- Histopathology of Age-Related Macular Degeneration and Implications for Pathogenesis and Therapy.Advances in experimental medicine and biology · 2021Article
- Risk factors for progression of age-related macular degeneration.Ophthalmic & physiological optics : the journal of the British College of Ophthalmic Opticians (Optometrists) · 2020Review
- Milk metabolites and neurodegeneration: Is there crosstalk?Annals of neurosciences · 2015Review
- ApoE4 induces synaptic and ERG impairments in the retina of young targeted replacement apoE4 mice.PloS one · 2013Article
- Evidence of association of APOE with age-related macular degeneration: a pooled analysis of 15 studies.Human mutation · 2011Article
- Variants in the APOE gene are associated with improved outcome after anti-VEGF treatment for neovascular AMD.Investigative ophthalmology & visual science · 2011Article
- Function and comorbidities of apolipoprotein e in Alzheimer's disease.International journal of Alzheimer's disease · 2011Article
- Cross-talk between apolipoprotein E and cytokines.Mediators of inflammation · 2011Review
- Retinal ultrastructure of murine models of dry age-related macular degeneration (AMD).Progress in retinal and eye research · 2010Review
- Mediators of ocular angiogenesis.Journal of genetics · 2009Review
- The molecular genetic basis of age-related macular degeneration: an overview.Journal of genetics · 2009Review
- Chlamydia pneumoniae infection, complement factor H variants and age-related macular degeneration.The British journal of ophthalmology · 2009Article
- Normal aging involves modulation of specific inflammatory markers in the rat retina and choroid.The journals of gerontology. Series A, Biological sciences and medical sciences · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Age-related macular degeneration (AMD) is the leading cause of visual impairment and blindness among the elderly in Western countries. Genetic factors, age, cigarette smoking, nutrition, and exposure to light have been identified as AMD risk factors. In this study, we investigated the association between ApoE C112R/R158C single nucleotide polymorphisms (which determine the E2, E3, and E4 isoforms) and age-related macular degeneration (AMD), and the mechanism underlying the association. Genomic DNA was extracted from 133 clinically screened controls, 94 volunteers with a younger mean age, 120 patients with advanced AMD, and 40 archived ocular AMD slides for single nucleotide polymorphism typing. The effects of recombinant ApoE isoforms on CCL2 (a chemokine), CX3CR1 (a chemokine receptor), and VEGF (a cytokine) expression in cultured human retinal pigment epithelium (RPE) cells were tested and serum cholesterol profiles of the clinically screened subjects were analyzed. ApoE112R (E4) distribution differed significantly between AMD patients and controls. ApoE112R allele frequency was 10.9% in the AMD group when compared with 16.5% in the younger controls and 18.8% in the clinically screened controls. The pathologically diagnosed archived AMD cases had the lowest allele frequency of 5%. No significant differences in ApoE158C (E2) distribution were observed among the groups. A meta-analysis of 8 cohorts including 4,289 subjects showed a strong association between AMD and 112R, but not 158C. In vitro studies found that recombinant ApoE suppresses CCL2 and VEGF expression in RPE cells. However, the E4 isoform showed more suppression than E3 in both cases. These results further confirm the association between ApoE112R and a decreased risk of AMD development. The underlying mechanisms may involve differential regulation of both CCL2 and VEGF by the ApoE isoforms.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.