FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4224233571> ?p ?o ?g. }

• W4224233571 endingPage "100159" @default.
• W4224233571 startingPage "100159" @default.
• W4224233571 abstract "PurposeTo investigate the association between the apolipoprotein E (APOE) E4 dementia-risk allele and prospective longitudinal retinal thinning in a cohort study of suspect and early manifest glaucoma.DesignRetrospective analysis of prospective cohort data.ParticipantsThis study included all available eyes from participants recruited to the Progression Risk of Glaucoma: Relevant SNPs [single nucleotide polymorphisms] with Significant Association (PROGRESSA) study with genotyping data from which APOE genotypes could be determined.MethodsApolipoprotein E alleles and genotypes were determined in PROGRESSA, and their distributions were compared with an age-matched and ancestrally matched normative cohort, the Blue Mountains Eye Study. Structural parameters of neuroretinal atrophy measured using spectral-domain OCT were compared within the PROGRESSA cohort on the basis of APOE E4 allele status.Main Outcome MeasuresLongitudinal rates of thinning in the macular ganglion cell–inner plexiform layer (mGCIPL) complex and the peripapillary retinal nerve fiber layer (pRNFL).ResultsRates of mGCIPL complex thinning were faster in participants harboring ≥1 copies of the APOE E4 allele (β = –0.13 μm/year; P ≤0.001). This finding was strongest in eyes affected by normal-tension glaucoma (NTG; β = –0.20 μm/year; P = 0.003). Apolipoprotein E E4 allele carriers were also more likely to be lost to follow-up (P = 0.01) and to demonstrate a thinner average mGCIPL complex (70.9 μm vs. 71.9 μm; P = 0.011) and pRNFL (77.6 μm vs. 79.2 μm; P = 0.045) after a minimum of 3 years of monitoring.ConclusionsThe APOE E4 allele was associated with faster rates of mCGIPL complex thinning, particularly in eyes with NTG. These results suggest that the APOE E4 allele may be a risk factor for retinal ganglion cell degeneration in glaucoma. To investigate the association between the apolipoprotein E (APOE) E4 dementia-risk allele and prospective longitudinal retinal thinning in a cohort study of suspect and early manifest glaucoma. Retrospective analysis of prospective cohort data. This study included all available eyes from participants recruited to the Progression Risk of Glaucoma: Relevant SNPs [single nucleotide polymorphisms] with Significant Association (PROGRESSA) study with genotyping data from which APOE genotypes could be determined. Apolipoprotein E alleles and genotypes were determined in PROGRESSA, and their distributions were compared with an age-matched and ancestrally matched normative cohort, the Blue Mountains Eye Study. Structural parameters of neuroretinal atrophy measured using spectral-domain OCT were compared within the PROGRESSA cohort on the basis of APOE E4 allele status. Longitudinal rates of thinning in the macular ganglion cell–inner plexiform layer (mGCIPL) complex and the peripapillary retinal nerve fiber layer (pRNFL). Rates of mGCIPL complex thinning were faster in participants harboring ≥1 copies of the APOE E4 allele (β = –0.13 μm/year; P ≤0.001). This finding was strongest in eyes affected by normal-tension glaucoma (NTG; β = –0.20 μm/year; P = 0.003). Apolipoprotein E E4 allele carriers were also more likely to be lost to follow-up (P = 0.01) and to demonstrate a thinner average mGCIPL complex (70.9 μm vs. 71.9 μm; P = 0.011) and pRNFL (77.6 μm vs. 79.2 μm; P = 0.045) after a minimum of 3 years of monitoring. The APOE E4 allele was associated with faster rates of mCGIPL complex thinning, particularly in eyes with NTG. These results suggest that the APOE E4 allele may be a risk factor for retinal ganglion cell degeneration in glaucoma." @default.
• W4224233571 created "2022-04-26" @default.
• W4224233571 creator A5003148662 @default.
• W4224233571 creator A5005522131 @default.
• W4224233571 creator A5008259206 @default.
• W4224233571 creator A5010178491 @default.
• W4224233571 creator A5010716388 @default.
• W4224233571 creator A5012599011 @default.
• W4224233571 creator A5017757731 @default.
• W4224233571 creator A5020493237 @default.
• W4224233571 creator A5027915808 @default.
• W4224233571 creator A5029948119 @default.
• W4224233571 creator A5033888317 @default.
• W4224233571 creator A5034340164 @default.
• W4224233571 creator A5036614947 @default.
• W4224233571 creator A5037433676 @default.
• W4224233571 creator A5037639355 @default.
• W4224233571 creator A5039731589 @default.
• W4224233571 creator A5040284130 @default.
• W4224233571 creator A5041104671 @default.
• W4224233571 creator A5047701250 @default.
• W4224233571 creator A5053943974 @default.
• W4224233571 creator A5054972306 @default.
• W4224233571 creator A5060388119 @default.
• W4224233571 creator A5062605162 @default.
• W4224233571 creator A5068570514 @default.
• W4224233571 creator A5069803192 @default.
• W4224233571 creator A5070884587 @default.
• W4224233571 creator A5074017926 @default.
• W4224233571 creator A5077384288 @default.
• W4224233571 creator A5078949408 @default.
• W4224233571 creator A5085105499 @default.
• W4224233571 creator A5086317817 @default.
• W4224233571 date "2022-06-01" @default.
• W4224233571 modified "2023-10-14" @default.
• W4224233571 title "The APOE E4 Allele Is Associated with Faster Rates of Neuroretinal Thinning in a Prospective Cohort Study of Suspect and Early Glaucoma" @default.
• W4224233571 cites W137929997 @default.
• W4224233571 cites W1523693806 @default.
• W4224233571 cites W1589866722 @default.
• W4224233571 cites W1804927859 @default.
• W4224233571 cites W1855997172 @default.
• W4224233571 cites W1856328802 @default.
• W4224233571 cites W1967251284 @default.
• W4224233571 cites W1972120835 @default.
• W4224233571 cites W1972971823 @default.
• W4224233571 cites W1993510118 @default.
• W4224233571 cites W1996603221 @default.
• W4224233571 cites W2003384166 @default.
• W4224233571 cites W2006109464 @default.
• W4224233571 cites W2014516884 @default.
• W4224233571 cites W2019610144 @default.
• W4224233571 cites W2024475596 @default.
• W4224233571 cites W2026191355 @default.
• W4224233571 cites W2034742711 @default.
• W4224233571 cites W2037247417 @default.
• W4224233571 cites W2037548402 @default.
• W4224233571 cites W2039831788 @default.
• W4224233571 cites W2040206211 @default.
• W4224233571 cites W2056516296 @default.
• W4224233571 cites W2058034919 @default.
• W4224233571 cites W2065974896 @default.
• W4224233571 cites W2081045709 @default.
• W4224233571 cites W2089750946 @default.
• W4224233571 cites W2089961311 @default.
• W4224233571 cites W2097450082 @default.
• W4224233571 cites W2099573670 @default.
• W4224233571 cites W2101873043 @default.
• W4224233571 cites W2113129492 @default.
• W4224233571 cites W2115738813 @default.
• W4224233571 cites W2136795277 @default.
• W4224233571 cites W2139923031 @default.
• W4224233571 cites W2140718540 @default.
• W4224233571 cites W2148732309 @default.
• W4224233571 cites W2150396276 @default.
• W4224233571 cites W2154886355 @default.
• W4224233571 cites W2163305295 @default.
• W4224233571 cites W2193309973 @default.
• W4224233571 cites W2241634696 @default.
• W4224233571 cites W2346619519 @default.
• W4224233571 cites W239648239 @default.
• W4224233571 cites W2401910999 @default.
• W4224233571 cites W2510973425 @default.
• W4224233571 cites W2525643635 @default.
• W4224233571 cites W2581573924 @default.
• W4224233571 cites W2616963645 @default.
• W4224233571 cites W2793736115 @default.
• W4224233571 cites W2810823800 @default.
• W4224233571 cites W2810823899 @default.
• W4224233571 cites W2884647899 @default.
• W4224233571 cites W2886040290 @default.
• W4224233571 cites W2886450553 @default.
• W4224233571 cites W2894334919 @default.
• W4224233571 cites W2900342065 @default.
• W4224233571 cites W2916982356 @default.
• W4224233571 cites W2965285787 @default.
• W4224233571 cites W2965401191 @default.
• W4224233571 cites W3000547714 @default.
• W4224233571 cites W3014226248 @default.

• next