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Article ; Online: APOE genotype-specific methylation patterns are linked to Alzheimer disease pathology and estrogen response.

Panitch, Rebecca / Sahelijo, Nathan / Hu, Junming / Nho, Kwangsik / Bennett, David A / Lunetta, Kathryn L / Au, Rhoda / Stein, Thor D / Farrer, Lindsay A / Jun, Gyungah R

Translational psychiatry

2024 Volume 14, Issue 1, Page(s) 129

Abstract: The joint effects of APOE genotype and DNA methylation on Alzheimer disease (AD) risk is relatively unknown. We conducted genome-wide methylation analyses using 2,021 samples in blood (91 AD cases, 329 mild cognitive impairment, 1,391 controls) and 697 ... ...

Abstract	The joint effects of APOE genotype and DNA methylation on Alzheimer disease (AD) risk is relatively unknown. We conducted genome-wide methylation analyses using 2,021 samples in blood (91 AD cases, 329 mild cognitive impairment, 1,391 controls) and 697 samples in brain (417 AD cases, 280 controls). We identified differentially methylated levels in AD compared to controls in an APOE genotype-specific manner at 25 cytosine-phosphate-guanine (CpG) sites in brain and 36 CpG sites in blood. Additionally, we identified seven CpG sites in the APOE region containing TOMM40, APOE, and APOC1 genes with P < 5 × 10
MeSH term(s)	Humans ; Alzheimer Disease/metabolism ; Apolipoprotein E4/genetics ; Apolipoproteins E/genetics ; DNA Methylation ; Estrogens ; Genotype
Chemical Substances	Apolipoprotein E4 ; Apolipoproteins E ; Estrogens ; ApoE protein, human
Language	English
Publishing date	2024-02-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	2609311-X
ISSN	2158-3188 ; 2158-3188
ISSN (online)	2158-3188
ISSN	2158-3188
DOI	10.1038/s41398-024-02834-x
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Article ; Online: Blood and brain transcriptome analysis reveals APOE genotype-mediated and immune-related pathways involved in Alzheimer disease.

Panitch, Rebecca / Hu, Junming / Xia, Weiming / Bennett, David A / Stein, Thor D / Farrer, Lindsay A / Jun, Gyungah R

Alzheimer's research & therapy

2022 Volume 14, Issue 1, Page(s) 30

Abstract: Background: While Alzheimer disease (AD) is generally considered as a brain disorder, blood biomarkers may be useful for the diagnosis and prediction of AD brain pathology. The APOE ε4 allele has shown cerebrovascular effects including acceleration of ... ...

Abstract	Background: While Alzheimer disease (AD) is generally considered as a brain disorder, blood biomarkers may be useful for the diagnosis and prediction of AD brain pathology. The APOE ε4 allele has shown cerebrovascular effects including acceleration of blood-brain barrier (BBB) breakdown. Methods: We evaluated the differential expression of previously established AD genes in brains from 344 pathologically confirmed AD cases and 232 controls and in blood from 112 pathologically confirmed AD cases and 67 controls from the Religious Orders Study and Memory and Aging Project. Differential gene expression between AD cases and controls was analyzed in the blood and brain jointly using a multivariate approach in the total sample and within APOE genotype groups. Gene set enrichment analysis was performed within APOE genotype groups using the results from the combined blood and brain analyses to identify biologically important pathways. Gene co-expression networks in brain and blood samples were investigated using weighted correlation network analysis. Top-ranked genes from networks and pathways were further evaluated with vascular injury traits. Results: We observed differentially expressed genes with P < 0.05 in both brain and blood for established AD genes INPP5D (upregulated) and HLA-DQA1 (downregulated). PIGHP1 and FRAS1 were differentially expressed at the transcriptome-wide level (P < 3.3 × 10 Conclusion: These results suggest that the APOE genotype contributes to unique expression network profiles in both blood and brain. Several genes in these networks are associated with measures of vascular injury and potentially contribute to ε4's effect on the BBB.
MeSH term(s)	Alzheimer Disease/genetics ; Apolipoprotein E4/genetics ; Apolipoproteins E/genetics ; Brain ; Gene Expression Profiling ; Genotype ; Humans
Chemical Substances	Apolipoprotein E4 ; Apolipoproteins E
Language	English
Publishing date	2022-02-09
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2506521-X
ISSN	1758-9193 ; 1758-9193
ISSN (online)	1758-9193
ISSN	1758-9193
DOI	10.1186/s13195-022-00975-z
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Article ; Online: Comparison of methods for multivariate gene-based association tests for complex diseases using common variants.

Chung, Jaeyoon / Jun, Gyungah R / Dupuis, Josée / Farrer, Lindsay A

European journal of human genetics : EJHG

2019 Volume 27, Issue 5, Page(s) 811–823

Abstract: Complex diseases are usually associated with multiple correlated phenotypes, and the analysis of composite scores or disease status may not fully capture the complexity (or multidimensionality). Joint analysis of multiple disease-related phenotypes in ... ...

Abstract	Complex diseases are usually associated with multiple correlated phenotypes, and the analysis of composite scores or disease status may not fully capture the complexity (or multidimensionality). Joint analysis of multiple disease-related phenotypes in genetic tests could potentially increase power to detect association of a disease with common SNPs (or genes). Gene-based tests are designed to identify genes containing multiple risk variants that individually are weakly associated with a univariate trait. We combined three multivariate association tests (O'Brien method, TATES, and MultiPhen) with two gene-based association tests (GATES and VEGAS) and compared performance (type I error and power) of six multivariate gene-based methods using simulated data. Data (n = 2000) for genetic sequence and correlated phenotypes were simulated by varying causal variant proportions and phenotype correlations for various scenarios. These simulations showed that two multivariate association tests (TATES and MultiPhen, but not O'Brien) paired with VEGAS have inflated type I error in all scenarios, while the three multivariate association tests paired with GATES have correct type I error. MultiPhen paired with GATES has higher power than competing methods if the correlations among phenotypes are low (r < 0.57). We applied these gene-based association methods to a GWAS dataset from the Alzheimer's Disease Genetics Consortium containing three neuropathological traits related to Alzheimer disease (neuritic plaque, neurofibrillary tangles, and cerebral amyloid angiopathy) measured in 3500 autopsied brains. Gene-level significant evidence (P < 2.7 × 10
MeSH term(s)	Alzheimer Disease/genetics ; Computer Simulation ; Disease/genetics ; Genome-Wide Association Study ; Humans ; Multivariate Analysis
Language	English
Publishing date	2019-01-25
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1141470-4
ISSN	1476-5438 ; 1018-4813
ISSN (online)	1476-5438
ISSN	1018-4813
DOI	10.1038/s41431-018-0327-8
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Article ; Online: Alzheimer's disease heterogeneity explained by polygenic risk scores derived from brain transcriptomic profiles.

Chung, Jaeyoon / Sahelijo, Nathan / Maruyama, Toru / Hu, Junming / Panitch, Rebecca / Xia, Weiming / Mez, Jesse / Stein, Thor D / Saykin, Andrew J / Takeyama, Haruko / Farrer, Lindsay A / Crane, Paul K / Nho, Kwangsik / Jun, Gyungah R

Alzheimer's & dementia : the journal of the Alzheimer's Association

2023 Volume 19, Issue 11, Page(s) 5173–5184

Abstract: Introduction: Alzheimer's disease (AD) is heterogeneous, both clinically and neuropathologically. We investigated whether polygenic risk scores (PRSs) integrated with transcriptome profiles from AD brains can explain AD clinical heterogeneity.: ... ...

Abstract	Introduction: Alzheimer's disease (AD) is heterogeneous, both clinically and neuropathologically. We investigated whether polygenic risk scores (PRSs) integrated with transcriptome profiles from AD brains can explain AD clinical heterogeneity. Methods: We conducted co-expression network analysis and identified gene sets (modules) that were preserved in three AD transcriptome datasets and associated with AD-related neuropathological traits including neuritic plaques (NPs) and neurofibrillary tangles (NFTs). We computed the module-based PRSs (mbPRSs) for each module and tested associations with mbPRSs for cognitive test scores, cognitively defined AD subgroups, and brain imaging data. Results: Of the modules significantly associated with NPs and/or NFTs, the mbPRSs from two modules (M6 and M9) showed distinct associations with language and visuospatial functioning, respectively. They matched clinical subtypes and brain atrophy at specific regions. Discussion: Our findings demonstrate that polygenic profiling based on co-expressed gene sets can explain heterogeneity in AD patients, enabling genetically informed patient stratification and precision medicine in AD. Highlights: Co-expression gene-network analysis in Alzheimer's disease (AD) brains identified gene sets (modules) associated with AD heterogeneity. AD-associated modules were selected when genes in each module were enriched for neuritic plaques and neurofibrillary tangles. Polygenic risk scores from two selected modules were linked to the matching cognitively defined AD subgroups (language and visuospatial subgroups). Polygenic risk scores from the two modules were associated with cognitive performance in language and visuospatial domains and the associations were confirmed in regional-specific brain atrophy data.
MeSH term(s)	Humans ; Alzheimer Disease/pathology ; Transcriptome ; Plaque, Amyloid/genetics ; Plaque, Amyloid/pathology ; Brain/pathology ; Risk Factors ; Atrophy/pathology
Language	English
Publishing date	2023-05-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2211627-8
ISSN	1552-5279 ; 1552-5260
ISSN (online)	1552-5279
ISSN	1552-5260
DOI	10.1002/alz.13069
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Article ; Online: Cytokine Levels in Human Vitreous in Proliferative Diabetic Retinopathy.

Loporchio, Dean F / Tam, Emily K / Cho, Jane / Chung, Jaeyoon / Jun, Gyungah R / Xia, Weiming / Fiorello, Marissa G / Siegel, Nicole H / Ness, Steven / Stein, Thor D / Subramanian, Manju L

Cells

2021 Volume 10, Issue 5

Abstract: In this study, we compare the vitreous cytokine profile in patients with proliferative diabetic retinopathy (PDR) to that of patients without PDR. The identification of novel cytokines involved in the pathogenesis of PDR provides candidate therapeutic ... ...

Abstract	In this study, we compare the vitreous cytokine profile in patients with proliferative diabetic retinopathy (PDR) to that of patients without PDR. The identification of novel cytokines involved in the pathogenesis of PDR provides candidate therapeutic targets that may stand alone or work synergistically with current therapies in the management of diabetic retinopathy. Undiluted vitreous humor specimens were collected from 74 patients undergoing vitrectomy for various vitreoretinal disorders. Quantitative immunoassay was performed for a panel of 36 neuroinflammatory cytokines in each specimen and assessed to identify differences between PDR (
MeSH term(s)	C-Reactive Protein/metabolism ; Diabetic Retinopathy/metabolism ; Female ; Fibroblast Growth Factor 2/metabolism ; Humans ; Intercellular Adhesion Molecule-1/metabolism ; Interleukins/metabolism ; Male ; Middle Aged ; Vascular Cell Adhesion Molecule-1/metabolism ; Vascular Endothelial Growth Factor A/metabolism ; Vitreous Body/metabolism
Chemical Substances	Interleukins ; Vascular Cell Adhesion Molecule-1 ; Vascular Endothelial Growth Factor A ; Fibroblast Growth Factor 2 (103107-01-3) ; Intercellular Adhesion Molecule-1 (126547-89-5) ; C-Reactive Protein (9007-41-4)
Language	English
Publishing date	2021-04-30
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10051069
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Article ; Online: Integrative brain transcriptome analysis links complement component 4 and HSPA2 to the APOE ε2 protective effect in Alzheimer disease.

Panitch, Rebecca / Hu, Junming / Chung, Jaeyoon / Zhu, Congcong / Meng, Gaoyuan / Xia, Weiming / Bennett, David A / Lunetta, Kathryn L / Ikezu, Tsuneya / Au, Rhoda / Stein, Thor D / Farrer, Lindsay A / Jun, Gyungah R

Molecular psychiatry

2021 Volume 26, Issue 10, Page(s) 6054–6064

Abstract: Mechanisms underlying the protective effect of apolipoprotein E (APOE) ε2 against Alzheimer disease (AD) are not well understood. We analyzed gene expression data derived from autopsied brains donated by 982 individuals including 135 APOE ɛ2/ɛ3 carriers. ...

Abstract	Mechanisms underlying the protective effect of apolipoprotein E (APOE) ε2 against Alzheimer disease (AD) are not well understood. We analyzed gene expression data derived from autopsied brains donated by 982 individuals including 135 APOE ɛ2/ɛ3 carriers. Complement pathway genes C4A and C4B were among the most significantly differentially expressed genes between ɛ2/ɛ3 AD cases and controls. We also identified an APOE ε2/ε3 AD-specific co-expression network enriched for astrocytes, oligodendrocytes and oligodendrocyte progenitor cells containing the genes C4A, C4B, and HSPA2. These genes were significantly associated with the ratio of phosphorylated tau at position 231 to total Tau but not with amyloid-β 42 level, suggesting this APOE ɛ2 related co-expression network may primarily be involved with tau pathology. HSPA2 expression was oligodendrocyte-specific and significantly associated with C4B protein. Our findings provide the first evidence of a crucial role of the complement pathway in the protective effect of APOE ε2 for AD.
MeSH term(s)	Alzheimer Disease/genetics ; Apolipoprotein E2/genetics ; Brain ; Complement C4/genetics ; Gene Expression Profiling ; Genotype ; HSP70 Heat-Shock Proteins/genetics ; Humans
Chemical Substances	Apolipoprotein E2 ; Complement C4 ; HSP70 Heat-Shock Proteins ; HSPA2 protein, human
Language	English
Publishing date	2021-09-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/s41380-021-01266-z
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Article ; Online: Neurofilament light chain in the vitreous humor of the eye.

Subramanian, Manju L / Vig, Viha / Chung, Jaeyoon / Fiorello, Marissa G / Xia, Weiming / Zetterberg, Henrik / Blennow, Kaj / Zetterberg, Madeleine / Shareef, Farah / Siegel, Nicole H / Ness, Steven / Jun, Gyungah R / Stein, Thor D

Alzheimer's research & therapy

2020 Volume 12, Issue 1, Page(s) 111

Abstract: Background: Neurofilament light chain (NfL) is a promising biomarker of neurodegeneration in the cerebrospinal fluid and blood. This study investigated the presence of NfL in the vitreous humor and its associations with amyloid beta, tau, inflammatory ... ...

Abstract	Background: Neurofilament light chain (NfL) is a promising biomarker of neurodegeneration in the cerebrospinal fluid and blood. This study investigated the presence of NfL in the vitreous humor and its associations with amyloid beta, tau, inflammatory cytokines and vascular proteins, apolipoprotein E (APOE) genotypes, Mini-Mental State Examination (MMSE) scores, systemic disease, and ophthalmic diseases. Methods: This is a single-site, prospective, cross-sectional cohort study. Undiluted vitreous fluid (0.5-1.0 mL) was aspirated during vitrectomy, and whole blood was drawn for APOE genotyping. NfL, amyloid beta (Aβ), total Tau (t-Tau), phosphorylated Tau (p-Tau181), inflammatory cytokines, chemokines, and vascular proteins in the vitreous were quantitatively measured by immunoassay. The main outcome measures were the detection of NfL levels in the vitreous humor and its associations with the aforementioned proteins. Linear regression was used to test the associations of NfL with other proteins, APOE genotypes, MMSE scores, and ophthalmic and systemic diseases after adjustment for age, sex, education level, and other eye diseases. Results: NfL was detected in all 77 vitreous samples. NfL was not found to be associated with ophthalmic conditions, APOE genotypes, MMSE scores, or systemic disease (p > 0.05). NfL levels were positively associated with increased vitreous levels of Aβ Conclusion: NfL is detectable in the vitreous humor of the eye and significantly associated with amyloid beta, t-tau, and select inflammatory and vascular proteins in the vitreous. Additionally, NfL was not associated with patients' clinical eye condition. Our results serve as a foundation for further investigation of NfL in the ocular fluids to inform us about the potential utility of its presence in the eye.
MeSH term(s)	Alzheimer Disease ; Amyloid beta-Peptides ; Biomarkers ; Cross-Sectional Studies ; Humans ; Intermediate Filaments ; Neurofilament Proteins ; Prospective Studies ; Vascular Endothelial Growth Factor A ; Vitreous Body ; tau Proteins
Chemical Substances	Amyloid beta-Peptides ; Biomarkers ; Neurofilament Proteins ; Vascular Endothelial Growth Factor A ; tau Proteins
Language	English
Publishing date	2020-09-17
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2506521-X
ISSN	1758-9193 ; 1758-9193
ISSN (online)	1758-9193
ISSN	1758-9193
DOI	10.1186/s13195-020-00677-4
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Article ; Online: Protein phosphatase 2A and complement component 4 are linked to the protective effect of APOE ɛ2 for Alzheimer's disease.

Alzheimer's & dementia : the journal of the Alzheimer's Association

2022 Volume 18, Issue 11, Page(s) 2042–2054

Abstract: Introduction: The apolipoprotein E (APOE) ɛ2 allele reduces risk against Alzheimer's disease (AD) but mechanisms underlying this effect are largely unknown.: Methods: We conducted a genome-wide association study for AD among 2096 ɛ2 carriers. The ... ...

Abstract	Introduction: The apolipoprotein E (APOE) ɛ2 allele reduces risk against Alzheimer's disease (AD) but mechanisms underlying this effect are largely unknown. Methods: We conducted a genome-wide association study for AD among 2096 ɛ2 carriers. The potential role of the top-ranked gene and complement 4 (C4) proteins, which were previously linked to AD in ɛ2 carriers, was investigated using human isogenic APOE allele-specific induced pluripotent stem cell (iPSC)-derived neurons and astrocytes and in 224 neuropathologically examined human brains. Results: PPP2CB rs117296832 was the second most significantly associated single nucleotide polymorphism among ɛ2 carriers (P = 1.1 × 10 Discussion: PP2A may be linked to classical complement activation leading to AD-related tau pathology.
MeSH term(s)	Humans ; Apolipoprotein E2/genetics ; Alzheimer Disease/pathology ; Protein Phosphatase 2/genetics ; Genome-Wide Association Study ; Apolipoproteins E/genetics ; Complement C4/genetics ; Apolipoprotein E4/genetics ; tau Proteins/genetics
Chemical Substances	Apolipoprotein E2 ; Protein Phosphatase 2 (EC 3.1.3.16) ; Apolipoproteins E ; Complement C4 ; Apolipoprotein E4 ; tau Proteins
Language	English
Publishing date	2022-02-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2211627-8
ISSN	1552-5279 ; 1552-5260
ISSN (online)	1552-5279
ISSN	1552-5260
DOI	10.1002/alz.12607
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Article: Cross-sectional and longitudinal evaluation of plasma glial fibrillary acidic protein to detect and predict clinical syndromes of Alzheimer's disease.

Ally, Madeline / Sugarman, Michael A / Zetterberg, Henrik / Blennow, Kaj / Ashton, Nicholas J / Karikari, Thomas K / Aparicio, Hugo J / Frank, Brandon / Tripodis, Yorghos / Martin, Brett / Palmisano, Joseph N / Steinberg, Eric G / Simkin, Irene / Farrer, Lindsay A / Jun, Gyungah R / Turk, Katherine W / Budson, Andrew E / O'Connor, Maureen K / Au, Rhoda /

Goldstein, Lee E / Kowall, Neil W / Killiany, Ronald / Stern, Robert A / Stein, Thor D / McKee, Ann C / Qiu, Wei Qiao / Mez, Jesse / Alosco, Michael L

Alzheimer's & dementia (Amsterdam, Netherlands)

2023 Volume 15, Issue 4, Page(s) e12492

Abstract: Introduction: This study examined plasma glial fibrillary acidic protein (GFAP) as a biomarker of cognitive impairment due to Alzheimer's disease (AD) with and against plasma neurofilament light chain (NfL), and phosphorylated tau (p-tau): Methods: ... ...

Abstract	Introduction: This study examined plasma glial fibrillary acidic protein (GFAP) as a biomarker of cognitive impairment due to Alzheimer's disease (AD) with and against plasma neurofilament light chain (NfL), and phosphorylated tau (p-tau) Methods: Plasma samples were analyzed using Simoa platform for 567 participants spanning the AD continuum. Cognitive diagnosis, neuropsychological testing, and dementia severity were examined for cross-sectional and longitudinal outcomes. Results: Plasma GFAP discriminated AD dementia from normal cognition (adjusted mean difference = 0.90 standard deviation [SD]) and mild cognitive impairment (adjusted mean difference = 0.72 SD), and demonstrated superior discrimination compared to alternative plasma biomarkers. Higher GFAP was associated with worse dementia severity and worse performance on 11 of 12 neuropsychological tests. Longitudinally, GFAP predicted decline in memory, but did not predict conversion to mild cognitive impairment or dementia. Discussion: Plasma GFAP was associated with clinical outcomes related to suspected AD and could be of assistance in a plasma biomarker panel to detect in vivo AD.
Language	English
Publishing date	2023-10-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	2832898-X
ISSN	2352-8729
ISSN	2352-8729
DOI	10.1002/dad2.12492
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Article ; Online: Aldose Reductase Polymorphisms, Fasting Blood Glucose, and Age-Related Cortical Cataract.

Tan, Ava Grace / Kifley, Annette / Holliday, Elizabeth G / Klein, Barbara E K / Iyengar, Sudha K / Lee, Kristine E / Jun, Gyungah R / Cumming, Robert G / Zhao, Wanting / Wong, Tien Yin / Cheng, Ching-Yu / Mitchell, Paul / Wang, Jie Jin

Investigative ophthalmology & visual science

2018 Volume 59, Issue 11, Page(s) 4755–4762

Abstract: Purpose: To determine whether there is an association between polymorphisms of the AKR1B1 gene and cortical cataract in the presence of hyperglycemia.: Methods: In the second cross section of the Blue Mountains Eye Study (BMES), 3508 participants ( ... ...

Abstract	Purpose: To determine whether there is an association between polymorphisms of the AKR1B1 gene and cortical cataract in the presence of hyperglycemia. Methods: In the second cross section of the Blue Mountains Eye Study (BMES), 3508 participants (2334 at 5-year follow-up and 1174 newly recruited participants) were examined during 1997 to 2000. Cataract was graded from lens photographs using the Wisconsin Cataract Grading System. Fasting blood glucose (FBG) was measured. Continuous imputed dosages of minor alleles of 17 AKR1B1 single nucleotide polymorphisms (SNPs) were assessed for associations with prevalent cortical cataract. Gene-environment interactions between SNPs and FBG were examined. Odds ratios (OR) and 95% confidence intervals (CI) for prevalent cortical cataract were estimated using logistic regression adjusting for age, sex, smoking, hypertension, education, and myopia. A P value of 0.005 was considered statistically significant after correction for 10 independent tests. Replication of significant associations found in the BMES sample was conducted in the Singapore Epidemiology of Eye Diseases (SEED) study (n = 10,033). Results: No polymorphism was associated with prevalent cortical cataract. A significant interaction was observed between rs9640883 and FBG (Pinteraction = 0.004), with increased cortical cataract prevalence associated with rs9640883 minor allele dosage in those with FBG >6.0 mM (strata-specific OR 1.72, 95% CI 1.09-2.72). No similar association was found in participants with normal FBG (OR 0.85, 95% CI 0.69-1.04). This interaction was not evident in the SEED study. Conclusions: The identified interaction between rs9640883 and FBG in relation to cortical cataract was not replicated but may warrant further investigation.
MeSH term(s)	Aged ; Aged, 80 and over ; Aldehyde Reductase/genetics ; Blood Glucose/metabolism ; Cataract/blood ; Cataract/epidemiology ; Cataract/genetics ; Female ; Gene-Environment Interaction ; Genotyping Techniques ; Humans ; Hyperglycemia/blood ; Male ; Middle Aged ; New South Wales/epidemiology ; Polymorphism, Single Nucleotide ; Prevalence
Chemical Substances	Blood Glucose ; AKR1B1 protein, human (EC 1.1.1.21) ; Aldehyde Reductase (EC 1.1.1.21)
Language	English
Publishing date	2018-09-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	391794-0
ISSN	1552-5783 ; 0146-0404
ISSN (online)	1552-5783
ISSN	0146-0404
DOI	10.1167/iovs.18-24353
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