Plasma levels of apolipoprotein E and risk of dementia in the general population
Objective The apolipoprotein E (APOE) ε4 allele is a major genetic risk factor for Alzheimer disease and dementia. However, it remains unclear whether plasma levels of apoE confer additional risk. We tested this hypothesis. Methods Using 75,708 participants from the general population, we tested whe...
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| Published in | Annals of neurology Vol. 77; no. 2; pp. 301 - 311 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Blackwell Publishing Ltd
01.02.2015
Wiley Subscription Services, Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0364-5134 1531-8249 1531-8249 |
| DOI | 10.1002/ana.24326 |
Cover
| Abstract | Objective
The apolipoprotein E (APOE) ε4 allele is a major genetic risk factor for Alzheimer disease and dementia. However, it remains unclear whether plasma levels of apoE confer additional risk. We tested this hypothesis.
Methods
Using 75,708 participants from the general population, we tested whether low plasma levels of apoE at study enrollment were associated with increased risk of future Alzheimer disease and all dementia, and whether this association was independent of ε2/ε3/ε4 APOE genotype.
Results
Multifactorially adjusted hazard ratios (HRs) for Alzheimer disease and all dementia increased from the highest to the lowest apoE tertile (p for trends < 1 × 10−6). Multifactorially adjusted HRs for lowest versus highest tertile were 2.68 (95% confidence interval [CI] = 2.04–3.52) and 1.80 (95% CI = 1.52–2.13) for Alzheimer disease and all dementia, respectively. After further adjustment for ε2/ε3/ε4 APOE genotype, plasma apoE tertiles remained associated with Alzheimer disease (p for trend = 0.007) and all dementia (p for trend = 0.04). Plasma apoE tertiles did not interact with ε2/ε3/ε4 APOE genotype on risk of Alzheimer disease (p = 0.53) or all dementia (p = 0.79). In a subanalysis, the −219G>T GT promoter genotype, associated with low plasma apoE levels, remained significantly associated with increased risk of Alzheimer disease after adjustment for ε2/ε3/ε4 APOE genotype (HR = 1.56, 95% CI = 1.05–2.30).
Interpretation
Low plasma levels of apoE are associated with increased risk of future Alzheimer disease and all dementia in the general population, independent of ε2/ε3/ε4 APOE genotype. This is clinically relevant, because no plasma biomarkers are currently implemented. Hence, plasma levels of apoE may be a new, easily accessible preclinical biomarker. Ann Neurol 2015;77:301–311 |
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| AbstractList | The apolipoprotein E (APOE) ε4 allele is a major genetic risk factor for Alzheimer disease and dementia. However, it remains unclear whether plasma levels of apoE confer additional risk. We tested this hypothesis.OBJECTIVEThe apolipoprotein E (APOE) ε4 allele is a major genetic risk factor for Alzheimer disease and dementia. However, it remains unclear whether plasma levels of apoE confer additional risk. We tested this hypothesis.Using 75,708 participants from the general population, we tested whether low plasma levels of apoE at study enrollment were associated with increased risk of future Alzheimer disease and all dementia, and whether this association was independent of ε2/ε3/ε4 APOE genotype.METHODSUsing 75,708 participants from the general population, we tested whether low plasma levels of apoE at study enrollment were associated with increased risk of future Alzheimer disease and all dementia, and whether this association was independent of ε2/ε3/ε4 APOE genotype.Multifactorially adjusted hazard ratios (HRs) for Alzheimer disease and all dementia increased from the highest to the lowest apoE tertile (p for trends < 1 × 10(-6) ). Multifactorially adjusted HRs for lowest versus highest tertile were 2.68 (95% confidence interval [CI] = 2.04-3.52) and 1.80 (95% CI = 1.52-2.13) for Alzheimer disease and all dementia, respectively. After further adjustment for ε2/ε3/ε4 APOE genotype, plasma apoE tertiles remained associated with Alzheimer disease (p for trend = 0.007) and all dementia (p for trend = 0.04). Plasma apoE tertiles did not interact with ε2/ε3/ε4 APOE genotype on risk of Alzheimer disease (p = 0.53) or all dementia (p = 0.79). In a subanalysis, the -219G>T GT promoter genotype, associated with low plasma apoE levels, remained significantly associated with increased risk of Alzheimer disease after adjustment for ε2/ε3/ε4 APOE genotype (HR = 1.56, 95% CI = 1.05-2.30).RESULTSMultifactorially adjusted hazard ratios (HRs) for Alzheimer disease and all dementia increased from the highest to the lowest apoE tertile (p for trends < 1 × 10(-6) ). Multifactorially adjusted HRs for lowest versus highest tertile were 2.68 (95% confidence interval [CI] = 2.04-3.52) and 1.80 (95% CI = 1.52-2.13) for Alzheimer disease and all dementia, respectively. After further adjustment for ε2/ε3/ε4 APOE genotype, plasma apoE tertiles remained associated with Alzheimer disease (p for trend = 0.007) and all dementia (p for trend = 0.04). Plasma apoE tertiles did not interact with ε2/ε3/ε4 APOE genotype on risk of Alzheimer disease (p = 0.53) or all dementia (p = 0.79). In a subanalysis, the -219G>T GT promoter genotype, associated with low plasma apoE levels, remained significantly associated with increased risk of Alzheimer disease after adjustment for ε2/ε3/ε4 APOE genotype (HR = 1.56, 95% CI = 1.05-2.30).Low plasma levels of apoE are associated with increased risk of future Alzheimer disease and all dementia in the general population, independent of ε2/ε3/ε4 APOE genotype. This is clinically relevant, because no plasma biomarkers are currently implemented. Hence, plasma levels of apoE may be a new, easily accessible preclinical biomarker.INTERPRETATIONLow plasma levels of apoE are associated with increased risk of future Alzheimer disease and all dementia in the general population, independent of ε2/ε3/ε4 APOE genotype. This is clinically relevant, because no plasma biomarkers are currently implemented. Hence, plasma levels of apoE may be a new, easily accessible preclinical biomarker. Objective The apolipoprotein E (APOE) epsilon 4 allele is a major genetic risk factor for Alzheimer disease and dementia. However, it remains unclear whether plasma levels of apoE confer additional risk. We tested this hypothesis. Methods Using 75,708 participants from the general population, we tested whether low plasma levels of apoE at study enrollment were associated with increased risk of future Alzheimer disease and all dementia, and whether this association was independent of epsilon 2/ epsilon 3/ epsilon 4 APOE genotype. Results Multifactorially adjusted hazard ratios (HRs) for Alzheimer disease and all dementia increased from the highest to the lowest apoE tertile (p for trends<1 10 super(-6)). Multifactorially adjusted HRs for lowest versus highest tertile were 2.68 (95% confidence interval [CI]=2.04-3.52) and 1.80 (95% CI=1.52-2.13) for Alzheimer disease and all dementia, respectively. After further adjustment for epsilon 2/ epsilon 3/ epsilon 4 APOE genotype, plasma apoE tertiles remained associated with Alzheimer disease (p for trend=0.007) and all dementia (p for trend=0.04). Plasma apoE tertiles did not interact with epsilon 2/ epsilon 3/ epsilon 4 APOE genotype on risk of Alzheimer disease (p=0.53) or all dementia (p=0.79). In a subanalysis, the -219G>T GT promoter genotype, associated with low plasma apoE levels, remained significantly associated with increased risk of Alzheimer disease after adjustment for epsilon 2/ epsilon 3/ epsilon 4 APOE genotype (HR=1.56, 95% CI=1.05-2.30). Interpretation Low plasma levels of apoE are associated with increased risk of future Alzheimer disease and all dementia in the general population, independent of epsilon 2/ epsilon 3/ epsilon 4 APOE genotype. This is clinically relevant, because no plasma biomarkers are currently implemented. Hence, plasma levels of apoE may be a new, easily accessible preclinical biomarker. Ann Neurol 2015; 77:301-311 The apolipoprotein E (APOE) ε4 allele is a major genetic risk factor for Alzheimer disease and dementia. However, it remains unclear whether plasma levels of apoE confer additional risk. We tested this hypothesis. Using 75,708 participants from the general population, we tested whether low plasma levels of apoE at study enrollment were associated with increased risk of future Alzheimer disease and all dementia, and whether this association was independent of ε2/ε3/ε4 APOE genotype. Multifactorially adjusted hazard ratios (HRs) for Alzheimer disease and all dementia increased from the highest to the lowest apoE tertile (p for trends < 1 × 10(-6) ). Multifactorially adjusted HRs for lowest versus highest tertile were 2.68 (95% confidence interval [CI] = 2.04-3.52) and 1.80 (95% CI = 1.52-2.13) for Alzheimer disease and all dementia, respectively. After further adjustment for ε2/ε3/ε4 APOE genotype, plasma apoE tertiles remained associated with Alzheimer disease (p for trend = 0.007) and all dementia (p for trend = 0.04). Plasma apoE tertiles did not interact with ε2/ε3/ε4 APOE genotype on risk of Alzheimer disease (p = 0.53) or all dementia (p = 0.79). In a subanalysis, the -219G>T GT promoter genotype, associated with low plasma apoE levels, remained significantly associated with increased risk of Alzheimer disease after adjustment for ε2/ε3/ε4 APOE genotype (HR = 1.56, 95% CI = 1.05-2.30). Low plasma levels of apoE are associated with increased risk of future Alzheimer disease and all dementia in the general population, independent of ε2/ε3/ε4 APOE genotype. This is clinically relevant, because no plasma biomarkers are currently implemented. Hence, plasma levels of apoE may be a new, easily accessible preclinical biomarker. Objective The apolipoprotein E (APOE) ε4 allele is a major genetic risk factor for Alzheimer disease and dementia. However, it remains unclear whether plasma levels of apoE confer additional risk. We tested this hypothesis. Methods Using 75,708 participants from the general population, we tested whether low plasma levels of apoE at study enrollment were associated with increased risk of future Alzheimer disease and all dementia, and whether this association was independent of ε2/ε3/ε4 APOE genotype. Results Multifactorially adjusted hazard ratios (HRs) for Alzheimer disease and all dementia increased from the highest to the lowest apoE tertile (p for trends < 1 × 10−6). Multifactorially adjusted HRs for lowest versus highest tertile were 2.68 (95% confidence interval [CI] = 2.04–3.52) and 1.80 (95% CI = 1.52–2.13) for Alzheimer disease and all dementia, respectively. After further adjustment for ε2/ε3/ε4 APOE genotype, plasma apoE tertiles remained associated with Alzheimer disease (p for trend = 0.007) and all dementia (p for trend = 0.04). Plasma apoE tertiles did not interact with ε2/ε3/ε4 APOE genotype on risk of Alzheimer disease (p = 0.53) or all dementia (p = 0.79). In a subanalysis, the −219G>T GT promoter genotype, associated with low plasma apoE levels, remained significantly associated with increased risk of Alzheimer disease after adjustment for ε2/ε3/ε4 APOE genotype (HR = 1.56, 95% CI = 1.05–2.30). Interpretation Low plasma levels of apoE are associated with increased risk of future Alzheimer disease and all dementia in the general population, independent of ε2/ε3/ε4 APOE genotype. This is clinically relevant, because no plasma biomarkers are currently implemented. Hence, plasma levels of apoE may be a new, easily accessible preclinical biomarker. Ann Neurol 2015;77:301–311 Objective The apolipoprotein E (APOE) [epsi]4 allele is a major genetic risk factor for Alzheimer disease and dementia. However, it remains unclear whether plasma levels of apoE confer additional risk. We tested this hypothesis. Methods Using 75,708 participants from the general population, we tested whether low plasma levels of apoE at study enrollment were associated with increased risk of future Alzheimer disease and all dementia, and whether this association was independent of [epsi]2/[epsi]3/[epsi]4 APOE genotype. Results Multifactorially adjusted hazard ratios (HRs) for Alzheimer disease and all dementia increased from the highest to the lowest apoE tertile (p for trends<1 × 10-6). Multifactorially adjusted HRs for lowest versus highest tertile were 2.68 (95% confidence interval [CI]=2.04-3.52) and 1.80 (95% CI=1.52-2.13) for Alzheimer disease and all dementia, respectively. After further adjustment for [epsi]2/[epsi]3/[epsi]4 APOE genotype, plasma apoE tertiles remained associated with Alzheimer disease (p for trend=0.007) and all dementia (p for trend=0.04). Plasma apoE tertiles did not interact with [epsi]2/[epsi]3/[epsi]4 APOE genotype on risk of Alzheimer disease (p=0.53) or all dementia (p=0.79). In a subanalysis, the -219G>T GT promoter genotype, associated with low plasma apoE levels, remained significantly associated with increased risk of Alzheimer disease after adjustment for [epsi]2/[epsi]3/[epsi]4 APOE genotype (HR=1.56, 95% CI=1.05-2.30). Interpretation Low plasma levels of apoE are associated with increased risk of future Alzheimer disease and all dementia in the general population, independent of [epsi]2/[epsi]3/[epsi]4 APOE genotype. This is clinically relevant, because no plasma biomarkers are currently implemented. Hence, plasma levels of apoE may be a new, easily accessible preclinical biomarker. Ann Neurol 2015;77:301-311 |
| Author | Tybjærg-Hansen, Anne Nordestgaard, Børge G. Frikke-Schmidt, Ruth Rasmussen, Katrine L. |
| Author_xml | – sequence: 1 givenname: Katrine L. surname: Rasmussen fullname: Rasmussen, Katrine L. organization: Department of Clinical Biochemistry, Rigshospitalet, Copenhagen – sequence: 2 givenname: Anne surname: Tybjærg-Hansen fullname: Tybjærg-Hansen, Anne organization: Department of Clinical Biochemistry, Rigshospitalet, Copenhagen – sequence: 3 givenname: Børge G. surname: Nordestgaard fullname: Nordestgaard, Børge G. organization: Copenhagen University Hospital and Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen – sequence: 4 givenname: Ruth surname: Frikke-Schmidt fullname: Frikke-Schmidt, Ruth email: ruth.frikke-schmidt@regionh.dk organization: Department of Clinical Biochemistry, Rigshospitalet, Copenhagen |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25469919$$D View this record in MEDLINE/PubMed |
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| Copyright | 2014 American Neurological Association 2014 American Neurological Association. 2015 American Neurological Association |
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| References | Vijayaraghavan S, Maetzler W, Reinmold M, et al. High apolipoprotein E in cerebrospinal fluid of patients with Lewy body disorders is associated with dementia. Alzheimers Dement 2014;10:530.e1-540.e1. Cruchaga C, Kauwe JS, Nowotny P, et al. Cerebrospinal fluid apoE levels: an endophenotype for genetic studies for Alzheimer's disease. Hum Mol Genet 2012;21:4558-4571. Clarke R, Shipley M, Lewington S, et al. Underestimation of risk associations due to regression dilution in long-term follow-up of prospective studies. Am J Epidemiol 1999;150:341-353. Cramer PE, Cirrito JR, Wesson DW, et al. ApoE-directed therapeutics rapidly clear beta-amyloid and reverse deficits in AD mouse models. Science 2012;335:1503-1506. Harold D, Abraham R, Hollingworth P, et al. Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease. Nat Genet 2009;41:1088-1093. World Health Organization and Alzheimer's Disease International. Dementia: a public health priority. Geneva, Switzerland: WHO Press, 2012. Ulrich JD, Burchett JM, Restivo JL, et al. In vivo measurement of apolipoprotein E from the brain interstitial fluid using microdialysis. Mol Neurodegener 2013;8:13. Corder EH, Saunders AM, Strittmatter WJ, et al. Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families. Science 1993;261:921-923. Bekris LM, Galloway NM, Montine TJ, et al. APOE mRNA and protein expression in postmortem brain are modulated by an extended haplotype structure. Am J Med Genet Part B 2010;153B:409-417. Bales KR, Verina T, Cummins DJ, et al. Apolipoprotein E is essential for amyloid deposition in the APP(V717F) transgenic mouse model of Alzheimer's disease. Proc Natl Acad Sci U S A 1999;96:15233-15238. Daneman R, Zhou L, Kebede AA, Barres BA. Pericytes are required for blood-brain barrier integrity during embryogenesis. Nature 2010;468:562-566. Siest G, Bertrand P, Qin B, et al. Apolipoprotein E polymorphism and serum concentration in Alzheimer's disease in nine European centres: the ApoEurope study. ApoEurope group. Clin Chem Lab Med 2000;38:721-730. Wahrle SE, Holtzman DM. Differential metabolism of apoE isoforms in plasma and CSF. Exp Neurol 2003;183:4-6. Martel CL, Mackic JB, Matsubara E, et al. Isoform-specific effects of apolipoprotein E2, E3, and E4 on cerebral capillary sequestration and blood-brain barrier transport of circulating Alzheimer's amyloid beta. J Neurochem 1997;69:1995-2004. Mahley RW, Weisgraber KH, Huang Y. Apolipoprotein E: structure determines function, from atherosclerosis to Alzheimer's disease to AIDS. J Lipid Res 2009;50(suppl):S183-S188. Zlokovic BV. Neurovascular pathways to neurodegeneration in Alzheimer's disease and other disorders. Nat Rev Neurosci 2011;12:723-738. Hu WT, Holtzman DM, Fagan AM, et al. Plasma multianalyte profiling in mild cognitive impairment and Alzheimer disease. Neurology 2012;79:897-905. Verghese PB, Castellano JM, Holtzman DM. Apolipoprotein E in Alzheimer's disease and other neurological disorders. Lancet Neurol 2011;10:241-252. Frikke-Schmidt R, Nordestgaard BG, Stene MC, et al. Association of loss-of-function mutations in the ABCA1 gene with high-density lipoprotein cholesterol levels and risk of ischemic heart disease. JAMA 2008;299:2524-2532. Barret JC, Fry B, Maller J, Daly MJ. Haploview: analysis and visualization of LD and haplotype maps. Bioinformatics 2005;21:263-265. Simon R, Girod M, Fonbonne C, et al. Total ApoE and ApoE4 isoform assay in an Alzheimer's disease case-control study by targeted mass spectrometry (n = 669): a pilot assay for methionine-containing proteotypic peptides. Mol Cell Proteomics 2012;11:1389-1403. Yu CE, Seltman H, Peskind ER, el al. Comprehensive analysis of APOE and selected proximate markers for late-onset Alzheimer's disease: patterns of linkage disequilibrium and disease/marker association. Genomics 2007;89:655-665. Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem 1972;18:499-502. Bell RD, Winkler EA, Singh I, et al. Apolipoprotein E controls cerebrovascular integrity via cyclophilin A. Nature 2012;485:512-516. Armulik A, Genove G, Mae M, et al. Pericytes regulate the blood-brain barrier. Nature 2010;468:557-561. Deane R, Sagare A, Hamm K, et al. apoE isoform-specific disruption of amyloid beta clearance from mouse brain. J Clin Invest 2008;118:4002-4013. Utermann G, Hees M, Steinmetz A. Polymorphism of apolipoprotein E and occurrence of dysbetalipoproteinaemia in man. Nature 1977;269:604-607. Lista S, Faltraco F, Prvulovic D, Hampel H. Blood and plasma-based proteomic biomarker research in Alzheimer's disease. Prog Neurobiol 2013;101-102:1-17. Frikke-Schmidt R, Nordestgaard BG, Agerholm-Larsen B, et al. Context-dependent and invariant associations between lipids, lipoproteins, and apolipoproteins and apolipoprotein E genotype. J Lipid Res 2000;41:1812-1822. Soares HD, Potter WZ, Pickering E, et al. Plasma biomarkers associated with the apolipoprotein E genotype and Alzheimer disease. Arch Neurol 2012;69:1310-1317. Bales KR, Verina T, Dodel RC, et al. Lack of apolipoprotein E dramatically reduces amyloid beta-peptide deposition. Nat Genet 1997;17:263-264. Naj AC, Jun G, Beecham GW, et al. Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer's disease. Nat Genet 2011;43:436-441. Mawuenyega KG, Sigurdson W, Ovod V, et al. Decreased clearance of CNS beta-amyloid in Alzheimer's disease. Science 2010;330:1774. Hollingworth P, Harold D, Sims R, et al. Common variants at ABCA7, MS4A6A/MS4A4E, EPHA1, CD33 and CD2AP are associated with Alzheimer's disease. Nat Genet 2011;43:429-435. Zacho J, Tybjaerg-Hansen A, Jensen JS, et al. Genetically elevated C-reactive protein and ischemic vascular disease. N Engl J Med 2008;359:1897-1908. Seshadri S, Fitzpatrick AL, Ikram MA, et al. Genome-wide analysis of genetic loci associated with Alzheimer disease. JAMA 2010;303:1832-1840. Jack CR Jr, Knopman DS, Jagust WJ, et al. Tracking pathophysiological processes in Alzheimer's disease: an updated hypothetical model of dynamic biomarkers. Lancet Neurol 2013;12:207-216. Kamstrup PR, Tybjaerg-Hansen A, Steffensen R, Nordestgaard BG. Genetically elevated lipoprotein(a) and increased risk of myocardial infarction. JAMA 2009;301:2331-2339. Frikke-Schmidt R, Sing CF, Nordestgaard BG, Tybjaerg-Hansen A. Gender- and age-specific contributions of additional DNA sequence variation in the 5′ regulatory region of the APOE gene to prediction of measures of lipid metabolism. Hum Genet 2004;115:331-345. Linton MF, Gish R, Hubl ST, et al. Phenotypes of apolipoprotein B and apolipoprotein E after liver transplantation. J Clin Invest 1991;88:270-281. Querfurth HW, LaFerla FM. Alzheimer's disease. N Engl J Med 2010;362:329-344. Lambert JC, Heath S, Even G, et al. Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer's disease. Nat Genet 2009;41:1094-1099. Yu CE, Devlin B, Galloway N, et al. ADLAPH: A molecular haplotyping method based on allele-discriminating long-range PCR. Genomics 2004;84:600-612. DeMattos RB, Cirrito JR, Parsadanian M, et al. ApoE and clusterin cooperatively suppress Abeta levels and deposition: evidence that ApoE regulates extracellular Abeta metabolism in vivo. Neuron 2004;41:193-202. 2004; 41 2009; 41 2004; 84 2012; 485 2012 2010; 303 2010; 468 2010; 153B 1999; 150 1997; 69 2000; 41 2010; 362 1993; 261 2011; 10 2005; 21 1977; 269 2011; 12 2013; 101–102 2012; 79 2013; 8 2012; 11 2004; 115 2000; 38 2001 2009; 50 2013; 12 1991; 88 2010; 330 2003; 183 2008; 118 1997; 17 2011; 43 2008; 359 1999; 96 2008; 299 2012; 69 2012; 335 2007; 89 2012; 21 2009; 301 1972; 18 2014; 10 e_1_2_8_28_1 e_1_2_8_29_1 e_1_2_8_24_1 e_1_2_8_25_1 e_1_2_8_46_1 e_1_2_8_26_1 e_1_2_8_27_1 Bekris LM (e_1_2_8_35_1) 2010; 153 e_1_2_8_2_1 e_1_2_8_5_1 e_1_2_8_4_1 e_1_2_8_7_1 e_1_2_8_6_1 e_1_2_8_9_1 e_1_2_8_8_1 e_1_2_8_20_1 e_1_2_8_43_1 e_1_2_8_21_1 e_1_2_8_42_1 e_1_2_8_22_1 e_1_2_8_45_1 e_1_2_8_23_1 e_1_2_8_44_1 e_1_2_8_41_1 e_1_2_8_40_1 e_1_2_8_17_1 e_1_2_8_18_1 e_1_2_8_39_1 Frikke‐Schmidt R (e_1_2_8_16_1) 2000; 41 e_1_2_8_19_1 e_1_2_8_13_1 e_1_2_8_36_1 e_1_2_8_15_1 e_1_2_8_38_1 World Health Organization and Alzheimer's Disease International (e_1_2_8_3_1) 2012 e_1_2_8_37_1 Mahley RW (e_1_2_8_14_1) 2001 e_1_2_8_32_1 e_1_2_8_10_1 e_1_2_8_31_1 e_1_2_8_11_1 e_1_2_8_34_1 e_1_2_8_12_1 e_1_2_8_33_1 e_1_2_8_30_1 25583643 - Ann Neurol. 2015 Feb;77(2):204-5 |
| References_xml | – reference: Bell RD, Winkler EA, Singh I, et al. Apolipoprotein E controls cerebrovascular integrity via cyclophilin A. Nature 2012;485:512-516. – reference: DeMattos RB, Cirrito JR, Parsadanian M, et al. ApoE and clusterin cooperatively suppress Abeta levels and deposition: evidence that ApoE regulates extracellular Abeta metabolism in vivo. Neuron 2004;41:193-202. – reference: Armulik A, Genove G, Mae M, et al. Pericytes regulate the blood-brain barrier. Nature 2010;468:557-561. – reference: Ulrich JD, Burchett JM, Restivo JL, et al. In vivo measurement of apolipoprotein E from the brain interstitial fluid using microdialysis. Mol Neurodegener 2013;8:13. – reference: Hollingworth P, Harold D, Sims R, et al. Common variants at ABCA7, MS4A6A/MS4A4E, EPHA1, CD33 and CD2AP are associated with Alzheimer's disease. Nat Genet 2011;43:429-435. – reference: Cramer PE, Cirrito JR, Wesson DW, et al. ApoE-directed therapeutics rapidly clear beta-amyloid and reverse deficits in AD mouse models. Science 2012;335:1503-1506. – reference: Kamstrup PR, Tybjaerg-Hansen A, Steffensen R, Nordestgaard BG. Genetically elevated lipoprotein(a) and increased risk of myocardial infarction. JAMA 2009;301:2331-2339. – reference: Deane R, Sagare A, Hamm K, et al. apoE isoform-specific disruption of amyloid beta clearance from mouse brain. J Clin Invest 2008;118:4002-4013. – reference: Seshadri S, Fitzpatrick AL, Ikram MA, et al. Genome-wide analysis of genetic loci associated with Alzheimer disease. JAMA 2010;303:1832-1840. – reference: Lista S, Faltraco F, Prvulovic D, Hampel H. Blood and plasma-based proteomic biomarker research in Alzheimer's disease. Prog Neurobiol 2013;101-102:1-17. – reference: Yu CE, Seltman H, Peskind ER, el al. Comprehensive analysis of APOE and selected proximate markers for late-onset Alzheimer's disease: patterns of linkage disequilibrium and disease/marker association. Genomics 2007;89:655-665. – reference: Bekris LM, Galloway NM, Montine TJ, et al. APOE mRNA and protein expression in postmortem brain are modulated by an extended haplotype structure. Am J Med Genet Part B 2010;153B:409-417. – reference: Mawuenyega KG, Sigurdson W, Ovod V, et al. Decreased clearance of CNS beta-amyloid in Alzheimer's disease. Science 2010;330:1774. – reference: Verghese PB, Castellano JM, Holtzman DM. Apolipoprotein E in Alzheimer's disease and other neurological disorders. Lancet Neurol 2011;10:241-252. – reference: Lambert JC, Heath S, Even G, et al. Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer's disease. Nat Genet 2009;41:1094-1099. – reference: Siest G, Bertrand P, Qin B, et al. Apolipoprotein E polymorphism and serum concentration in Alzheimer's disease in nine European centres: the ApoEurope study. ApoEurope group. Clin Chem Lab Med 2000;38:721-730. – reference: Daneman R, Zhou L, Kebede AA, Barres BA. Pericytes are required for blood-brain barrier integrity during embryogenesis. Nature 2010;468:562-566. – reference: Soares HD, Potter WZ, Pickering E, et al. Plasma biomarkers associated with the apolipoprotein E genotype and Alzheimer disease. Arch Neurol 2012;69:1310-1317. – reference: Barret JC, Fry B, Maller J, Daly MJ. Haploview: analysis and visualization of LD and haplotype maps. Bioinformatics 2005;21:263-265. – reference: Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem 1972;18:499-502. – reference: Frikke-Schmidt R, Sing CF, Nordestgaard BG, Tybjaerg-Hansen A. Gender- and age-specific contributions of additional DNA sequence variation in the 5′ regulatory region of the APOE gene to prediction of measures of lipid metabolism. Hum Genet 2004;115:331-345. – reference: Zlokovic BV. Neurovascular pathways to neurodegeneration in Alzheimer's disease and other disorders. Nat Rev Neurosci 2011;12:723-738. – reference: Cruchaga C, Kauwe JS, Nowotny P, et al. Cerebrospinal fluid apoE levels: an endophenotype for genetic studies for Alzheimer's disease. Hum Mol Genet 2012;21:4558-4571. – reference: Mahley RW, Weisgraber KH, Huang Y. Apolipoprotein E: structure determines function, from atherosclerosis to Alzheimer's disease to AIDS. J Lipid Res 2009;50(suppl):S183-S188. – reference: Wahrle SE, Holtzman DM. Differential metabolism of apoE isoforms in plasma and CSF. Exp Neurol 2003;183:4-6. – reference: Bales KR, Verina T, Cummins DJ, et al. Apolipoprotein E is essential for amyloid deposition in the APP(V717F) transgenic mouse model of Alzheimer's disease. Proc Natl Acad Sci U S A 1999;96:15233-15238. – reference: Bales KR, Verina T, Dodel RC, et al. Lack of apolipoprotein E dramatically reduces amyloid beta-peptide deposition. Nat Genet 1997;17:263-264. – reference: Naj AC, Jun G, Beecham GW, et al. Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer's disease. Nat Genet 2011;43:436-441. – reference: Querfurth HW, LaFerla FM. Alzheimer's disease. N Engl J Med 2010;362:329-344. – reference: Clarke R, Shipley M, Lewington S, et al. Underestimation of risk associations due to regression dilution in long-term follow-up of prospective studies. Am J Epidemiol 1999;150:341-353. – reference: Linton MF, Gish R, Hubl ST, et al. Phenotypes of apolipoprotein B and apolipoprotein E after liver transplantation. J Clin Invest 1991;88:270-281. – reference: Yu CE, Devlin B, Galloway N, et al. ADLAPH: A molecular haplotyping method based on allele-discriminating long-range PCR. Genomics 2004;84:600-612. – reference: Utermann G, Hees M, Steinmetz A. Polymorphism of apolipoprotein E and occurrence of dysbetalipoproteinaemia in man. Nature 1977;269:604-607. – reference: Harold D, Abraham R, Hollingworth P, et al. Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease. Nat Genet 2009;41:1088-1093. – reference: Hu WT, Holtzman DM, Fagan AM, et al. Plasma multianalyte profiling in mild cognitive impairment and Alzheimer disease. Neurology 2012;79:897-905. – reference: World Health Organization and Alzheimer's Disease International. Dementia: a public health priority. Geneva, Switzerland: WHO Press, 2012. – reference: Corder EH, Saunders AM, Strittmatter WJ, et al. Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families. Science 1993;261:921-923. – reference: Frikke-Schmidt R, Nordestgaard BG, Agerholm-Larsen B, et al. Context-dependent and invariant associations between lipids, lipoproteins, and apolipoproteins and apolipoprotein E genotype. J Lipid Res 2000;41:1812-1822. – reference: Martel CL, Mackic JB, Matsubara E, et al. Isoform-specific effects of apolipoprotein E2, E3, and E4 on cerebral capillary sequestration and blood-brain barrier transport of circulating Alzheimer's amyloid beta. J Neurochem 1997;69:1995-2004. – reference: Simon R, Girod M, Fonbonne C, et al. Total ApoE and ApoE4 isoform assay in an Alzheimer's disease case-control study by targeted mass spectrometry (n = 669): a pilot assay for methionine-containing proteotypic peptides. Mol Cell Proteomics 2012;11:1389-1403. – reference: Zacho J, Tybjaerg-Hansen A, Jensen JS, et al. Genetically elevated C-reactive protein and ischemic vascular disease. N Engl J Med 2008;359:1897-1908. – reference: Frikke-Schmidt R, Nordestgaard BG, Stene MC, et al. Association of loss-of-function mutations in the ABCA1 gene with high-density lipoprotein cholesterol levels and risk of ischemic heart disease. JAMA 2008;299:2524-2532. – reference: Jack CR Jr, Knopman DS, Jagust WJ, et al. Tracking pathophysiological processes in Alzheimer's disease: an updated hypothetical model of dynamic biomarkers. Lancet Neurol 2013;12:207-216. – reference: Vijayaraghavan S, Maetzler W, Reinmold M, et al. High apolipoprotein E in cerebrospinal fluid of patients with Lewy body disorders is associated with dementia. 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apolipoprotein E in cerebrospinal fluid of patients with Lewy body disorders is associated with dementia publication-title: Alzheimers Dement – volume: 468 start-page: 562 year: 2010 end-page: 566 article-title: Pericytes are required for blood‐brain barrier integrity during embryogenesis publication-title: Nature – volume: 43 start-page: 429 year: 2011 end-page: 435 article-title: Common variants at ABCA7, MS4A6A/MS4A4E, EPHA1, CD33 and CD2AP are associated with Alzheimer's disease publication-title: Nat Genet – volume: 79 start-page: 897 year: 2012 end-page: 905 article-title: Plasma multianalyte profiling in mild cognitive impairment and Alzheimer disease publication-title: Neurology – volume: 43 start-page: 436 year: 2011 end-page: 441 article-title: Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late‐onset Alzheimer's disease publication-title: Nat Genet – volume: 69 start-page: 1310 year: 2012 end-page: 1317 article-title: Plasma biomarkers associated with the apolipoprotein E genotype and Alzheimer disease publication-title: Arch Neurol – volume: 89 start-page: 655 year: 2007 end-page: 665 article-title: Comprehensive analysis of APOE and selected proximate markers for late‐onset Alzheimer's disease: patterns of linkage disequilibrium and disease/marker association publication-title: Genomics – volume: 468 start-page: 557 year: 2010 end-page: 561 article-title: Pericytes regulate the blood‐brain barrier publication-title: Nature – volume: 183 start-page: 4 year: 2003 end-page: 6 article-title: Differential metabolism of apoE isoforms in plasma and CSF publication-title: Exp Neurol – volume: 69 start-page: 1995 year: 1997 end-page: 2004 article-title: Isoform‐specific effects of apolipoprotein E2, E3, and E4 on cerebral capillary sequestration and blood‐brain barrier transport of circulating Alzheimer's amyloid beta publication-title: J Neurochem – volume: 362 start-page: 329 year: 2010 end-page: 344 article-title: Alzheimer's 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The apolipoprotein E (APOE) ε4 allele is a major genetic risk factor for Alzheimer disease and dementia. However, it remains unclear whether plasma... The apolipoprotein E (APOE) ε4 allele is a major genetic risk factor for Alzheimer disease and dementia. However, it remains unclear whether plasma levels of... Objective The apolipoprotein E (APOE) [epsi]4 allele is a major genetic risk factor for Alzheimer disease and dementia. However, it remains unclear whether... Objective The apolipoprotein E (APOE) epsilon 4 allele is a major genetic risk factor for Alzheimer disease and dementia. However, it remains unclear whether... |
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| SubjectTerms | Aged Apolipoproteins E - blood Biomarkers - blood Dementia - blood Dementia - diagnosis Dementia - epidemiology Denmark - epidemiology Female Follow-Up Studies Humans Male Middle Aged Population Surveillance - methods Prospective Studies Risk Factors |
| Title | Plasma levels of apolipoprotein E and risk of dementia in the general population |
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