Sex modifies the APOE-related risk of developing Alzheimer disease
Objective The APOE4 allele is the strongest genetic risk factor for sporadic Alzheimer disease (AD). Case–control studies suggest the APOE4 link to AD is stronger in women. We examined the APOE4‐by‐sex interaction in conversion risk (from healthy aging to mild cognitive impairment (MCI)/AD or from M...
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| Published in | Annals of neurology Vol. 75; no. 4; pp. 563 - 573 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Blackwell Publishing Ltd
01.04.2014
Wiley Subscription Services, Inc |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Objective
The APOE4 allele is the strongest genetic risk factor for sporadic Alzheimer disease (AD). Case–control studies suggest the APOE4 link to AD is stronger in women. We examined the APOE4‐by‐sex interaction in conversion risk (from healthy aging to mild cognitive impairment (MCI)/AD or from MCI to AD) and cerebrospinal fluid (CSF) biomarker levels.
Methods
Cox proportional hazards analysis was used to compute hazard ratios (HRs) for an APOE‐by‐sex interaction on conversion in controls (n = 5,496) and MCI patients (n = 2,588). The interaction was also tested in CSF biomarker levels of 980 subjects from the Alzheimer's Disease Neuroimaging Initiative.
Results
Among controls, male and female carriers were more likely to convert to MCI/AD, but the effect was stronger in women (HR = 1.81 for women; HR = 1.27 for men; interaction: p = 0.011). The interaction remained significant in a predefined subanalysis restricted to APOE3/3 and APOE3/4 genotypes. Among MCI patients, both male and female APOE4 carriers were more likely to convert to AD (HR = 2.16 for women; HR = 1.64 for men); the interaction was not significant (p = 0.14). In the subanalysis restricted to APOE3/3 and APOE3/4 genotypes, the interaction was significant (p = 0.02; HR = 2.17 for women; HR = 1.51 for men). The APOE4‐by‐sex interaction on biomarker levels was significant for MCI patients for total tau and the tau‐to‐Aβ ratio (p = 0.009 and p = 0.02, respectively; more AD‐like in women).
Interpretation
APOE4 confers greater AD risk in women. Biomarker results suggest that increased APOE‐related risk in women may be associated with tau pathology. These findings have important clinical implications and suggest novel research approaches into AD pathogenesis. Ann Neurol 2014;75:563–573 |
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| AbstractList | Objective The APOE4 allele is the strongest genetic risk factor for sporadic Alzheimer disease (AD). Case-control studies suggest the APOE4 link to AD is stronger in women. We examined the APOE4-by-sex interaction in conversion risk (from healthy aging to mild cognitive impairment (MCI)/AD or from MCI to AD) and cerebrospinal fluid (CSF) biomarker levels. Methods Cox proportional hazards analysis was used to compute hazard ratios (HRs) for an APOE-by-sex interaction on conversion in controls (n = 5,496) and MCI patients (n = 2,588). The interaction was also tested in CSF biomarker levels of 980 subjects from the Alzheimer's Disease Neuroimaging Initiative. Results Among controls, male and female carriers were more likely to convert to MCI/AD, but the effect was stronger in women (HR = 1.81 for women; HR = 1.27 for men; interaction: p = 0.011). The interaction remained significant in a predefined subanalysis restricted to APOE3/3 and APOE3/4 genotypes. Among MCI patients, both male and female APOE4 carriers were more likely to convert to AD (HR = 2.16 for women; HR = 1.64 for men); the interaction was not significant (p = 0.14). In the subanalysis restricted to APOE3/3 and APOE3/4 genotypes, the interaction was significant (p = 0.02; HR = 2.17 for women; HR = 1.51 for men). The APOE4-by-sex interaction on biomarker levels was significant for MCI patients for total tau and the tau-to-A[beta] ratio (p = 0.009 and p = 0.02, respectively; more AD-like in women). Interpretation APOE4 confers greater AD risk in women. Biomarker results suggest that increased APOE-related risk in women may be associated with tau pathology. These findings have important clinical implications and suggest novel research approaches into AD pathogenesis. Ann Neurol 2014; 75:563-573 The APOE4 allele is the strongest genetic risk factor for sporadic Alzheimer disease (AD). Case-control studies suggest the APOE4 link to AD is stronger in women. We examined the APOE4-by-sex interaction in conversion risk (from healthy aging to mild cognitive impairment (MCI)/AD or from MCI to AD) and cerebrospinal fluid (CSF) biomarker levels.OBJECTIVEThe APOE4 allele is the strongest genetic risk factor for sporadic Alzheimer disease (AD). Case-control studies suggest the APOE4 link to AD is stronger in women. We examined the APOE4-by-sex interaction in conversion risk (from healthy aging to mild cognitive impairment (MCI)/AD or from MCI to AD) and cerebrospinal fluid (CSF) biomarker levels.Cox proportional hazards analysis was used to compute hazard ratios (HRs) for an APOE-by-sex interaction on conversion in controls (n = 5,496) and MCI patients (n = 2,588). The interaction was also tested in CSF biomarker levels of 980 subjects from the Alzheimer's Disease Neuroimaging Initiative.METHODSCox proportional hazards analysis was used to compute hazard ratios (HRs) for an APOE-by-sex interaction on conversion in controls (n = 5,496) and MCI patients (n = 2,588). The interaction was also tested in CSF biomarker levels of 980 subjects from the Alzheimer's Disease Neuroimaging Initiative.Among controls, male and female carriers were more likely to convert to MCI/AD, but the effect was stronger in women (HR = 1.81 for women; HR = 1.27 for men; interaction: p = 0.011). The interaction remained significant in a predefined subanalysis restricted to APOE3/3 and APOE3/4 genotypes. Among MCI patients, both male and female APOE4 carriers were more likely to convert to AD (HR = 2.16 for women; HR = 1.64 for men); the interaction was not significant (p = 0.14). In the subanalysis restricted to APOE3/3 and APOE3/4 genotypes, the interaction was significant (p = 0.02; HR = 2.17 for women; HR = 1.51 for men). The APOE4-by-sex interaction on biomarker levels was significant for MCI patients for total tau and the tau-to-Aβ ratio (p = 0.009 and p = 0.02, respectively; more AD-like in women).RESULTSAmong controls, male and female carriers were more likely to convert to MCI/AD, but the effect was stronger in women (HR = 1.81 for women; HR = 1.27 for men; interaction: p = 0.011). The interaction remained significant in a predefined subanalysis restricted to APOE3/3 and APOE3/4 genotypes. Among MCI patients, both male and female APOE4 carriers were more likely to convert to AD (HR = 2.16 for women; HR = 1.64 for men); the interaction was not significant (p = 0.14). In the subanalysis restricted to APOE3/3 and APOE3/4 genotypes, the interaction was significant (p = 0.02; HR = 2.17 for women; HR = 1.51 for men). The APOE4-by-sex interaction on biomarker levels was significant for MCI patients for total tau and the tau-to-Aβ ratio (p = 0.009 and p = 0.02, respectively; more AD-like in women).APOE4 confers greater AD risk in women. Biomarker results suggest that increased APOE-related risk in women may be associated with tau pathology. These findings have important clinical implications and suggest novel research approaches into AD pathogenesis.INTERPRETATIONAPOE4 confers greater AD risk in women. Biomarker results suggest that increased APOE-related risk in women may be associated with tau pathology. These findings have important clinical implications and suggest novel research approaches into AD pathogenesis. Objective The APOE4 allele is the strongest genetic risk factor for sporadic Alzheimer disease (AD). Case-control studies suggest the APOE4 link to AD is stronger in women. We examined the APOE4-by-sex interaction in conversion risk (from healthy aging to mild cognitive impairment (MCI)/AD or from MCI to AD) and cerebrospinal fluid (CSF) biomarker levels. Methods Cox proportional hazards analysis was used to compute hazard ratios (HRs) for an APOE-by-sex interaction on conversion in controls (n = 5,496) and MCI patients (n = 2,588). The interaction was also tested in CSF biomarker levels of 980 subjects from the Alzheimer's Disease Neuroimaging Initiative. Results Among controls, male and female carriers were more likely to convert to MCI/AD, but the effect was stronger in women (HR = 1.81 for women; HR = 1.27 for men; interaction: p = 0.011). The interaction remained significant in a predefined subanalysis restricted to APOE3/3 and APOE3/4 genotypes. Among MCI patients, both male and female APOE4 carriers were more likely to convert to AD (HR = 2.16 for women; HR = 1.64 for men); the interaction was not significant (p = 0.14). In the subanalysis restricted to APOE3/3 and APOE3/4 genotypes, the interaction was significant (p = 0.02; HR = 2.17 for women; HR = 1.51 for men). The APOE4-by-sex interaction on biomarker levels was significant for MCI patients for total tau and the tau-to-A[beta] ratio (p = 0.009 and p = 0.02, respectively; more AD-like in women). Interpretation APOE4 confers greater AD risk in women. Biomarker results suggest that increased APOE-related risk in women may be associated with tau pathology. These findings have important clinical implications and suggest novel research approaches into AD pathogenesis. Ann Neurol 2014;75:563-573 [PUBLICATION ABSTRACT] Objective The APOE4 allele is the strongest genetic risk factor for sporadic Alzheimer disease (AD). Case–control studies suggest the APOE4 link to AD is stronger in women. We examined the APOE4‐by‐sex interaction in conversion risk (from healthy aging to mild cognitive impairment (MCI)/AD or from MCI to AD) and cerebrospinal fluid (CSF) biomarker levels. Methods Cox proportional hazards analysis was used to compute hazard ratios (HRs) for an APOE‐by‐sex interaction on conversion in controls (n = 5,496) and MCI patients (n = 2,588). The interaction was also tested in CSF biomarker levels of 980 subjects from the Alzheimer's Disease Neuroimaging Initiative. Results Among controls, male and female carriers were more likely to convert to MCI/AD, but the effect was stronger in women (HR = 1.81 for women; HR = 1.27 for men; interaction: p = 0.011). The interaction remained significant in a predefined subanalysis restricted to APOE3/3 and APOE3/4 genotypes. Among MCI patients, both male and female APOE4 carriers were more likely to convert to AD (HR = 2.16 for women; HR = 1.64 for men); the interaction was not significant (p = 0.14). In the subanalysis restricted to APOE3/3 and APOE3/4 genotypes, the interaction was significant (p = 0.02; HR = 2.17 for women; HR = 1.51 for men). The APOE4‐by‐sex interaction on biomarker levels was significant for MCI patients for total tau and the tau‐to‐Aβ ratio (p = 0.009 and p = 0.02, respectively; more AD‐like in women). Interpretation APOE4 confers greater AD risk in women. Biomarker results suggest that increased APOE‐related risk in women may be associated with tau pathology. These findings have important clinical implications and suggest novel research approaches into AD pathogenesis. Ann Neurol 2014;75:563–573 The APOE4 allele is the strongest genetic risk factor for sporadic Alzheimer disease (AD). Case-control studies suggest the APOE4 link to AD is stronger in women. We examined the APOE4-by-sex interaction in conversion risk (from healthy aging to mild cognitive impairment (MCI)/AD or from MCI to AD) and cerebrospinal fluid (CSF) biomarker levels. Cox proportional hazards analysis was used to compute hazard ratios (HRs) for an APOE-by-sex interaction on conversion in controls (n = 5,496) and MCI patients (n = 2,588). The interaction was also tested in CSF biomarker levels of 980 subjects from the Alzheimer's Disease Neuroimaging Initiative. Among controls, male and female carriers were more likely to convert to MCI/AD, but the effect was stronger in women (HR = 1.81 for women; HR = 1.27 for men; interaction: p = 0.011). The interaction remained significant in a predefined subanalysis restricted to APOE3/3 and APOE3/4 genotypes. Among MCI patients, both male and female APOE4 carriers were more likely to convert to AD (HR = 2.16 for women; HR = 1.64 for men); the interaction was not significant (p = 0.14). In the subanalysis restricted to APOE3/3 and APOE3/4 genotypes, the interaction was significant (p = 0.02; HR = 2.17 for women; HR = 1.51 for men). The APOE4-by-sex interaction on biomarker levels was significant for MCI patients for total tau and the tau-to-Aβ ratio (p = 0.009 and p = 0.02, respectively; more AD-like in women). APOE4 confers greater AD risk in women. Biomarker results suggest that increased APOE-related risk in women may be associated with tau pathology. These findings have important clinical implications and suggest novel research approaches into AD pathogenesis. |
| Author | Henderson, Victor W. Greicius, Michael D. Tian, Lu Altmann, Andre |
| Author_xml | – sequence: 1 givenname: Andre surname: Altmann fullname: Altmann, Andre organization: Stanford Center for Memory Disorders, Department of Neurology and Neurological Sciences, Stanford University, CA, Stanford – sequence: 2 givenname: Lu surname: Tian fullname: Tian, Lu organization: Department of Health Research and Policy, Stanford University, CA, Stanford – sequence: 3 givenname: Victor W. surname: Henderson fullname: Henderson, Victor W. organization: Stanford Center for Memory Disorders, Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA – sequence: 4 givenname: Michael D. surname: Greicius fullname: Greicius, Michael D. email: greicius@stanford.edu organization: Stanford Center for Memory Disorders, Department of Neurology and Neurological Sciences, Stanford University, CA, Stanford |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24623176$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | 2014 American Neurological Association 2014 American Neurological Association. |
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| CorporateAuthor | Alzheimer's Disease Neuroimaging Initiative Investigators |
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Biol Psychiatry 2004;56:670-676. Morris JC, Weintraub S, Chui HC, et al. The Uniform Data Set (UDS): clinical and cognitive variables and descriptive data from Alzheimer Disease Centers. Alzheimer Dis Assoc Disord 2006;20:210-216. Huang Y. Abeta-independent roles of apolipoprotein E4 in the pathogenesis of Alzheimer's disease. Trends Mol Med 2010;16:287-294. Payami H, Zareparsi S, Montee KR, et al. Gender difference in apolipoprotein E-associated risk for familial Alzheimer disease: a possible clue to the higher incidence of Alzheimer disease in women. Am J Hum Genet 1996;58:803-811. Cruchaga C, Kauwe JS, Harari O, et al. GWAS of cerebrospinal fluid tau levels identifies risk variants for Alzheimer's disease. Neuron 2013;78:256-268. 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. Marquis S, Moore MM, Howieson DB, et al. 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Ann N Y Acad Sci 2004;1019:24-28. Beydoun MA, Boueiz A, Abougergi MS, et al. Sex differences in the association of the apolipoprotein E epsilon 4 allele with incidence of dementia, cognitive impairment, and decline. Neurobiol Aging 2012;33:720-731 e4. Shaw LM, Vanderstichele H, Knapik-Czajka M, et al. Cerebrospinal fluid biomarker signature in Alzheimer's disease neuroimaging initiative subjects. Ann Neurol 2009;65:403-413. Ward A, Crean S, Mercaldi CJ, et al. Prevalence of apolipoprotein E4 genotype and homozygotes (APOE e4/4) among patients diagnosed with Alzheimer's disease: a systematic review and meta-analysis. Neuroepidemiology 2012;38:1-17. Weiner MW, Aisen PS, Jack CR Jr, et al. The Alzheimer's disease neuroimaging initiative: progress report and future plans. Alzheimers Dement 2010;6:202.e7-211.e7. McKhann G, Drachman D, Folstein M, et al. 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Neuropsychology 2013;27:86-94. Tsai WY. Testing the assumption of independence of truncation time and failure time. Biometrika 1990;77:169-177. Elias-Sonnenschein LS, Bertram L, Visser PJ. Relationship between genetic risk factors and markers for Alzheimer's disease pathology. Biomark Med 2012;6:477-495. Farrer LA, Cupples LA, Haines JL, et al. Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease. A meta-analysis. APOE and Alzheimer Disease Meta Analysis Consortium. JAMA 1997;278:1349-1356. Damoiseaux JS, Seeley WW, Zhou J, et al. Gender modulates the APOE epsilon4 effect in healthy older adults: convergent evidence from functional brain connectivity and spinal fluid tau levels. J Neurosci 2012;32:8254-8262. Bretsky PM, Buckwalter JG, Seeman TE, et al. Evidence for an interaction between apolipoprotein E genotype, gender, and Alzheimer disease. Alzheimer Dis Assoc Disord 1999;13:216-221. Beekly DL, Ramos EM, Lee WW, et al. The National Alzheimer's Coordinating Center (NACC) database: the Uniform Data Set. Alzheimer Dis Assoc Disord 2007;21:249-258. 1997; 278 2009; 23 2004; 63 2002; 59 2010; 16 1990; 77 2009; 65 2013; 27 1994; 271 2009; 132 2006; 7 1993; 261 2012; 38 1996; 58 2011; 3 2012; 33 2012; 32 2011; 7 2009; 28 2006; 63 2006; 20 2013; 78 2004; 56 1984; 34 1999; 13 2012; 6 2007; 21 2010; 2 1998; 95 2010; 6 2004; 1019 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_26_1 e_1_2_8_27_1 Schuff N (e_1_2_8_7_1) 2009; 132 e_1_2_8_3_1 e_1_2_8_2_1 e_1_2_8_5_1 e_1_2_8_4_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_21_1 e_1_2_8_22_1 e_1_2_8_23_1 e_1_2_8_17_1 e_1_2_8_19_1 e_1_2_8_13_1 e_1_2_8_14_1 e_1_2_8_15_1 e_1_2_8_16_1 Payami H (e_1_2_8_18_1) 1996; 58 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_12_1 e_1_2_8_33_1 e_1_2_8_30_1 |
| References_xml | – reference: Sunderland T, Mirza N, Putnam KT, et al. Cerebrospinal fluid beta-amyloid1-42 and tau in control subjects at risk for Alzheimer's disease: the effect of APOE epsilon4 allele. Biol Psychiatry 2004;56:670-676. – reference: Ward A, Crean S, Mercaldi CJ, et al. Prevalence of apolipoprotein E4 genotype and homozygotes (APOE e4/4) among patients diagnosed with Alzheimer's disease: a systematic review and meta-analysis. Neuroepidemiology 2012;38:1-17. – reference: Beekly DL, Ramos EM, Lee WW, et al. The National Alzheimer's Coordinating Center (NACC) database: the Uniform Data Set. Alzheimer Dis Assoc Disord 2007;21:249-258. – reference: Weiner MW, Aisen PS, Jack CR Jr, et al. The Alzheimer's disease neuroimaging initiative: progress report and future plans. Alzheimers Dement 2010;6:202.e7-211.e7. – reference: Payami H, Montee KR, Kaye JA, et al. Alzheimer's disease, apolipoprotein E4, and gender. JAMA 1994;271:1316-1317. – reference: Sperling RA, Aisen PS, Beckett LA, et al. Toward defining the preclinical stages of Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement 2011;7:280-292. – reference: Farlow MR. Should the ApoE genotype be a covariate for clinical trials in Alzheimer disease? Alzheimers Res Ther 2010;2:15. – reference: Brainerd CJ, Reyna VF, Petersen RC, et al. The apolipoprotein E genotype predicts longitudinal transitions to mild cognitive impairment but not to Alzheimer's dementia: findings from a nationally representative study. Neuropsychology 2013;27:86-94. – reference: Marquis S, Moore MM, Howieson DB, et al. Independent predictors of cognitive decline in healthy elderly persons. Arch Neurol 2002;59:601-606. – reference: Shaw LM, Vanderstichele H, Knapik-Czajka M, et al. Cerebrospinal fluid biomarker signature in Alzheimer's disease neuroimaging initiative subjects. Ann Neurol 2009;65:403-413. – reference: Bretsky PM, Buckwalter JG, Seeman TE, et al. Evidence for an interaction between apolipoprotein E genotype, gender, and Alzheimer disease. Alzheimer Dis Assoc Disord 1999;13:216-221. – reference: Tsai WY. Testing the assumption of independence of truncation time and failure time. Biometrika 1990;77:169-177. – reference: Raber J, Wong D, Buttini M, et al. Isoform-specific effects of human apolipoprotein E on brain function revealed in ApoE knockout mice: increased susceptibility of females. Proc Natl Acad Sci U S A 1998;95:10914-10919. – reference: Farrer LA, Cupples LA, Haines JL, et al. Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease. A meta-analysis. APOE and Alzheimer Disease Meta Analysis Consortium. JAMA 1997;278:1349-1356. – reference: Elias-Sonnenschein LS, Bertram L, Visser PJ. Relationship between genetic risk factors and markers for Alzheimer's disease pathology. Biomark Med 2012;6:477-495. – reference: Sperling RA, Jack CR Jr, Aisen PS. Testing the right target and right drug at the right stage. Sci Transl Med 2011;3:111cm33. – reference: Beydoun MA, Boueiz A, Abougergi MS, et al. Sex differences in the association of the apolipoprotein E epsilon 4 allele with incidence of dementia, cognitive impairment, and decline. Neurobiol Aging 2012;33:720-731 e4. – reference: Cruchaga C, Kauwe JS, Harari O, et al. GWAS of cerebrospinal fluid tau levels identifies risk variants for Alzheimer's disease. Neuron 2013;78:256-268. – reference: Manolio TA, Bailey-Wilson JE, Collins FS. Genes, environment and the value of prospective cohort studies. Nat Rev Genet 2006;7:812-820. – reference: Bunce D, Fratiglioni L, Small BJ, et al. APOE and cognitive decline in preclinical Alzheimer disease and non-demented aging. Neurology 2004;63:816-821. – reference: Schuff N, Woerner N, Boreta L, et al. MRI of hippocampal volume loss in early Alzheimer's disease in relation to ApoE genotype and biomarkers. Brain 2009;132(pt 4):1067-1077. – reference: McKhann G, Drachman D, Folstein M, et al. Clinical diagnosis of Alzheimer's disease: report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease. Neurology 1984;34:939-944. – reference: Gail MH, Graubard B, Williamson DE, Flegal KM. Comments on 'Choice of time scale and its effect on significance of predictors in longitudinal studies.' Stat Med 2009;28:1315-1317. – reference: Huang Y. Abeta-independent roles of apolipoprotein E4 in the pathogenesis of Alzheimer's disease. Trends Mol Med 2010;16:287-294. – reference: Corder EH, Ghebremedhin E, Taylor MG, et al. The biphasic relationship between regional brain senile plaque and neurofibrillary tangle distributions: modification by age, sex, and APOE polymorphism. Ann N Y Acad Sci 2004;1019:24-28. – 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: Damoiseaux JS, Seeley WW, Zhou J, et al. Gender modulates the APOE epsilon4 effect in healthy older adults: convergent evidence from functional brain connectivity and spinal fluid tau levels. J Neurosci 2012;32:8254-8262. – reference: Geda YE, Knopman DS, Mrazek DA, et al. Depression, apolipoprotein E genotype, and the incidence of mild cognitive impairment: a prospective cohort study. Arch Neurol 2006;63:435-440. – reference: Payami H, Zareparsi S, Montee KR, et al. Gender difference in apolipoprotein E-associated risk for familial Alzheimer disease: a possible clue to the higher incidence of Alzheimer disease in women. Am J Hum Genet 1996;58:803-811. – reference: Morris JC, Weintraub S, Chui HC, et al. The Uniform Data Set (UDS): clinical and cognitive variables and descriptive data from Alzheimer Disease Centers. Alzheimer Dis Assoc Disord 2006;20:210-216. – reference: Wilson RS, Schneider JA, Barnes LL, et al. The apolipoprotein E epsilon 4 allele and decline in different cognitive systems during a 6-year period. Arch Neurol 2002;59:1154-1160. – reference: Weintraub S, Salmon D, Mercaldo N, et al. The Alzheimer's Disease Centers' Uniform Data Set (UDS): the neuropsychologic test battery. 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A meta‐analysis publication-title: JAMA – volume: 2 start-page: 15 year: 2010 article-title: Should the ApoE genotype be a covariate for clinical trials in Alzheimer disease? publication-title: Alzheimers Res Ther – volume: 27 start-page: 86 year: 2013 end-page: 94 article-title: The apolipoprotein E genotype predicts longitudinal transitions to mild cognitive impairment but not to Alzheimer's dementia: findings from a nationally representative study publication-title: Neuropsychology – volume: 20 start-page: 210 year: 2006 end-page: 216 article-title: The Uniform Data Set (UDS): clinical and cognitive variables and descriptive data from Alzheimer Disease Centers publication-title: Alzheimer Dis Assoc Disord – volume: 21 start-page: 249 year: 2007 end-page: 258 article-title: The National Alzheimer's Coordinating Center (NACC) database: the Uniform Data Set publication-title: Alzheimer Dis Assoc Disord – volume: 78 start-page: 256 year: 2013 end-page: 268 article-title: GWAS of 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volume: 132 start-page: 1067 issue: pt 4 year: 2009 end-page: 1077 article-title: MRI of hippocampal volume loss in early Alzheimer's disease in relation to ApoE genotype and biomarkers publication-title: Brain – volume: 261 start-page: 921 year: 1993 end-page: 923 article-title: Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families publication-title: Science – volume: 63 start-page: 816 year: 2004 end-page: 821 article-title: APOE and cognitive decline in preclinical Alzheimer disease and non‐demented aging publication-title: Neurology – volume: 1019 start-page: 24 year: 2004 end-page: 28 article-title: The biphasic relationship between regional brain senile plaque and neurofibrillary tangle distributions: modification by age, sex, and APOE polymorphism publication-title: Ann N Y Acad Sci – volume: 56 start-page: 670 year: 2004 end-page: 676 article-title: Cerebrospinal fluid beta‐amyloid1‐42 and tau in control subjects at risk for Alzheimer's disease: the effect of APOE epsilon4 allele publication-title: Biol Psychiatry – volume: 6 start-page: 477 year: 2012 end-page: 495 article-title: Relationship between genetic risk factors and markers for Alzheimer's disease pathology publication-title: Biomark Med – volume: 271 start-page: 1316 year: 1994 end-page: 1317 article-title: Alzheimer's disease, apolipoprotein E4, and gender publication-title: JAMA – volume: 58 start-page: 803 year: 1996 end-page: 811 article-title: Gender difference in apolipoprotein E‐associated risk for familial Alzheimer disease: a possible clue to the higher incidence of Alzheimer disease in women publication-title: Am J Hum Genet – volume: 77 start-page: 169 year: 1990 end-page: 177 article-title: Testing the assumption of independence of truncation time and failure time publication-title: Biometrika – volume: 3 start-page: 111cm33 year: 2011 article-title: Testing the right target and right drug at the right stage publication-title: Sci Transl Med – volume: 33 start-page: 720 year: 2012 end-page: 731 article-title: Sex differences in the association of the apolipoprotein E epsilon 4 allele with incidence of dementia, cognitive impairment, and decline publication-title: Neurobiol Aging – volume: 63 start-page: 435 year: 2006 end-page: 440 article-title: Depression, apolipoprotein E genotype, and the incidence of mild cognitive impairment: a prospective cohort study publication-title: Arch Neurol – volume: 59 start-page: 601 year: 2002 end-page: 606 article-title: Independent predictors of cognitive decline in healthy elderly persons publication-title: Arch Neurol – volume: 95 start-page: 10914 year: 1998 end-page: 10919 article-title: Isoform‐specific effects of human apolipoprotein E on brain function revealed in ApoE knockout mice: increased susceptibility of females publication-title: Proc Natl Acad Sci U S A – volume: 7 start-page: 812 year: 2006 end-page: 820 article-title: Genes, environment and the value of 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The APOE4 allele is the strongest genetic risk factor for sporadic Alzheimer disease (AD). Case–control studies suggest the APOE4 link to AD is... The APOE4 allele is the strongest genetic risk factor for sporadic Alzheimer disease (AD). Case-control studies suggest the APOE4 link to AD is stronger in... Objective The APOE4 allele is the strongest genetic risk factor for sporadic Alzheimer disease (AD). Case-control studies suggest the APOE4 link to AD is... |
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| SubjectTerms | Aged Aged, 80 and over Alzheimer Disease - cerebrospinal fluid Alzheimer Disease - genetics Amyloid beta-Peptides - cerebrospinal fluid Apolipoproteins E - classification Apolipoproteins E - genetics Biomarkers Case-Control Studies Cognitive Dysfunction - genetics Databases, Factual - statistics & numerical data Female Follow-Up Studies Genetic Predisposition to Disease - genetics Genetic Testing Health risk assessment Humans Male Medical research Proportional Hazards Models Risk Factors Sex Factors tau Proteins - cerebrospinal fluid |
| Title | Sex modifies the APOE-related risk of developing Alzheimer disease |
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