SNPs Associated with Cerebrospinal Fluid Phospho-Tau Levels Influence Rate of Decline in Alzheimer's Disease
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{"title"=>"SNPs Associated with Cerebrospinal Fluid Phospho-Tau Levels Influence Rate of Decline in Alzheimer's Disease", "type"=>"journal", "authors"=>[{"first_name"=>"Carlos", "last_name"=>"Cruchaga"}, {"first_name"=>"John S. K.", "last_name"=>"Kauwe"}, {"first_name"=>"Kevin", "last_name"=>"Mayo"}, {"first_name"=>"Noah", "last_name"=>"Spiegel"}, {"first_name"=>"Sarah", "last_name"=>"Bertelsen"}, {"first_name"=>"Petra", "last_name"=>"Nowotny"}, {"first_name"=>"Aarti R.", "last_name"=>"Shah"}, {"first_name"=>"Richard", "last_name"=>"Abraham"}, {"first_name"=>"Paul", "last_name"=>"Hollingworth"}, {"first_name"=>"Denise", "last_name"=>"Harold"}, {"first_name"=>"Michael M.", "last_name"=>"Owen"}, {"first_name"=>"Julie", "last_name"=>"Williams"}, {"first_name"=>"Simon", "last_name"=>"Lovestone"}, {"first_name"=>"Elaine R.", "last_name"=>"Peskind"}, {"first_name"=>"Ge", "last_name"=>"Li"}, {"first_name"=>"James B.", "last_name"=>"Leverenz"}, {"first_name"=>"Douglas", "last_name"=>"Galasko"}, {"first_name"=>"John C.", "last_name"=>"Morris"}, {"first_name"=>"Anne M.", "last_name"=>"Fagan"}, {"first_name"=>"David M.", "last_name"=>"Holtzman"}, {"first_name"=>"Alison M.", "last_name"=>"Goate"}], "year"=>2010, "source"=>"PLoS Genetics", "identifiers"=>{"pmid"=>"20862329", "isbn"=>"1553-7404 (Electronic)\\n1553-7390 (Linking)", "doi"=>"10.1371/journal.pgen.1001101", "issn"=>"1553-7404"}, "id"=>"769db9fc-9ca8-36ae-82c3-d535c6f32ae0", "abstract"=>"Alzheimer's Disease (AD) is a complex and multifactorial disease. While large genome-wide association studies have had some success in identifying novel genetic risk factors for AD, case-control studies are less likely to uncover genetic factors that influence progression of disease. An alternative approach to identifying genetic risk for AD is the use of quantitative traits or endophenotypes. The use of endophenotypes has proven to be an effective strategy, implicating genetic risk factors in several diseases, including anemia, osteoporosis and heart disease. In this study we identify a genetic factor associated with the rate of decline in AD patients and present a methodology for identification of other such factors. We have used an established biomarker for AD, cerebrospinal fluid (CSF) tau phosphorylated at threonine 181 (ptau(181)) levels as an endophenotype for AD, identifying a SNP, rs1868402, in the gene encoding the regulatory sub-unit of protein phosphatase B, associated with CSF ptau(181) levels in two independent CSF series (P(combined) = 1.17 x 10(-05)). We show no association of rs1868402 with risk for AD or age at onset, but detected a very significant association with rate of progression of disease that is consistent in two independent series (P(combined) = 1.17 x 10(-05)). Our analyses suggest that genetic variants associated with CSF ptau(181) levels may have a greater impact on rate of progression, while genetic variants such as APOE4, that are associated with CSF Aβ(42) levels influence risk and onset but not the rate of progression. Our results also suggest that drugs that inhibit or decrease tau phosphorylation may slow cognitive decline in individuals with very mild dementia or delay the appearance of memory problems in elderly individuals with low CSF Aβ(42) levels. Finally, we believe genome-wide association studies of CSF tau/ptau(181) levels should identify novel genetic variants which will likely influence rate of progression of AD.", "link"=>"http://www.mendeley.com/research/snps-associated-cerebrospinal-fluid-phosphotau-levels-influence-rate-decline-alzheimers-disease-5", "reader_count"=>74, "reader_count_by_academic_status"=>{"Unspecified"=>4, "Professor > Associate Professor"=>4, "Researcher"=>24, "Student > Doctoral Student"=>6, "Student > Ph. D. Student"=>15, "Student > Postgraduate"=>1, "Other"=>6, "Student > Master"=>8, "Student > Bachelor"=>4, "Lecturer > Senior Lecturer"=>1, "Professor"=>1}, "reader_count_by_user_role"=>{"Unspecified"=>4, "Professor > Associate Professor"=>4, "Researcher"=>24, "Student > Doctoral Student"=>6, "Student > Ph. D. Student"=>15, "Student > Postgraduate"=>1, "Other"=>6, "Student > Master"=>8, "Student > Bachelor"=>4, "Lecturer > Senior Lecturer"=>1, "Professor"=>1}, "reader_count_by_subject_area"=>{"Unspecified"=>8, "Biochemistry, Genetics and Molecular Biology"=>5, "Nursing and Health Professions"=>1, "Agricultural and Biological Sciences"=>38, "Medicine and Dentistry"=>13, "Neuroscience"=>4, "Pharmacology, Toxicology and Pharmaceutical Science"=>1, "Psychology"=>2, "Computer Science"=>1, "Decision Sciences"=>1}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>13}, "Neuroscience"=>{"Neuroscience"=>4}, "Decision Sciences"=>{"Decision Sciences"=>1}, "Psychology"=>{"Psychology"=>2}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>38}, "Computer Science"=>{"Computer Science"=>1}, "Nursing and Health Professions"=>{"Nursing and Health Professions"=>1}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>5}, "Unspecified"=>{"Unspecified"=>8}, "Pharmacology, Toxicology and Pharmaceutical Science"=>{"Pharmacology, Toxicology and Pharmaceutical Science"=>1}}, "reader_count_by_country"=>{"United States"=>5, "Italy"=>1, "France"=>1, "Germany"=>2, "Spain"=>2}, "group_count"=>1}

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Figshare

  • {"files"=>["https://ndownloader.figshare.com/files/830270"], "description"=>"<p>Rate of progression is defined as the change in the Clinical Dementia Rating sum of boxes (SB-CDR) score per year. Association of SNPs with progression was calculated using a mixed linear model (PROC MIXED) after controlling for age, sex, <i>APOE</i>, <i>initial CDR</i>, CSF ptau<sub>181</sub> and Aβ<sub>42</sub> levels. <b>A</b>. Minor allele carriers of rs1868402, are associated with higher CSF ptau<sub>181</sub> levels, and show a 6 fold faster progression than homozygotes for the major allele (CDR-SB/year: 0.58 vs 0.09; p = 0.0026) in individuals from the WU-ADRC-CSF with low CSF Aβ<sub>42</sub> levels (<500pg/ml). For this SNP the dominant model was used because it showed the best fit in all the analyses. <b>B</b>. rs3785883 genotypes do not have significantly different progression rates <i>P</i> = 0.057. The genotype frequency distribution for rs3785883 with disease progression is most likely not significant due to the low statistical power. AA carriers show a CDR-SB of 1.01, AG of 0.47 and GG 0.26 (p = 0.057). The additive model was used because it showed the best fit. <b>C</b>. Rs1868402 and rs3785883 show an epistatic interaction. Carriers of the alleles associated with higher CSF ptau<sub>181</sub> levels (CT+CC for rs1868402 and AA for 3785883) showed a CDR-SB/year of 1.02 vs −0.006 for carriers of alleles associated with lowest CSF ptau<sub>181</sub> levels. LP indicates lumbar puncture.</p>", "links"=>[], "tags"=>["variants", "csf", "levels", "progression"], "article_id"=>500610, "categories"=>["Neuroscience", "Genetics"], "users"=>["Carlos Cruchaga", "John S. K. Kauwe", "Kevin Mayo", "Noah Spiegel", "Sarah Bertelsen", "Petra Nowotny", "Aarti R. Shah", "Richard Abraham", "Paul Hollingworth", "Denise Harold", "Michael M. Owen", "Julie Williams", "Simon Lovestone", "Elaine R. Peskind", "Ge Li", "James B. Leverenz", "Douglas Galasko", "John C. Morris", "Anne M. Fagan", "David M. Holtzman", "Alison M. Goate"], "doi"=>"https://dx.doi.org/10.1371/journal.pgen.1001101.g003", "stats"=>{"downloads"=>0, "page_views"=>6, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Genetic_variants_associated_with_CSF_ptau_181_levels_are_also_associated_with_rate_of_progression_of_AD_/500610", "title"=>"Genetic variants associated with CSF ptau<sub>181</sub> levels are also associated with rate of progression of AD.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2010-09-16 00:10:10"}
  • {"files"=>["https://ndownloader.figshare.com/files/829975"], "description"=>"<p><b>A</b>. Association of rs1868402 with CSF ptau<sub>181</sub> levels (WU-ADRC-CSF n = 353) was tested by an Analyses of Covariance (ANCOVA) including CDR, age and <i>APOE</i> genotype as covariates. <b>B</b>: Minor allele carriers of rs1868402 have significantly lower <i>PPP3R1</i> mRNA levels in individuals with AD pathology (n = 82). <b>C</b>: Minor allele carriers of rs1868402 have significantly higher numbers of tangles (n = 82). <b>D</b>: <i>PPP3R1</i> mRNA expression correlates with tangle counts in individuals with AD pathological changes (n = 82). The p-value is for the correlation between mRNA levels and genotypes.</p>", "links"=>[], "tags"=>["csf", "mrna", "levels", "tangle"], "article_id"=>500316, "categories"=>["Neuroscience", "Genetics"], "users"=>["Carlos Cruchaga", "John S. K. Kauwe", "Kevin Mayo", "Noah Spiegel", "Sarah Bertelsen", "Petra Nowotny", "Aarti R. Shah", "Richard Abraham", "Paul Hollingworth", "Denise Harold", "Michael M. Owen", "Julie Williams", "Simon Lovestone", "Elaine R. Peskind", "Ge Li", "James B. Leverenz", "Douglas Galasko", "John C. Morris", "Anne M. Fagan", "David M. Holtzman", "Alison M. Goate"], "doi"=>"https://dx.doi.org/10.1371/journal.pgen.1001101.g001", "stats"=>{"downloads"=>1, "page_views"=>7, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Rs1868402_is_associated_with_CSF_ptau_181_levels_PPP3R1_mRNA_expression_levels_and_tangle_counts_/500316", "title"=>"Rs1868402 is associated with CSF ptau<sub>181</sub> levels, <i>PPP3R1</i> mRNA expression levels and tangle counts.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2010-09-16 00:05:16"}
  • {"files"=>["https://ndownloader.figshare.com/files/413158", "https://ndownloader.figshare.com/files/413192", "https://ndownloader.figshare.com/files/413226", "https://ndownloader.figshare.com/files/413261", "https://ndownloader.figshare.com/files/413303"], "description"=>"<div><p>Alzheimer's Disease (AD) is a complex and multifactorial disease. While large genome-wide association studies have had some success in identifying novel genetic risk factors for AD, case-control studies are less likely to uncover genetic factors that influence progression of disease. An alternative approach to identifying genetic risk for AD is the use of quantitative traits or endophenotypes. The use of endophenotypes has proven to be an effective strategy, implicating genetic risk factors in several diseases, including anemia, osteoporosis and heart disease. In this study we identify a genetic factor associated with the rate of decline in AD patients and present a methodology for identification of other such factors. We have used an established biomarker for AD, cerebrospinal fluid (CSF) tau phosphorylated at threonine 181 (ptau<sub>181</sub>) levels as an endophenotype for AD, identifying a SNP, rs1868402, in the gene encoding the regulatory sub-unit of protein phosphatase B, associated with CSF ptau<sub>181</sub> levels in two independent CSF series . We show no association of rs1868402 with risk for AD or age at onset, but detected a very significant association with rate of progression of disease that is consistent in two independent series . Our analyses suggest that genetic variants associated with CSF ptau<sub>181</sub> levels may have a greater impact on rate of progression, while genetic variants such as <em>APOE4</em>, that are associated with CSF Aβ<sub>42</sub> levels influence risk and onset but not the rate of progression. Our results also suggest that drugs that inhibit or decrease tau phosphorylation may slow cognitive decline in individuals with very mild dementia or delay the appearance of memory problems in elderly individuals with low CSF Aβ<sub>42</sub> levels. Finally, we believe genome-wide association studies of CSF tau/ptau<sub>181</sub> levels should identify novel genetic variants which will likely influence rate of progression of AD.</p></div>", "links"=>[], "tags"=>["snps", "cerebrospinal", "phospho-tau", "levels"], "article_id"=>141611, "categories"=>["Neuroscience", "Genetics"], "users"=>["Carlos Cruchaga", "John S. K. Kauwe", "Kevin Mayo", "Noah Spiegel", "Sarah Bertelsen", "Petra Nowotny", "Aarti R. Shah", "Richard Abraham", "Paul Hollingworth", "Denise Harold", "Michael M. Owen", "Julie Williams", "Simon Lovestone", "Elaine R. Peskind", "Ge Li", "James B. Leverenz", "Douglas Galasko", "John C. Morris", "Anne M. Fagan", "David M. Holtzman", "Alison M. Goate"], "doi"=>["https://dx.doi.org/10.1371/journal.pgen.1001101.s001", "https://dx.doi.org/10.1371/journal.pgen.1001101.s002", "https://dx.doi.org/10.1371/journal.pgen.1001101.s003", "https://dx.doi.org/10.1371/journal.pgen.1001101.s004", "https://dx.doi.org/10.1371/journal.pgen.1001101.s005"], "stats"=>{"downloads"=>28, "page_views"=>35, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/SNPs_Associated_with_Cerebrospinal_Fluid_Phospho_Tau_Levels_Influence_Rate_of_Decline_in_Alzheimer_s_Disease/141611", "title"=>"SNPs Associated with Cerebrospinal Fluid Phospho-Tau Levels Influence Rate of Decline in Alzheimer's Disease", "pos_in_sequence"=>0, "defined_type"=>4, "published_date"=>"2010-09-16 00:26:51"}
  • {"files"=>["https://ndownloader.figshare.com/files/830179"], "description"=>"<p>Survival fractions were calculated using the Kaplan-Meier method and significant differences were calculated by Log-rank test. Association with age at onset was calculated in a combined series with samples from WU-ADRC-CC, ADNI-CC and MRC.</p>", "links"=>[], "tags"=>["curves", "comparing", "onset", "genotypes"], "article_id"=>500524, "categories"=>["Neuroscience", "Genetics"], "users"=>["Carlos Cruchaga", "John S. K. Kauwe", "Kevin Mayo", "Noah Spiegel", "Sarah Bertelsen", "Petra Nowotny", "Aarti R. Shah", "Richard Abraham", "Paul Hollingworth", "Denise Harold", "Michael M. Owen", "Julie Williams", "Simon Lovestone", "Elaine R. Peskind", "Ge Li", "James B. Leverenz", "Douglas Galasko", "John C. Morris", "Anne M. Fagan", "David M. Holtzman", "Alison M. Goate"], "doi"=>"https://dx.doi.org/10.1371/journal.pgen.1001101.g002", "stats"=>{"downloads"=>0, "page_views"=>1, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Survival_curves_comparing_age_at_onset_of_LOAD_between_the_different_genotypes_of_rs1868402_/500524", "title"=>"Survival curves comparing age at onset of LOAD between the different genotypes of rs1868402.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2010-09-16 00:08:44"}
  • {"files"=>["https://ndownloader.figshare.com/files/830579"], "description"=>"<p>The p-value and the OR for rs1868402 were calculated by comparing the rs1868402 allele frequency in the lowest quartile vs the highest quartile of CSF ptau<sub>181</sub> levels, after correction for covariates in the WU-ADRC-CSF (n = 353)+ADNI-CSF (n = 266) samples. CSF Samples from the UW could not be included in this analysis because there is no study analyzing the correlation between the CSF Aβ<sub>42</sub> levels and PET-PIB signal in this dataset, and therefore the threshold of CSF Aβ<sub>42</sub> levels for PIB positivity is unknown. OR (95%) = Odds ratio with the 95% confidence interval: Odds ratios were calculated comparing the highest vs lowest quartile of CSF ptau<sub>181</sub> levels. Samples were stratified based on CSF Aβ<sub>42</sub> levels as an approximation of Aβ deposition. For the ADRC samples individuals with Aβ<sub>42</sub> levels less than 500 pg/ml were considered positive for Aβ deposition and for ADNI samples the Aβ<sub>42</sub> cutoff value of 192 pg/ml was used.</p><p>Values in boldface indicate significant p-values.</p>A<p>Dominant model.</p>B<p>effects and the standard error of the mean are given in units of standard deviation.</p>", "links"=>[], "tags"=>["1868402", "csf", "levels", "individuals"], "article_id"=>500915, "categories"=>["Neuroscience", "Genetics"], "users"=>["Carlos Cruchaga", "John S. K. Kauwe", "Kevin Mayo", "Noah Spiegel", "Sarah Bertelsen", "Petra Nowotny", "Aarti R. Shah", "Richard Abraham", "Paul Hollingworth", "Denise Harold", "Michael M. Owen", "Julie Williams", "Simon Lovestone", "Elaine R. Peskind", "Ge Li", "James B. Leverenz", "Douglas Galasko", "John C. Morris", "Anne M. Fagan", "David M. Holtzman", "Alison M. Goate"], "doi"=>"https://dx.doi.org/10.1371/journal.pgen.1001101.t004", "stats"=>{"downloads"=>7, "page_views"=>7, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Rs_1868402_is_associated_with_CSF_ptau_181_levels_in_individuals_with_A_946_deposition_/500915", "title"=>"Rs 1868402 is associated with CSF ptau<sub>181</sub> levels in individuals with Aβ deposition.", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2010-09-16 00:15:15"}
  • {"files"=>["https://ndownloader.figshare.com/files/830443"], "description"=>"<p>CSF Aß<sub>42</sub>, tau and ptau<sub>181</sub> levels for the Washington University Alzheimer's Disease Reseach Center (ADRC), Alzheimer's Disease Neuroimaging Initiative (ADNI) and for the University of Washington, Seattle (UW). For each phenotype the mean in pg/ml with the standard deviation and range is shown.</p>", "links"=>[], "tags"=>["biomarker"], "article_id"=>500788, "categories"=>["Neuroscience", "Genetics"], "users"=>["Carlos Cruchaga", "John S. K. Kauwe", "Kevin Mayo", "Noah Spiegel", "Sarah Bertelsen", "Petra Nowotny", "Aarti R. Shah", "Richard Abraham", "Paul Hollingworth", "Denise Harold", "Michael M. Owen", "Julie Williams", "Simon Lovestone", "Elaine R. Peskind", "Ge Li", "James B. Leverenz", "Douglas Galasko", "John C. Morris", "Anne M. Fagan", "David M. Holtzman", "Alison M. Goate"], "doi"=>"https://dx.doi.org/10.1371/journal.pgen.1001101.t002", "stats"=>{"downloads"=>1, "page_views"=>6, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Summary_of_biomarker_characteristics_/500788", "title"=>"Summary of biomarker characteristics.", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2010-09-16 00:13:08"}
  • {"files"=>["https://ndownloader.figshare.com/files/830503"], "description"=>"<p>NPs that passed FDR correction in the WU-ADRC-CSF series were followed up in a replication series composed of CSF samples from ADNI-CSF and UW. Both series (WU-ADRC-CSF and Replication) were combined to increase the statistical power. In the WU-ADRC-CSF and replication series; p-values in bold denote values that are significant after FDR correction. In the Combined Series we applied Bonferroni correction. Threshold for Bonferroni correction is 1.3×10<sup>−04</sup>.</p><p>For each SNP the rs number and P values for association with ptau<sub>181</sub> before and after FDR correction are shown.</p>A<p>Dominant model.</p>B<p>Recessive model.</p>C<p>effects and the standard error of the mean are given in units of standard deviation.</p>", "links"=>[], "tags"=>["csf", "levels", "replication"], "article_id"=>500853, "categories"=>["Neuroscience", "Genetics"], "users"=>["Carlos Cruchaga", "John S. K. Kauwe", "Kevin Mayo", "Noah Spiegel", "Sarah Bertelsen", "Petra Nowotny", "Aarti R. Shah", "Richard Abraham", "Paul Hollingworth", "Denise Harold", "Michael M. Owen", "Julie Williams", "Simon Lovestone", "Elaine R. Peskind", "Ge Li", "James B. Leverenz", "Douglas Galasko", "John C. Morris", "Anne M. Fagan", "David M. Holtzman", "Alison M. Goate"], "doi"=>"https://dx.doi.org/10.1371/journal.pgen.1001101.t003", "stats"=>{"downloads"=>1, "page_views"=>3, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_SNPs_associated_with_CSF_ptau_181_levels_in_the_initial_series_the_replication_series_and_the_combined_dataset_/500853", "title"=>"SNPs associated with CSF ptau<sub>181</sub> levels in the initial series, the replication series and the combined dataset.", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2010-09-16 00:14:13"}
  • {"files"=>["https://ndownloader.figshare.com/files/830707"], "description"=>"<p>Rs1868402 is associated with progression rate and shows epistasis with rs3785883, which is also associated with CSF tau levels <a href=\"http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1001101#pgen.1001101-Kauwe1\" target=\"_blank\">[27]</a>.</p><p>Rate of progression were analyzed by the change of the Clinical Dementia Rating sum of boxes (CDR-SB) score per year in individuals with low CSF Aβ<sub>42</sub> levels (ADRC<500pg/ml; ADNI<192pg/ml) and in samples with no CSF data. Association of SNPs with progression was calculated with mixed linear models (proc mixed) after controlling for age, sex, <i>APOE</i>, CDR and/or CSF ptau<sub>181</sub> and Aβ<sub>42</sub>.</p>", "links"=>[], "tags"=>["genetics and genomics/complex traits", "genetics and genomics/genetics of disease", "neurological disorders/alzheimer disease", "neurological disorders/neurogenetics"], "article_id"=>501046, "categories"=>["Neuroscience", "Genetics"], "users"=>["Carlos Cruchaga", "John S. K. Kauwe", "Kevin Mayo", "Noah Spiegel", "Sarah Bertelsen", "Petra Nowotny", "Aarti R. Shah", "Richard Abraham", "Paul Hollingworth", "Denise Harold", "Michael M. Owen", "Julie Williams", "Simon Lovestone", "Elaine R. Peskind", "Ge Li", "James B. Leverenz", "Douglas Galasko", "John C. Morris", "Anne M. Fagan", "David M. Holtzman", "Alison M. Goate"], "doi"=>"https://dx.doi.org/10.1371/journal.pgen.1001101.t006", "stats"=>{"downloads"=>1, "page_views"=>2, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Association_with_rate_of_disease_progression_/501046", "title"=>"Association with rate of disease progression.", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2010-09-16 00:17:26"}
  • {"files"=>["https://ndownloader.figshare.com/files/830640"], "description"=>"<p>rs1868402 was genotyped in the MRC, WU-ADRC-CC and ADNI-CC series. Number of cases and controls, minor allele and minor allele frequency (MAF) for each series and for the combined series are showed. P-value for the dominant (rs1868402) model were calculated by logistic regression including <i>APOE</i>, age, gender and series as covariates.</p>", "links"=>[], "tags"=>["genetics and genomics/complex traits", "genetics and genomics/genetics of disease", "neurological disorders/alzheimer disease", "neurological disorders/neurogenetics"], "article_id"=>500984, "categories"=>["Neuroscience", "Genetics"], "users"=>["Carlos Cruchaga", "John S. K. Kauwe", "Kevin Mayo", "Noah Spiegel", "Sarah Bertelsen", "Petra Nowotny", "Aarti R. Shah", "Richard Abraham", "Paul Hollingworth", "Denise Harold", "Michael M. Owen", "Julie Williams", "Simon Lovestone", "Elaine R. Peskind", "Ge Li", "James B. Leverenz", "Douglas Galasko", "John C. Morris", "Anne M. Fagan", "David M. Holtzman", "Alison M. Goate"], "doi"=>"https://dx.doi.org/10.1371/journal.pgen.1001101.t005", "stats"=>{"downloads"=>0, "page_views"=>8, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Rs1868402_is_not_associated_with_risk_for_AD_/500984", "title"=>"Rs1868402 is not associated with risk for AD.", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2010-09-16 00:16:24"}
  • {"files"=>["https://ndownloader.figshare.com/files/830381"], "description"=>"<p>Sample size (n), age, percentage of males, percentage of <i>APOE4</i> allele carriers, and clinical dementia rating (CDR) for each sample. For the cases age at onset is shown and for controls the age at last assessment.</p><p>Washington University Alzheimer's Disease Research Center (ADRC), Alzheimer's Disease Neuroimaging Initiative (ADNI) and for the University of Washington, Seattle (UW). Cerebrospinal Fluid (CSF). Case-control (CC).</p>", "links"=>[], "tags"=>["genetics and genomics/complex traits", "genetics and genomics/genetics of disease", "neurological disorders/alzheimer disease", "neurological disorders/neurogenetics"], "article_id"=>500732, "categories"=>["Neuroscience", "Genetics"], "users"=>["Carlos Cruchaga", "John S. K. Kauwe", "Kevin Mayo", "Noah Spiegel", "Sarah Bertelsen", "Petra Nowotny", "Aarti R. Shah", "Richard Abraham", "Paul Hollingworth", "Denise Harold", "Michael M. Owen", "Julie Williams", "Simon Lovestone", "Elaine R. Peskind", "Ge Li", "James B. Leverenz", "Douglas Galasko", "John C. Morris", "Anne M. Fagan", "David M. Holtzman", "Alison M. Goate"], "doi"=>"https://dx.doi.org/10.1371/journal.pgen.1001101.t001", "stats"=>{"downloads"=>0, "page_views"=>3, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Summary_of_sample_characteristics_/500732", "title"=>"Summary of sample characteristics.", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2010-09-16 00:12:12"}
  • {"files"=>["https://ndownloader.figshare.com/files/830766"], "description"=>"<p>P-values for the association of rs1868402 (<i>PPP3R1</i>) and <i>APOE4</i> with CSF Aß<sub>42</sub> and ptau<sub>181</sub> levels, risk for AD, age at onset and disease progression are shown.</p><p>*Sample size = 846; WU-ADRC-CSF+ADNI-CSF+UW.</p><p>**Sample size = 2322 MRC+WU ADRC-CC+ADNI-CC.</p><p>***Sample size<b> = 259</b>; WU-ADRC-CSF+ADNI-CSF with low CSF Aβ<sub>42</sub> levels.</p><p>Significant p-values are in bold.</p>", "links"=>[], "tags"=>["csf", "levels", "variants"], "article_id"=>501117, "categories"=>["Neuroscience", "Genetics"], "users"=>["Carlos Cruchaga", "John S. K. Kauwe", "Kevin Mayo", "Noah Spiegel", "Sarah Bertelsen", "Petra Nowotny", "Aarti R. Shah", "Richard Abraham", "Paul Hollingworth", "Denise Harold", "Michael M. Owen", "Julie Williams", "Simon Lovestone", "Elaine R. Peskind", "Ge Li", "James B. Leverenz", "Douglas Galasko", "John C. Morris", "Anne M. Fagan", "David M. Holtzman", "Alison M. Goate"], "doi"=>"https://dx.doi.org/10.1371/journal.pgen.1001101.t007", "stats"=>{"downloads"=>4, "page_views"=>5, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Variants_that_modify_CSF_A_42_levels_affect_risk_for_AD_whereas_variants_associated_with_CSF_ptau_181_levels_affect_rate_of_progression_/501117", "title"=>"Variants that modify CSF Aβ<sub>42</sub> levels affect risk for AD, whereas variants associated with CSF ptau<sub>181</sub> levels affect rate of progression.", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2010-09-16 00:18:37"}

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Relative Metric

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