31 results on '"Jager, Philip L De"'
Search Results
2. Association of whole-person eigen-polygenic risk scores with Alzheimer's disease.
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Kharaghani, Amin, Tio, Earvin S, Milic, Milos, Bennett, David A, Jager, Philip L De, Schneider, Julie A, Sun, Lei, and Felsky, Daniel
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- 2024
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3. Not all roads lead to the immune system: the genetic basis of multiple sclerosis severity.
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Jokubaitis, Vilija G, Campagna, Maria Pia, Ibrahim, Omar, Stankovich, Jim, Kleinova, Pavlina, Matesanz, Fuencisla, Hui, Daniel, Eichau, Sara, Slee, Mark, Lechner-Scott, Jeannette, Lea, Rodney, Kilpatrick, Trevor J, Kalincik, Tomas, Jager, Philip L De, Beecham, Ashley, McCauley, Jacob L, Taylor, Bruce V, Vucic, Steve, Laverick, Louise, and Vodehnalova, Karolina
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MULTIPLE sclerosis ,DELAYED onset of disease ,SINGLE nucleotide polymorphisms ,MACHINE learning ,MEDICAL registries ,GENOME-wide association studies ,IMMUNE system - Abstract
Multiple sclerosis is a leading cause of neurological disability in adults. Heterogeneity in multiple sclerosis clinical presentation has posed a major challenge for identifying genetic variants associated with disease outcomes. To overcome this challenge, we used prospectively ascertained clinical outcomes data from the largest international multiple sclerosis Registry, MSBase. We assembled a cohort of deeply phenotyped individuals of European ancestry with relapse-onset multiple sclerosis. We used unbiased genome-wide association study and machine learning approaches to assess the genetic contribution to longitudinally defined multiple sclerosis severity phenotypes in 1,813 individuals. Our primary analyses did not identify any genetic variants of moderate to large effect sizes that met genome-wide significance thresholds. The strongest signal was associated with rs7289446 (β=-0.4882, P = 2.73 × 10-7), intronic to SEZ6L on chromosome 22. However, we demonstrate that clinical outcomes in relapse-onset multiple sclerosis are associated with multiple genetic loci of small effect sizes. Using a machine learning approach incorporating over 62,000 variants together with clinical and demographic variables available at multiple sclerosis disease onset, we could predict severity with an area under the receiver operator curve of 0.84 (95% CI 0.79-0.88). Our machine learning algorithm achieved positive predictive value for outcome assignation of 80% and negative predictive value of 88%. This outperformed our machine learning algorithm that contained clinical and demographic variables alone (area under the receiver operator curve 0.54, 95% CI 0.48-0.60). Secondary, sex-stratified analyses identified two genetic loci that met genome-wide significance thresholds. One in females (rs10967273; βfemale =0.8289, P = 3.52 × 10-08), the other in males (rs698805; βmale = -1.5395, P = 4.35 × 10-08), providing some evidence for sex dimorphism in multiple sclerosis severity. Tissue enrichment and pathway analyses identified an overrepresentation of genes expressed in central nervous system compartments generally, and specifically in the cerebellum (P = 0.023). These involved mitochondrial function, synaptic plasticity, oligodendroglial biology, cellular senescence, calcium and g-protein receptor signalling pathways. We further identified six variants with strong evidence for regulating clinical outcomes, the strongest signal again intronic to SEZ6L (adjusted hazard ratio 0.72, P = 4.85 × 10-4). Here we report a milestone in our progress towards understanding the clinical heterogeneity of multiple sclerosis outcomes, implicating functionally distinct mechanisms to multiple sclerosis risk. Importantly, we demonstrate that machine learning using common single nucleotide variant clusters, together with clinical variables readily available at diagnosis can improve prognostic capabilities at diagnosis, and with further validation has the potential to translate to meaningful clinical practice change. [ABSTRACT FROM AUTHOR]
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- 2023
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4. 5'RNA-Seq identifies Fhl1 as a genetic modifier in cardiomyopathy
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Christodoulou, Danos C., Wakimoto, Hiroko, Onoue, Kenji, Eminaga, Seda, Gorham, Joshua M., DePalma, Steve R., Herman, Daniel S., Teekakirikul, Polakit, Conner, David A., McKean, David M., Domenighetti, Andrea A., Aboukhalil, Anton, Chang, Stephen, Srivastava, Gyan, McDonough, Barbara, Jager, Philip L. De, Chen, Ju, Bulyk, Martha L., Muehlschlegel, Jochen D., Seidman, Christine E., and Seidman, J.G.
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Heart diseases -- Genetic aspects ,Gene mutations -- Identification and classification ,RNA sequencing -- Methods ,Cardiomyopathy -- Genetic aspects ,Health care industry - Abstract
The transcriptome is subject to multiple changes during pathogenesis, including the use of alternate 5' start-sites that can affect transcription levels and output. Current RNA sequencing techniques can assess mRNA levels, but do not robustly detect changes in 5' start-site use. Here, we developed a transcriptome sequencing strategy that detects genome-wide changes in start-site usage (5'RNA-Seq) and applied this methodology to identify regulatory events that occur in hypertrophic cardiomyopathy (HCM). Compared with transcripts from WT mice, 92 genes had altered start-site usage in a mouse model of HCM, including four-and-a-half LIM domains protein 1 (Fhl1). HCM-induced altered transcriptional regulation of Fhl1 resulted in robust myocyte expression of a distinct protein isoform, a response that was conserved in humans with genetic or acquired cardiomyopathies. Genetic ablation of Fhl1 in HCM mice was deleterious, which suggests that Fhl1 transcriptional changes provide salutary effects on stressed myocytes in this disease. Because Fhl1 is a chromosome X--encoded gene, stress-induced changes in its transcription may contribute to gender differences in the clinical severity of HCM. Our findings indicate that 5'RNA-Seq has the potential to identify genome-wide changes in 5' start-site usage that are associated with pathogenic phenotypes., Introduction Pathogenic mutations produce broad changes in cell biology, in part by affecting gene expression. Changes in gene expression include altering transcription levels and/or diversifying the transcriptome through alternative use [...]
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- 2014
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5. Additional file 1 of Genome-wide epistasis analysis for Alzheimer’s disease and implications for genetic risk prediction
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Wang, Hui, Bennett, David A., Jager, Philip L. De, Zhang, Qing-Ye, and Zhang, Hong-Yu
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Additional file 1: Figure S1. GWAS analysis of selected SNPs (N = 10389, SNPs = 36860). Figure S2. Visualization of SNP-SNP interactions. Figure S3. Performance of epistasis risk scores (ERSs), polygenic risk scores (PRSs) and combined risk scores (CRSs) in AD risk prediction using samples from ROS/MAP. Figure S4. Epistasis risk scores (ERSs) analysis after removing genetic interactions that showed main effects (P < 0.05) using samples from ADNI and ROS/MAP. Figure S5. Associations between PRSs (polygenic risk scores constructed by APOE, i.e., rs7412 and rs429358 and 20 SNPs identified by previous GWAS) and Alzheimer’s disease pathologies.
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- 2021
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6. Meta-analysis of epigenome-wide association studies in Alzheimer’s disease highlights 220 differentially methylated loci across cortex
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Smith, Rebecca G., Pishva, Ehsan, Shireby, Gemma, Smith, Adam R., Roubroeks, Janou A.Y., Hannon, Eilis, Wheildon, Gregory, Mastroeni, Diego, Gasparoni, Gilles, Riemenschneider, Matthias, Giese, Armin, Sharp, Andrew J., Schalkwyk, Leonard, Haroutunian, Vahram, Viechtbauer, Wolfgang, van den Hove, Daniel L.A., Weedon, Michael, Walter, Jörn, Coleman, Paul D., Bennett, David A., Jager, Philip L. De, Mill, Jonathan, and Lunnon, Katie
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Epigenome-wide association studies of Alzheimer’s disease have highlighted neuropathology-associated DNA methylation differences, although existing studies have been limited in sample size and utilized different brain regions. Here, we combine data from six methylomic studies of Alzheimer’s disease (N=1,453 unique individuals) to identify differential methylation associated with Braak stage in different brain regions and across cortex. At an experiment-wide significance threshold (P
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- 2020
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7. MSJ958362_supplemental_material – Supplemental material for Classifying multiple sclerosis patients on the basis of SDMT performance using machine learning
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Buyukturkoglu, Korhan, Zeng, Dana, Srinidhi Bharadwaj, Tozlu, Ceren, Enricomaria Mormina, Igwe, Kay C, Seonjoo Lee, Habeck, Christian, Brickman, Adam M, Riley, Claire S, Jager, Philip L De, Sumowski, James F, and Leavitt, Victoria M
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FOS: Clinical medicine ,111702 Aged Health Care ,FOS: Health sciences ,110904 Neurology and Neuromuscular Diseases - Abstract
Supplemental material, MSJ958362_supplemental_material for Classifying multiple sclerosis patients on the basis of SDMT performance using machine learning by Korhan Buyukturkoglu, Dana Zeng, Srinidhi Bharadwaj, Ceren Tozlu, Enricomaria Mormina, Kay C Igwe, Seonjoo Lee, Christian Habeck, Adam M Brickman, Claire S Riley, Philip L De Jager, James F Sumowski and Victoria M Leavitt in Multiple Sclerosis Journal
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- 2020
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8. Additional file 1 of Integrated analysis of the aging brain transcriptome and proteome in tauopathy
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Mangleburg, Carl Grant, Wu, Timothy, Yalamanchili, Hari K., Caiwei Guo, Hsieh, Yi-Chen, Duong, Duc M., Dammer, Eric B., Jager, Philip L. De, Seyfried, Nicholas T., Zhandong Liu, and Shulman, Joshua M.
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Additional file 1: Supplemental Figures. Figure S1. Expression of TauWT and TauR406W in transgenic flies. Figure S2. Venn diagrams showing overlaps in differential expressed genes. Figure S3. Potential impact of missingness on proteome analyses. Figure S4. Reverse transcription-quantitative PCR validation of differentially expressed genes. Figure S5. Western blot validation of differentially expressed genes from LC-MS/MS proteomics. Figure S6. Age and Tau are major drivers of gene expression differences among samples. Figure S7. TauWT-triggered differential expression in the transcriptome vs. proteome. Figure S8. Additional examples of differentially expressed transcripts and proteins in TauR406W flies. Figure S9. Overlap between TauR406W- and aging-induced gene expression changes. Figure S10. Weighted gene coexpression network analysis in TauR406W flies. Figure S11. Integration of Tau-induced transcriptome and proteome changes in gene expression clusters. Figure S12. Non-negative matrix factorization rank survey for unsupervised hierarchical clustering. Figure S13. WGCNA cluster dendrograms.
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- 2020
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9. Additional file 6 of BIN1 protein isoforms are differentially expressed in astrocytes, neurons, and microglia: neuronal and astrocyte BIN1 are implicated in tau pathology
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Taga, Mariko, Petyuk, Vladislav A., White, Charles, Marsh, Galina, Yiyi Ma, Hans-Ulrich Klein, Connor, Sarah M., Kroshilina, Alexandra, Yung, Christina J., Khairallah, Anthony, Olah, Marta, Schneider, Julie, Karhohs, Kyle, Carpenter, Anne E., Ransohoff, Richard, Bennett, David A., Crotti, Andrea, Bradshaw, Elizabeth M., and Jager, Philip L. De
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Data_FILES - Abstract
Additional file 6.
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- 2020
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10. Association between DNA Methylation Levels in Brain Tissue and Late-Life Depression in Community-Based Participants
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Hüls, Anke, primary, Robins, Chloe, additional, Conneely, Karen N., additional, Jager, Philip L. De, additional, Bennett, David A., additional, Epstein, Michael P., additional, Wingo, Thomas S., additional, and Wingo, Aliza P., additional
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- 2020
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11. Genetic control of the human brain proteome
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Robins, Chloe, primary, Wingo, Aliza P., additional, Fan, Wen, additional, Duong, Duc M., additional, Meigs, Jacob, additional, Gerasimov, Ekaterina S., additional, Dammer, Eric B., additional, Cutler, David J., additional, Jager, Philip L. De, additional, Bennett, David A., additional, Lah, James J., additional, Levey, Allan I., additional, Seyfried, Nicholas T., additional, and Wingo, Thomas S., additional
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- 2019
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12. Brain microRNAs associated with late-life depressive symptoms are also associated with cognitive trajectory and dementia
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Wingo, Thomas S., primary, Yang, Jingjing, additional, Fan, Wen, additional, Logsdon, Benjamin, additional, Canon, Se Min, additional, Yao, Bing, additional, Seyfried, Nicholas T., additional, Lah, James J., additional, Levey, Allan I, additional, Boyle, Patricia A., additional, Schneider, Julia A., additional, Jager, Philip L. De, additional, Bennett, David A., additional, and Wingo, Aliza P., additional
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- 2019
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13. Deconvolving the contributions of cell-type heterogeneity on cortical gene expression
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Patrick, Ellis, primary, Taga, Mariko, additional, Ergun, Ayla, additional, Ng, Bernard, additional, Casazza, William, additional, Cimpean, Maria, additional, Yung, Christina, additional, Schneider, Julie A, additional, Bennett, David A, additional, Gaiteri, Chris, additional, Jager, Philip L De, additional, Bradshaw, Elizabeth M, additional, and Mostafavi, Sara, additional
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- 2019
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14. Ninety-nine independent genetic loci influencing general cognitive function include genes associated with brain health and structure (N = 280,360)
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Davies, Gail, primary, Lam, Max, additional, Harris, Sarah E, additional, Trampush, Joey W, additional, Luciano, Michelle, additional, Hill, W David, additional, Hagenaars, Saskia P, additional, Ritchie, Stuart J, additional, Marioni, Riccardo E, additional, Fawns-Ritchie, Chloe, additional, Liewald, David CM, additional, Okely, Judith A, additional, Ahola-Olli, Ari V, additional, Barnes, Catriona LK, additional, Bertram, Lars, additional, Bis, Joshua C, additional, Burdick, Katherine E, additional, Christoforou, Andrea, additional, DeRosse, Pamela, additional, Djurovic, Srdjan, additional, Espeseth, Thomas, additional, Giakoumaki, Stella, additional, Giddaluru, Sudheer, additional, Gustavson, Daniel E, additional, Hayward, Caroline, additional, Hofer, Edith, additional, Ikram, M Arfan, additional, Karlsson, Robert, additional, Knowles, Emma, additional, Lahti, Jari, additional, Leber, Markus, additional, Li, Shuo, additional, Mather, Karen A, additional, Melle, Ingrid, additional, Morris, Derek, additional, Oldmeadow, Christopher, additional, Palviainen, Teemu, additional, Payton, Antony, additional, Pazoki, Raha, additional, Petrovic, Katja, additional, Reynolds, Chandra A, additional, Sargurupremraj, Muralidharan, additional, Scholz, Markus, additional, Smith, Jennifer A, additional, Smith, Albert V, additional, Terzikhan, Natalie, additional, Thalamuthu, Anbu, additional, Trompet, Stella, additional, Lee, Sven J van der, additional, Ware, Erin B, additional, Windham, B Gwen, additional, Wright, Margaret J, additional, Yang, Jingyun, additional, Yu, Jin, additional, Ames, David, additional, Amin, Najaf, additional, Amouyel, Philippe, additional, Andreassen, Ole A, additional, Armstrong, Nicola J, additional, Assareh, Amelia A, additional, Attia, John R, additional, Attix, Deborah, additional, Avramopoulos, Dimitrios, additional, Bennett, David A, additional, Böhmer, Anne C, additional, Boyle, Patricia A, additional, Brodaty, Henry, additional, Campbell, Harry, additional, Cannon, Tyrone D, additional, Cirulli, Elizabeth T, additional, Congdon, Eliza, additional, Conley, Emily Drabant, additional, Corley, Janie, additional, Cox, Simon R, additional, Dale, Anders M, additional, Dehghan, Abbas, additional, Dick, Danielle, additional, Dickinson, Dwight, additional, Eriksson, Johan G, additional, Evangelou, Evangelos, additional, Faul, Jessica D, additional, Ford, Ian, additional, Freimer, Nelson A, additional, Gao, He, additional, Giegling, Ina, additional, Gillespie, Nathan A, additional, Gordon, Scott D, additional, Gottesman, Rebecca F, additional, Griswold, Michael E, additional, Gudnason, Vilmundur, additional, Harris, Tamara B, additional, Hartmann, Annette M, additional, Hatzimanolis, Alex, additional, Heiss, Gerardo, additional, Holliday, Elizabeth G, additional, Joshi, Peter K, additional, Kähönen, Mika, additional, Kardia, Sharon LR, additional, Karlsson, Ida, additional, Kleineidam, Luca, additional, Knopman, David S, additional, Kochan, Nicole A, additional, Konte, Bettina, additional, Kwok, John B, additional, Hellard, Stephanie Le, additional, Lee, Teresa, additional, Lehtimäki, Terho, additional, Li, Shu-Chen, additional, Liu, Tian, additional, Koini, Marisa, additional, London, Edythe, additional, Longstreth, Will T, additional, Lopez, Oscar L, additional, Loukola, Anu, additional, Luck, Tobias, additional, Lundervold, Astri J, additional, Lundquist, Anders, additional, Lyytikäinen, Leo-Pekka, additional, Martin, Nicholas G, additional, Montgomery, Grant W, additional, Murray, Alison D, additional, Need, Anna C, additional, Noordam, Raymond, additional, Nyberg, Lars, additional, Ollier, William, additional, Papenberg, Goran, additional, Pattie, Alison, additional, Polasek, Ozren, additional, Poldrack, Russell A, additional, Psaty, Bruce M, additional, Reppermund, Simone, additional, Riedel-Heller, Steffi G, additional, Rose, Richard J, additional, Rotter, Jerome I, additional, Roussos, Panos, additional, Rovio, Suvi P, additional, Saba, Yasaman, additional, Sabb, Fred W, additional, Sachdev, Perminder S, additional, Satizabal, Claudia, additional, Schmid, Matthias, additional, Scott, Rodney J, additional, Scult, Matthew A, additional, Simino, Jeannette, additional, Slagboom, P Eline, additional, Smyrnis, Nikolaos, additional, Soumaré, Aïcha, additional, Stefanis, Nikos C, additional, Stott, David J, additional, Straub, Richard E, additional, Sundet, Kjetil, additional, Taylor, Adele M, additional, Taylor, Kent D, additional, Tzoulaki, Ioanna, additional, Tzourio, Christophe, additional, Uitterlinden, André, additional, Vitart, Veronique, additional, Voineskos, Aristotle N, additional, Kaprio, Jaakko, additional, Wagner, Michael, additional, Wagner, Holger, additional, Weinhold, Leonie, additional, Wen, K Hoyan, additional, Widen, Elisabeth, additional, Yang, Qiong, additional, Zhao, Wei, additional, Adams, Hieab HH, additional, Arking, Dan E, additional, Bilder, Robert M, additional, Bitsios, Panos, additional, Boerwinkle, Eric, additional, Chiba-Falek, Ornit, additional, Corvin, Aiden, additional, Jager, Philip L De, additional, Debette, Stéphanie, additional, Donohoe, Gary, additional, Elliott, Paul, additional, Fitzpatrick, Annette L, additional, Gill, Michael, additional, Glahn, David C, additional, Hägg, Sara, additional, Hansell, Narelle K, additional, Hariri, Ahmad R, additional, Ikram, M Kamran, additional, Jukema, J. Wouter, additional, Vuoksimaa, Eero, additional, Keller, Matthew C, additional, Kremen, William S, additional, Launer, Lenore, additional, Lindenberger, Ulman, additional, Palotie, Aarno, additional, Pedersen, Nancy L, additional, Pendleton, Neil, additional, Porteous, David J, additional, Räikkönen, Katri, additional, Raitakari, Olli T, additional, Ramirez, Alfredo, additional, Reinvang, Ivar, additional, Rudan, Igor, additional, Rujescu, Dan, additional, Schmidt, Reinhold, additional, Schmidt, Helena, additional, Schofield, Peter W, additional, Schofield, Peter R, additional, Starr, John M, additional, Steen, Vidar M, additional, Trollor, Julian N, additional, Turner, Steven T, additional, Duijn, Cornelia M Van, additional, Villringer, Arno, additional, Weinberger, Daniel R, additional, Weir, David R, additional, Wilson, James F, additional, Malhotra, Anil, additional, McIntosh, Andrew M, additional, Gale, Catharine R, additional, Seshadri, Sudha, additional, Mosley, Thomas H., additional, Bressler, Jan, additional, Lencz, Todd, additional, and Deary, Ian J, additional
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- 2017
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15. Sex differences in the genetic predictors of Alzheimer's pathology.
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Dumitrescu, Logan, Barnes, Lisa L, Thambisetty, Madhav, Beecham, Gary, Kunkle, Brian, Bush, William S, Gifford, Katherine A, Chibnik, Lori B, Mukherjee, Shubhabrata, Jager, Philip L De, Kukull, Walter, Crane, Paul K, Resnick, Susan M, Keene, C Dirk, Montine, Thomas J, Schellenberg, Gerard D, Deming, Yuetiva, Chao, Michael J, Huentelman, Matt, and Martin, Eden R
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ALZHEIMER'S disease ,NEUROFIBRILLARY tangles ,SEX (Biology) ,PATHOLOGY ,BRAIN banks - Abstract
Autopsy measures of Alzheimer's disease neuropathology have been leveraged as endophenotypes in previous genome-wide association studies (GWAS). However, despite evidence of sex differences in Alzheimer's disease risk, sex-stratified models have not been incorporated into previous GWAS analyses. We looked for sex-specific genetic associations with Alzheimer's disease endophenotypes from six brain bank data repositories. The pooled dataset included 2701 males and 3275 females, the majority of whom were diagnosed with Alzheimer's disease at autopsy (70%). Sex-stratified GWAS were performed within each dataset and then meta-analysed. Loci that reached genome-wide significance (P < 5 × 10-8) in stratified models were further assessed for sex interactions. Additional analyses were performed in independent datasets leveraging cognitive, neuroimaging and CSF endophenotypes, along with age-at-onset data. Outside of the APOE region, one locus on chromosome 7 (rs34331204) showed a sex-specific association with neurofibrillary tangles among males (P = 2.5 × 10-8) but not females (P = 0.85, sex-interaction P = 2.9 × 10-4). In follow-up analyses, rs34331204 was also associated with hippocampal volume, executive function, and age-at-onset only among males. These results implicate a novel locus that confers male-specific protection from tau pathology and highlight the value of assessing genetic associations in a sex-specific manner. [ABSTRACT FROM AUTHOR]
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- 2019
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16. Early complement genes are associated with visual system degeneration in multiple sclerosis.
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Fitzgerald, Kathryn C, Kim, Kicheol, Smith, Matthew D, Aston, Sean A, Fioravante, Nicholas, Rothman, Alissa M, Krieger, Stephen, Cofield, Stacey S, Kimbrough, Dorlan J, Bhargava, Pavan, Saidha, Shiv, Whartenby, Katharine A, Green, Ari J, Mowry, Ellen M, Cutter, Gary R, Lublin, Fred D, Baranzini, Sergio E, Jager, Philip L De, Calabresi, Peter A, and De Jager, Philip L
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OPTIC neuritis ,MULTIPLE sclerosis ,EYE ,VISUAL evoked potentials ,PROPORTIONAL hazards models ,OPTICAL coherence tomography ,VISUAL pathways - Abstract
Multiple sclerosis is a heterogeneous disease with an unpredictable course and a wide range of severity; some individuals rapidly progress to a disabled state whereas others experience only mild symptoms. Though genetic studies have identified variants that are associated with an increased risk of developing multiple sclerosis, no variants have been consistently associated with multiple sclerosis severity. In part, the lack of findings is related to inherent limitations of clinical rating scales; these scales are insensitive to early degenerative changes that underlie disease progression. Optical coherence tomography imaging of the retina and low-contrast letter acuity correlate with and predict clinical and imaging-based outcomes in multiple sclerosis. Therefore, they may serve as sensitive phenotypes to discover genetic predictors of disease course. We conducted a set of genome-wide association studies of longitudinal structural and functional visual pathway phenotypes in multiple sclerosis. First, we assessed genetic predictors of ganglion cell/inner plexiform layer atrophy in a discovery cohort of 374 patients with multiple sclerosis using mixed-effects models adjusting for age, sex, disease duration, optic neuritis and genetic ancestry and using a combination of single-variant and network-based analyses. For candidate variants identified in discovery, we conducted a similar set of analyses of ganglion cell/inner plexiform layer thinning in a replication cohort (n = 376). Second, we assessed genetic predictors of sustained loss of 5-letters in low-contrast letter acuity in discovery (n = 582) using multivariable-adjusted Cox proportional hazards models. We then evaluated candidate variants/pathways in a replication cohort. (n = 253). Results of both studies revealed novel subnetworks highly enriched for connected genes in early complement activation linked to measures of disease severity. Within these networks, C3 was the gene most strongly associated with ganglion cell/inner plexiform layer atrophy (P = 0.004) and C1QA and CR1 were top results in analysis of sustained low-contrast letter acuity loss. Namely, variant rs158772, linked to C1QA, and rs61822967, linked to CR1, were associated with 71% and 40% increases in risk of sustained LCLA loss, respectively, in meta-analysis pooling discovery and replication cohorts (rs158772: hazard ratio: 1.71; 95% confidence interval 1.30-2.25; P = 1.3 × 10-4; rs61822967: hazard ratio: 1.40; 95% confidence interval: 1.16-1.68; P = 4.1 × 10-4). In conclusion, early complement pathway gene variants were consistently associated with structural and functional measures of multiple sclerosis severity. These results from unbiased analyses are strongly supported by several prior reports that mechanistically implicated early complement factors in neurodegeneration. [ABSTRACT FROM AUTHOR]
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- 2019
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17. Candidate-based screening via gene modulation in human neurons and astrocytes implicates FERMT2 in A β and TAU proteostasis.
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Sullivan, Sarah E, Liao, Meichen, Smith, Robert V, White, Charles, Lagomarsino, Valentina N, Xu, Jishu, Taga, Mariko, Bennett, David A, Jager, Philip L De, and Young-Pearse, Tracy L
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- 2019
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18. Genes and Environment in Multiple Sclerosis project: A platform to investigate multiple sclerosis risk
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Xia, Zongqi, primary, White, Charles C., additional, Owen, Emily K., additional, Korff, Alina Von, additional, Clarkson, Sarah R., additional, McCabe, Cristin A., additional, Cimpean, Maria, additional, Winn, Phoebe A., additional, Hoesing, Ashley, additional, Steele, Sonya U., additional, Cortese, Irene C. M., additional, Chitnis, Tanuja, additional, Weiner, Howard L., additional, Reich, Daniel S., additional, Chibnik, Lori B., additional, and Jager, Philip L. De, additional
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- 2015
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19. Gene-wide analysis detects two new susceptibility genes for Alzheimer's disease
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Escott-Price, Valentina, Bellenguez, Céline, Wang, Li-San, Choi, Seung-Hoan, Harold, Denise, Jones, Lesley, Holmans, Peter, Gerrish, Amy, Vedernikov, Alexey, Richards, Alexander, DeStefano, Anita L., Lambert, Jean-Charles, Ibrahim-Verbaas, Carla A., Naj, Adam C., Sims, Rebecca, Jun, Gyungah, Bis, Joshua C., Beecham, Gary W., Grenier-Boley, Benjamin, Russo, Giancarlo, Thornton-Wells, Tricia A., Denning, Nicola, Smith, Albert V., Chouraki, Vincent, Thomas, Charlene, Ikram, M. Arfan, Zelenika, Diana, Vardarajan, Badri N., Kamatani, Yoichiro, Lin, Chiao-Feng, Schmidt, Helena, Kunkle, Brian, Dunstan, Melanie L., Vronskaya, Maria, Johnson, Andrew D., Ruiz, Agustin, Bihoreau, Marie-Thérèse, Reitz, Christiane, Pasquier, Florence, Hollingworth, Paul, Hanon, Olivier, Fitzpatrick, Annette L., Buxbaum, Joseph D., Campion, Dominique, Crane, Paul K., Baldwin, Clinton, Becker, Tim, Gudnason, Vilmundur, Cruchaga, Carlos, Craig, David, Amin, Najaf, Berr, Claudine, Lopez, Oscar L., Jager, Philip L. De, Deramecourt, Vincent, Johnston, Janet A., Evans, Denis, Lovestone, Simon, Letenneur, Luc, Hernández, Isabel, Rubinsztein, David C., Eiriksdottir, Gudny, Sleegers, Kristel, Goate, Alison M., Fiévet, Nathalie, Huentelman, Matthew J., Gill, Michael, Brown, Kristelle, Kamboh, M. Ilyas, Keller, Lina, Barberger-Gateau, Pascale, McGuinness, Bernadette, Larson, Eric B., Myers, Amanda J., Dufouil, Carole, Todd, Stephen, Wallon, David, Love, Seth, Rogaeva, Ekaterina, Gallacher, John, St George-Hyslop, Peter, Clarimon, Jordi, Lleo, Alberto, Bayer, Anthony, Tsuang, Debby W., Yu, Lei, Tsolaki, Magda, Bossù, Paola, Spalletta, Gianfranco, Proitsi, Petra, Collinge, John, Sorbi, Sandro, Sanchez Garcia, Florentino, Fox, Nick C., Hardy, John, Deniz Naranjo, Maria Candida, Bosco, Paolo, Clarke, Robert, Brayne, Carol, Galimberti, Daniela, Scarpini, Elio, Bonuccelli, Ubaldo, Mancuso, Michelangelo, Siciliano, Gabriele, Moebus, Susanne, Mecocci, Patrizia, Del Zompo, Maria, Maier, Wolfgang, Hampel, Harald, Pilotto, Alberto, Frank-García, Ana, Panza, Francesco, Solfrizzi, Vincenzo, Caffarra, Paolo, Nacmias, Benedetta, Perry, William, Mayhaus, Manuel, Lannfelt, Lars, Hakonarson, Hakon, Pichler, Sabrina, Carrasquillo, Minerva M., Ingelsson, Martin, Beekly, Duane, Alvarez, Victoria, Zou, Fanggeng, Valladares, Otto, Younkin, Steven G., Coto, Eliecer, Hamilton-Nelson, Kara L., Gu, Wei, Razquin, Cristina, Pastor, Pau, Mateo, Ignacio, Owen, Michael J., Faber, Kelley M., Jonsson, Palmi V., Combarros, Onofre, O'Donovan, Michael C., Cantwell, Laura B., Soininen, Hilkka, Blacker, Deborah, Mead, Simon, Mosley, Thomas H., Bennett, David A., Harris, Tamara B., Fratiglioni, Laura, Holmes, Clive, Bruijn, Renee F. A. G. de, Passmore, Peter, Montine, Thomas J., Bettens, Karolien, Rotter, Jerome I., Brice, Alexis, Morgan, Kevin, Foroud, Tatiana M., Kukull, Walter A., Hannequin, Didier, Powell, John F., Nalls, Michael A., Ritchie, Karen, Lunetta, Kathryn L., Kauwe, John S. K., Boerwinkle, Eric, Riemenschneider, Matthias, Boada, Mercè, Hiltunen, Mikko, Martin, Eden R., Schmidt, Reinhold, Rujescu, Dan, Dartigues, Jean-François, Mayeux, Richard, Tzourio, Christophe, Hofman, Albert, Nöthen, Markus Maria, Graff, Caroline, Psaty, Bruce M., Haines, Jonathan L., Lathrop, Mark, Pericak-Vance, Margaret Ann, Launer, Lenore J., Broeckhoven, Christine Van, Farrer, Lindsay A., Duijn, Cornelia M. van, Ramirez, Alfredo, Seshadri, Sudha, Schellenberg, Gerard D., Amouyel, Philippe, Williams, Julie, Escott-Price, Valentina, Bellenguez, Céline, Wang, Li-San, Choi, Seung-Hoan, Harold, Denise, Jones, Lesley, Holmans, Peter, Gerrish, Amy, Vedernikov, Alexey, Richards, Alexander, DeStefano, Anita L., Lambert, Jean-Charles, Ibrahim-Verbaas, Carla A., Naj, Adam C., Sims, Rebecca, Jun, Gyungah, Bis, Joshua C., Beecham, Gary W., Grenier-Boley, Benjamin, Russo, Giancarlo, Thornton-Wells, Tricia A., Denning, Nicola, Smith, Albert V., Chouraki, Vincent, Thomas, Charlene, Ikram, M. Arfan, Zelenika, Diana, Vardarajan, Badri N., Kamatani, Yoichiro, Lin, Chiao-Feng, Schmidt, Helena, Kunkle, Brian, Dunstan, Melanie L., Vronskaya, Maria, Johnson, Andrew D., Ruiz, Agustin, Bihoreau, Marie-Thérèse, Reitz, Christiane, Pasquier, Florence, Hollingworth, Paul, Hanon, Olivier, Fitzpatrick, Annette L., Buxbaum, Joseph D., Campion, Dominique, Crane, Paul K., Baldwin, Clinton, Becker, Tim, Gudnason, Vilmundur, Cruchaga, Carlos, Craig, David, Amin, Najaf, Berr, Claudine, Lopez, Oscar L., Jager, Philip L. De, Deramecourt, Vincent, Johnston, Janet A., Evans, Denis, Lovestone, Simon, Letenneur, Luc, Hernández, Isabel, Rubinsztein, David C., Eiriksdottir, Gudny, Sleegers, Kristel, Goate, Alison M., Fiévet, Nathalie, Huentelman, Matthew J., Gill, Michael, Brown, Kristelle, Kamboh, M. Ilyas, Keller, Lina, Barberger-Gateau, Pascale, McGuinness, Bernadette, Larson, Eric B., Myers, Amanda J., Dufouil, Carole, Todd, Stephen, Wallon, David, Love, Seth, Rogaeva, Ekaterina, Gallacher, John, St George-Hyslop, Peter, Clarimon, Jordi, Lleo, Alberto, Bayer, Anthony, Tsuang, Debby W., Yu, Lei, Tsolaki, Magda, Bossù, Paola, Spalletta, Gianfranco, Proitsi, Petra, Collinge, John, Sorbi, Sandro, Sanchez Garcia, Florentino, Fox, Nick C., Hardy, John, Deniz Naranjo, Maria Candida, Bosco, Paolo, Clarke, Robert, Brayne, Carol, Galimberti, Daniela, Scarpini, Elio, Bonuccelli, Ubaldo, Mancuso, Michelangelo, Siciliano, Gabriele, Moebus, Susanne, Mecocci, Patrizia, Del Zompo, Maria, Maier, Wolfgang, Hampel, Harald, Pilotto, Alberto, Frank-García, Ana, Panza, Francesco, Solfrizzi, Vincenzo, Caffarra, Paolo, Nacmias, Benedetta, Perry, William, Mayhaus, Manuel, Lannfelt, Lars, Hakonarson, Hakon, Pichler, Sabrina, Carrasquillo, Minerva M., Ingelsson, Martin, Beekly, Duane, Alvarez, Victoria, Zou, Fanggeng, Valladares, Otto, Younkin, Steven G., Coto, Eliecer, Hamilton-Nelson, Kara L., Gu, Wei, Razquin, Cristina, Pastor, Pau, Mateo, Ignacio, Owen, Michael J., Faber, Kelley M., Jonsson, Palmi V., Combarros, Onofre, O'Donovan, Michael C., Cantwell, Laura B., Soininen, Hilkka, Blacker, Deborah, Mead, Simon, Mosley, Thomas H., Bennett, David A., Harris, Tamara B., Fratiglioni, Laura, Holmes, Clive, Bruijn, Renee F. A. G. de, Passmore, Peter, Montine, Thomas J., Bettens, Karolien, Rotter, Jerome I., Brice, Alexis, Morgan, Kevin, Foroud, Tatiana M., Kukull, Walter A., Hannequin, Didier, Powell, John F., Nalls, Michael A., Ritchie, Karen, Lunetta, Kathryn L., Kauwe, John S. K., Boerwinkle, Eric, Riemenschneider, Matthias, Boada, Mercè, Hiltunen, Mikko, Martin, Eden R., Schmidt, Reinhold, Rujescu, Dan, Dartigues, Jean-François, Mayeux, Richard, Tzourio, Christophe, Hofman, Albert, Nöthen, Markus Maria, Graff, Caroline, Psaty, Bruce M., Haines, Jonathan L., Lathrop, Mark, Pericak-Vance, Margaret Ann, Launer, Lenore J., Broeckhoven, Christine Van, Farrer, Lindsay A., Duijn, Cornelia M. van, Ramirez, Alfredo, Seshadri, Sudha, Schellenberg, Gerard D., Amouyel, Philippe, and Williams, Julie
- Abstract
Background: Alzheimer's disease is a common debilitating dementia with known heritability, for which 20 late onset susceptibility loci have been identified, but more remain to be discovered. This study sought to identify new susceptibility genes, using an alternative gene-wide analytical approach which tests for patterns of association within genes, in the powerful genome-wide association dataset of the International Genomics of Alzheimer's Project Consortium, comprising over 7 m genotypes from 25,580 Alzheimer's cases and 48,466 controls. Principal findings: In addition to earlier reported genes, we detected genome-wide significant loci on chromosomes 8 (TP53INP1, p = 1.4×10−6) and 14 (IGHV1-67 p = 7.9×10−8) which indexed novel susceptibility loci. Significance: The additional genes identified in this study, have an array of functions previously implicated in Alzheimer's disease, including aspects of energy metabolism, protein degradation and the immune system and add further weight to these pathways as potential therapeutic targets in Alzheimer's disease.
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- 2014
20. Pervasive Sharing of Genetic Effects in Autoimmune Disease
- Author
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Whitaker College of Health Sciences and Technology, Hafler, David A., Rossin, Elizabeth, Cotsapas, Chris, Voight, Benjamin F., Lage, Kasper, Neale, Benjamin M., Wallace, Chris, Abecasis, Gonçalo R., Barrett, Jeffrey C., Behrens, Timothy, Cho, Judy, Jager, Philip L. De, Elder, James T., Graham, Robert R., Gregersen, Peter K., Klareskog, Lars, Siminovitch, Katherine A., Heel, David A. van, Wijmenga, Cisca, Worthington, Jane, Todd, John A., Rich, Stephen S., Daly, Mark J., Whitaker College of Health Sciences and Technology, Hafler, David A., Rossin, Elizabeth, Cotsapas, Chris, Voight, Benjamin F., Lage, Kasper, Neale, Benjamin M., Wallace, Chris, Abecasis, Gonçalo R., Barrett, Jeffrey C., Behrens, Timothy, Cho, Judy, Jager, Philip L. De, Elder, James T., Graham, Robert R., Gregersen, Peter K., Klareskog, Lars, Siminovitch, Katherine A., Heel, David A. van, Wijmenga, Cisca, Worthington, Jane, Todd, John A., Rich, Stephen S., and Daly, Mark J.
- Abstract
Genome-wide association (GWA) studies have identified numerous, replicable, genetic associations between common single nucleotide polymorphisms (SNPs) and risk of common autoimmune and inflammatory (immune-mediated) diseases, some of which are shared between two diseases. Along with epidemiological and clinical evidence, this suggests that some genetic risk factors may be shared across diseases—as is the case with alleles in the Major Histocompatibility Locus. In this work we evaluate the extent of this sharing for 107 immune disease-risk SNPs in seven diseases: celiac disease, Crohn's disease, multiple sclerosis, psoriasis, rheumatoid arthritis, systemic lupus erythematosus, and type 1 diabetes. We have developed a novel statistic for Cross Phenotype Meta-Analysis (CPMA) which detects association of a SNP to multiple, but not necessarily all, phenotypes. With it, we find evidence that 47/107 (44%) immune-mediated disease risk SNPs are associated to multiple—but not all—immune-mediated diseases (SNP-wise PCPMA<0.01). We also show that distinct groups of interacting proteins are encoded near SNPs which predispose to the same subsets of diseases; we propose these as the mechanistic basis of shared disease risk. We are thus able to leverage genetic data across diseases to construct biological hypotheses about the underlying mechanism of pathogenesis.
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- 2012
21. Genes and Environment in Multiple Sclerosis project: A platform to investigate multiple sclerosis risk.
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Xia, Zongqi, White, Charles C., Owen, Emily K., Korff, Alina Von, Clarkson, Sarah R., McCabe, Cristin A., Cimpean, Maria, Winn, Phoebe A., Hoesing, Ashley, Steele, Sonya U., Cortese, Irene C. M., Chitnis, Tanuja, Weiner, Howard L., Reich, Daniel S., Chibnik, Lori B., Jager, Philip L. De, Von Korff, Alina, and De Jager, Philip L
- Subjects
DISEASE susceptibility ,ECOLOGY ,FAMILIES ,GENETIC polymorphisms ,LONGITUDINAL method ,MULTIPLE sclerosis ,RESEARCH funding ,RISK assessment ,DISEASE incidence - Abstract
The Genes and Environment in Multiple Sclerosis project establishes a platform to investigate the events leading to multiple sclerosis (MS) in at-risk individuals. It has recruited 2,632 first-degree relatives from across the USA. Using an integrated genetic and environmental risk score, we identified subjects with twice the MS risk when compared to the average family member, and we report an initial incidence rate in these subjects that is 30 times greater than that of sporadic MS. We discuss the feasibility of large-scale studies of asymptomatic at-risk subjects that leverage modern tools of subject recruitment to execute collaborative projects. [ABSTRACT FROM AUTHOR]
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- 2016
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22. A whole-genome admixture scan finds a candidate locus for multiple sclerosis susceptibility
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Reich, David, primary, Patterson, Nick, additional, Jager, Philip L De, additional, McDonald, Gavin J, additional, Waliszewska, Alicja, additional, Tandon, Arti, additional, Lincoln, Robin R, additional, DeLoa, Cari, additional, Fruhan, Scott A, additional, Cabre, Philippe, additional, Bera, Odile, additional, Semana, Gilbert, additional, Kelly, M Ann, additional, Francis, David A, additional, Ardlie, Kristin, additional, Khan, Omar, additional, Cree, Bruce A C, additional, Hauser, Stephen L, additional, Oksenberg, Jorge R, additional, and Hafler, David A, additional
- Published
- 2005
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23. Association analysis of the R620W polymorphism of protein tyrosine phosphatase PTPN22 in systemic lupus erythematosus families: Increased t allele frequency in systemic lupus erythematosus patients with autoimmune thyroid disease
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Wu, Hui, primary, Cantor, Rita M., additional, Graham, Deborah S. Cunninghame, additional, Lingren, Cecilia M., additional, Farwell, Lisa, additional, Jager, Philip L. De, additional, Bottini, Nunzio, additional, Grossman, Jennifer M., additional, Wallace, Daniel J., additional, Hahn, Bevra H., additional, Julkunen, Heikki, additional, Hebert, Lee A., additional, Rovin, Brad H., additional, Birmingham, Dan J., additional, Rioux, John D., additional, Yu, C. Yung, additional, Kere, Juha, additional, Vyse, Timothy J., additional, and Tsao, Betty P., additional
- Published
- 2005
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24. Applying a new generation of genetic maps to understand human inflammatory disease
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Hafler, David A., primary and Jager, Philip L. De, additional
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- 2005
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25. Age at surgical menopause influences cognitive decline and Alzheimer pathology in older women
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Bove, Riley, Secor, Elizabeth, Chibnik, Lori B., Barnes, Lisa L., Schneider, Julie A., Bennett, David A., and Jager, Philip L. De
- Abstract
To determine the association between age at surgical menopause and both cognitive decline and Alzheimer disease (AD) pathology in 2 longitudinal cohorts.
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- 2014
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26. Clinical relevance and functional consequences of the TNFRSF1Amultiple sclerosis locus
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Ottoboni, Linda, Frohlich, Irene Y., Lee, Michelle, Healy, Brian C., Keenan, Brendan T., Xia, Zongqi, Chitnis, Tanuja, Guttmann, Charles R., Khoury, Samia J., Weiner, Howard L., Hafler, David A., and Jager, Philip L. De
- Abstract
We set out to characterize the clinical impact and functional consequences of rs1800693G, the multiple sclerosis (MS) susceptibility allele found in the TNFRSF1Alocus.
- Published
- 2013
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27. Genetic risk variants in African Americans with multiple sclerosis
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Isobe, Noriko, Gourraud, Pierre-Antoine, Harbo, Hanne F., Caillier, Stacy J., Santaniello, Adam, Khankhanian, Pouya, Maiers, Martin, Spellman, Stephen, Cereb, Nezih, Yang, SooYoung, Pando, Marcelo J., Piccio, Laura, Cross, Anne H., Jager, Philip L. De, Cree, Bruce A.C., Hauser, Stephen L., and Oksenberg, Jorge R.
- Abstract
To assess the association of established multiple sclerosis (MS) risk variants in 3,254 African Americans (1,162 cases and 2,092 controls).
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- 2013
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28. UNCOVERING THE GENETIC ARCHITECTURE OF MULTIPLE SCLEROSIS
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Esposito, Federica and Jager, Philip L. De
- Abstract
Multiple sclerosis (MS) is a disease in which genetic, environmental, and stochastic factors interact to trigger an inflammatory disease of the CNS that also has a neurodegenerative component. Over the past 3 years, progress in high-throughput technologies and analysis methods has synergized with the collaborative efforts of investigators studying MS genetics to enable the discovery of more than a dozen genes involved in making individuals susceptible to MS. These genes are beginning to suggest molecular pathways that may be particularly vulnerable to genetic variation in MS. Soon, a comprehensive map of common genetic variants affecting MS susceptibility will be assembled, and communal efforts will need to focus on the more challenging issue of understanding the genetic architecture of disease course and treatment response in MS. Early efforts integrating different dimensions of information, including genomics, imaging, transcriptomics, and proteomics, with precise phenotypic data from clinicians illustrate the way forward for prognostic algorithms in MS and suggest that these approaches will yield a new series of insights in the next decade.
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- 2010
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29. Neuropathologic intermediate phenotypes enhance association to Alzheimer susceptibility alleles
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Bennett, David A., Jager, Philip L. De, Leurgans, Sue E., and Schneider, Julie A.
- Abstract
The identification of susceptibility alleles to risk of Alzheimer disease (AD) is a major public health priority. Using apolipoprotein E genotype (APOE), we examined whether neuropathologic intermediate phenotypes, the pathology underlying clinical AD that presumably lies intermediate in the causal chain, would increase power for genetic associations.
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- 2009
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30. Corrigendum: Genetic variants associated with subjective well-being, depressive symptoms, and neuroticism identified through genome-wide analyses
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Okbay, Aysu, Baselmans, Bart M L, Neve, Jan-Emmanuel De, Turley, Patrick, Nivard, Michel G, Fontana, Mark Alan, Meddens, S Fleur W, Linnér, Richard Karlsson, Rietveld, Cornelius A, Derringer, Jaime, Gratten, Jacob, Lee, James J, Liu, Jimmy Z, de Vlaming, Ronald, Ahluwalia, Tarunveer S, Buchwald, Jadwiga, Cavadino, Alana, Frazier-Wood, Alexis C, Furlotte, Nicholas A, Garfield, Victoria, Geisel, Marie Henrike, Gonzalez, Juan R, Haitjema, Saskia, Karlsson, Robert, van der Laan, Sander W, Ladwig, Karl-Heinz, Lahti, Jari, van der Lee, Sven J, Lind, Penelope A, Liu, Tian, Matteson, Lindsay, Mihailov, Evelin, Miller, Michael B, Minica, Camelia C, Nolte, Ilja M, Mook-Kanamori, Dennis, van der Most, Peter J, Oldmeadow, Christopher, Qian, Yong, Raitakari, Olli, Rawal, Rajesh, Realo, Anu, Rueedi, Rico, Schmidt, Börge, Smith, Albert V, Stergiakouli, Evie, Tanaka, Toshiko, Taylor, Kent, Thorleifsson, Gudmar, Wedenoja, Juho, Wellmann, Juergen, Westra, Harm-Jan, Willems, Sara M, Zhao, Wei, Amin, Najaf, Bakshi, Andrew, Bergmann, Sven, Bjornsdottir, Gyda, Boyle, Patricia A, Cherney, Samantha, Cox, Simon R, Davies, Gail, Davis, Oliver S P, Ding, Jun, Direk, Nese, Eibich, Peter, Emeny, Rebecca T, Fatemifar, Ghazaleh, Faul, Jessica D, Ferrucci, Luigi, Forstner, Andreas J, Gieger, Christian, Gupta, Richa, Harris, Tamara B, Harris, Juliette M, Holliday, Elizabeth G, Hottenga, Jouke-Jan, Jager, Philip L De, Kaakinen, Marika A, Kajantie, Eero, Karhunen, Ville, Kolcic, Ivana, Kumari, Meena, Launer, Lenore J, Franke, Lude, Li-Gao, Ruifang, Liewald, David C, Koini, Marisa, Loukola, Anu, Marques-Vidal, Pedro, Montgomery, Grant W, Mosing, Miriam A, Paternoster, Lavinia, Pattie, Alison, Petrovic, Katja E, Pulkki-Råback, Laura, Quaye, Lydia, Räikkönen, Katri, Rudan, Igor, Scott, Rodney J, Smith, Jennifer A, Sutin, Angelina R, Trzaskowski, Maciej, Vinkhuyzen, Anna E, Yu, Lei, Zabaneh, Delilah, Attia, John R, Bennett, David A, Berger, Klaus, Bertram, Lars, Boomsma, Dorret I, Snieder, Harold, Chang, Shun-Chiao, Cucca, Francesco, Deary, Ian J, van Duijn, Cornelia M, Eriksson, Johan G, Bültmann, Ute, de Geus, Eco J C, Groenen, Patrick J F, Gudnason, Vilmundur, Hansen, Torben, Hartman, Catharine A, Haworth, Claire M A, Hayward, Caroline, Heath, Andrew C, Hinds, David A, Hyppönen, Elina, Iacono, William G, Järvelin, Marjo-Riitta, Jöckel, Karl-Heinz, Kaprio, Jaakko, Kardia, Sharon L R, Keltikangas-Järvinen, Liisa, Kraft, Peter, Kubzansky, Laura D, Lehtimäki, Terho, Magnusson, Patrik K E, Martin, Nicholas G, McGue, Matt, Metspalu, Andres, Mills, Melinda, de Mutsert, Renée, Oldehinkel, Albertine J, Pasterkamp, Gerard, Pedersen, Nancy L, Plomin, Robert, Polasek, Ozren, Power, Christine, Rich, Stephen S, Rosendaal, Frits R, den Ruijter, Hester M, Schlessinger, David, Schmidt, Helena, Svento, Rauli, Schmidt, Reinhold, Alizadeh, Behrooz Z, Sørensen, Thorkild I A, Spector, Tim D, Starr, John M, Stefansson, Kari, Steptoe, Andrew, Terracciano, Antonio, Thorsteinsdottir, Unnur, Thurik, A Roy, Timpson, Nicholas J, Tiemeier, Henning, Uitterlinden, André G, Vollenweider, Peter, Wagner, Gert G, Weir, David R, Yang, Jian, Conley, Dalton C, Smith, George Davey, Hofman, Albert, Johannesson, Magnus, Laibson, David I, Medland, Sarah E, Meyer, Michelle N, Pickrell, Joseph K, Esko, Tõnu, Krueger, Robert F, Beauchamp, Jonathan P, Koellinger, Philipp D, Benjamin, Daniel J, Bartels, Meike, and Cesarini, David
- Published
- 2016
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31. Role of the HLA DRB11501 Risk Haplotype in the Expression of Clinical and Radiographic Phenotypes of Multiple Sclerosis
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Jager, Philip L. De, Guttmann, Charles, Holland, Christopher, Wolfish, Cara R. G., Alkasab, Tarik, Hoffman, Kathryn, Bakshi, Rohit, Brass, Steven, Buckle, Guy, Chitnis, Tanuja, Dawson, David, Duan, Yang, Gauthier, Susan, Houtchens, Maria, Liptak, Zsuzsanna, Margolin, David, Napoli, Salvatore, Stazzone, Lynn, Khoury, Samia, Weiner, Howard, and Hafler, David
- Published
- 2006
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