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1. Genetic polymorphisms associated with adverse pregnancy outcomes in nulliparas.

Author

Khan, Raiyan, Guerrero, Rafael, Wapner, Ronald, Hahn, Matthew, Raja, Anita, Salleb-Aouissi, Ansaf, Grobman, William, Simhan, Hyagriv, Silver, Robert, Reddy, Uma, Radivojac, Predrag, Peer, Itsik, Haas, David, and Chung, Judith

Subjects
Fetal death, Genetic association, Gestational diabetes, Miscarriage, Preeclampsia, Pregnancy loss, Preterm birth, Stillbirth, Humans, Pregnancy, Female, Polymorphism, Single Nucleotide, Genome-Wide Association Study, Pregnancy Outcome, Diabetes, Gestational, Adult, Pre-Eclampsia, Genetic Predisposition to Disease, Parity
Abstract

Adverse pregnancy outcomes (APOs) affect a large proportion of pregnancies and represent an important cause of morbidity and mortality worldwide. Yet the pathophysiology of APOs is poorly understood, limiting our ability to prevent and treat these conditions. To search for genetic markers of maternal risk for four APOs, we performed multi-ancestry genome-wide association studies (GWAS) for pregnancy loss, gestational length, gestational diabetes, and preeclampsia. We clustered participants by their genetic ancestry and focused our analyses on three sub-cohorts with the largest sample sizes: European, African, and Admixed American. Association tests were carried out separately for each sub-cohort and then meta-analyzed together. Two novel loci were significantly associated with an increased risk of pregnancy loss: a cluster of SNPs located downstream of the TRMU gene (top SNP: rs142795512), and the SNP rs62021480 near RGMA. In the GWAS of gestational length we identified two new variants, rs2550487 and rs58548906 near WFDC1 and AC005052.1, respectively. Lastly, three new loci were significantly associated with gestational diabetes (top SNPs: rs72956265, rs10890563, rs79596863), located on or near ZBTB20, GUCY1A2, and RPL7P20, respectively. Fourteen loci previously correlated with preterm birth, gestational diabetes, and preeclampsia were found to be associated with these outcomes as well.

Published
2024

2. Contamination source modeling with SCRuB improves cancer phenotype prediction from microbiome data.

Author

Austin, George, Park, Heekuk, Meydan, Yoli, Seeram, Dwayne, Sezin, Tanya, Lou, Yue, Firek, Brian, Morowitz, Michael, Banfield, Jill, Christiano, Angela, Peer, Itsik, Uhlemann, Anne-Catrin, Shenhav, Liat, and Korem, Tal

Subjects
Humans, Microbiota, Phenotype, Neoplasms
Abstract

Sequencing-based approaches for the analysis of microbial communities are susceptible to contamination, which could mask biological signals or generate artifactual ones. Methods for in silico decontamination using controls are routinely used, but do not make optimal use of information shared across samples and cannot handle taxa that only partially originate in contamination or leakage of biological material into controls. Here we present Source tracking for Contamination Removal in microBiomes (SCRuB), a probabilistic in silico decontamination method that incorporates shared information across multiple samples and controls to precisely identify and remove contamination. We validate the accuracy of SCRuB in multiple data-driven simulations and experiments, including induced contamination, and demonstrate that it outperforms state-of-the-art methods by an average of 15-20 times. We showcase the robustness of SCRuB across multiple ecosystems, data types and sequencing depths. Demonstrating its applicability to microbiome research, SCRuB facilitates improved predictions of host phenotypes, most notably the prediction of treatment response in melanoma patients using decontaminated tumor microbiome data.

Published
2023

3. Searching and visualizing genetic associations of pregnancy traits by using GnuMoM2b.

Author

Yan, Qi, Guerrero, Rafael, Khan, Raiyan, Surujnarine, Andy, Wapner, Ronald, Hahn, Matthew, Raja, Anita, Salleb-Aouissi, Ansaf, Grobman, William, Simhan, Hyagriv, Blue, Nathan, Silver, Robert, Chung, Judith, Reddy, Uma, Radivojac, Predrag, Peer, Itsik, and Haas, David

Subjects
GWAS, PheWAS, adverse pregnancy outcomes, nuMoM2b, Pregnancy, Female, Humans, Genome-Wide Association Study, Phenotype, Risk Factors, Phenomics, Polymorphism, Single Nucleotide
Abstract

Adverse pregnancy outcomes (APOs) are major risk factors for womens health during pregnancy and even in the years after pregnancy. Due to the heterogeneity of APOs, only few genetic associations have been identified. In this report, we conducted genome-wide association studies (GWASs) of 479 traits that are possibly related to APOs using a large and racially diverse study, Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-Be (nuMoM2b). To display extensive results, we developed a web-based tool GnuMoM2b (https://gnumom2b.cumcobgyn.org/) for searching, visualizing, and sharing results from a GWAS of 479 pregnancy traits as well as phenome-wide association studies of more than 17 million single nucleotide polymorphisms. The genetic results from 3 ancestries (Europeans, Africans, and Admixed Americans) and meta-analyses are populated in GnuMoM2b. In conclusion, GnuMoM2b is a valuable resource for extraction of pregnancy-related genetic results and shows the potential to facilitate meaningful discoveries.

Published
2023

4. Functional variants in the LRRK2 gene confer shared effects on risk for Crohns disease and Parkinsons disease.

Author

Hui, Ken, Fernandez-Hernandez, Heriberto, Hu, Jianzhong, Schaffner, Adam, Pankratz, Nathan, Hsu, Nai-Yun, Chuang, Ling-Shiang, Carmi, Shai, Villaverde, Nicole, Li, Xianting, Rivas, Manual, Levine, Adam, Bao, Xiuliang, Labrias, Philippe, Haritunians, Talin, Ruane, Darren, Gettler, Kyle, Chen, Ernie, Li, Dalin, Schiff, Elena, Pontikos, Nikolas, Barzilai, Nir, Brant, Steven, Bressman, Susan, Cheifetz, Adam, Clark, Lorraine, Daly, Mark, Desnick, Robert, Duerr, Richard, Katz, Seymour, Lencz, Todd, Myers, Richard, Ostrer, Harry, Ozelius, Laurie, Payami, Haydeh, Peter, Yakov, Rioux, John, Segal, Anthony, Scott, William, Silverberg, Mark, Vance, Jeffery, Ubarretxena-Belandia, Iban, Foroud, Tatiana, Atzmon, Gil, Peer, Itsik, Ioannou, Yiannis, McGovern, Dermot, Yue, Zhenyu, Schadt, Eric, Cho, Judy, and Peter, Inga

Subjects
Alleles, Autophagy, Crohn Disease, Cytoskeleton, Exome, Gene Frequency, Gene Regulatory Networks, Genetic Loci, Genetic Predisposition to Disease, Genetic Variation, Genome, Human, Humans, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, Macrophages, Odds Ratio, Open Reading Frames, Parkinson Disease, Phenotype, Reproducibility of Results, Risk Factors, Exome Sequencing
Abstract

Crohns disease (CD), a form of inflammatory bowel disease, has a higher prevalence in Ashkenazi Jewish than in non-Jewish European populations. To define the role of nonsynonymous mutations, we performed exome sequencing of Ashkenazi Jewish patients with CD, followed by array-based genotyping and association analysis in 2066 CD cases and 3633 healthy controls. We detected association signals in the LRRK2 gene that conferred risk for CD (N2081D variant, P = 9.5 × 10-10) or protection from CD (N551K variant, tagging R1398H-associated haplotype, P = 3.3 × 10-8). These variants affected CD age of onset, disease location, LRRK2 activity, and autophagy. Bayesian network analysis of CD patient intestinal tissue further implicated LRRK2 in CD pathogenesis. Analysis of the extended LRRK2 locus in 24,570 CD cases, patients with Parkinsons disease (PD), and healthy controls revealed extensive pleiotropy, with shared genetic effects between CD and PD in both Ashkenazi Jewish and non-Jewish cohorts. The LRRK2 N2081D CD risk allele is located in the same kinase domain as G2019S, a mutation that is the major genetic cause of familial and sporadic PD. Like the G2019S mutation, the N2081D variant was associated with increased kinase activity, whereas neither N551K nor R1398H variants on the protective haplotype altered kinase activity. We also confirmed that R1398H, but not N551K, increased guanosine triphosphate binding and hydrolyzing enzyme (GTPase) activity, thereby deactivating LRRK2. The presence of shared LRRK2 alleles in CD and PD provides refined insight into disease mechanisms and may have major implications for the treatment of these two seemingly unrelated diseases.

Published
2018

5. De novo mutations in histone-modifying genes in congenital heart disease.

Author

Zaidi, Samir, Choi, Murim, Wakimoto, Hiroko, Ma, Lijiang, Jiang, Jianming, Overton, John, Romano-Adesman, Angela, Bjornson, Robert, Breitbart, Roger, Brown, Kerry, Carriero, Nicholas, Cheung, Yee, Deanfield, John, DePalma, Steve, Fakhro, Khalid, Glessner, Joseph, Hakonarson, Hakon, Italia, Michael, Kaltman, Jonathan, Kaski, Juan, Kim, Richard, Kline, Jennie, Lee, Teresa, Leipzig, Jeremy, Lopez, Alexander, Mane, Shrikant, Mitchell, Laura, Newburger, Jane, Parfenov, Michael, Peer, Itsik, Porter, George, Roberts, Amy, Sachidanandam, Ravi, Subramanian, Sailakshmi, Tikhonova, Irina, Wang, Wei, Warburton, Dorothy, White, Peter, Williams, Ismee, Zhao, Hongyu, Seidman, Jonathan, Brueckner, Martina, Chung, Wendy, Gelb, Bruce, Goldmuntz, Elizabeth, Seidman, Christine, Lifton, Richard, Seiden, Howard, State, Matthew, and Sanders, Stephan

Subjects
Adult, Case-Control Studies, Child, Chromatin, DNA Mutational Analysis, Enhancer Elements, Genetic, Exome, Female, Genes, Developmental, Heart Diseases, Histones, Humans, Lysine, Male, Methylation, Mutation, Odds Ratio, Promoter Regions, Genetic
Abstract

Congenital heart disease (CHD) is the most frequent birth defect, affecting 0.8% of live births. Many cases occur sporadically and impair reproductive fitness, suggesting a role for de novo mutations. Here we compare the incidence of de novo mutations in 362 severe CHD cases and 264 controls by analysing exome sequencing of parent-offspring trios. CHD cases show a significant excess of protein-altering de novo mutations in genes expressed in the developing heart, with an odds ratio of 7.5 for damaging (premature termination, frameshift, splice site) mutations. Similar odds ratios are seen across the main classes of severe CHD. We find a marked excess of de novo mutations in genes involved in the production, removal or reading of histone 3 lysine 4 (H3K4) methylation, or ubiquitination of H2BK120, which is required for H3K4 methylation. There are also two de novo mutations in SMAD2, which regulates H3K27 methylation in the embryonic left-right organizer. The combination of both activating (H3K4 methylation) and inactivating (H3K27 methylation) chromatin marks characterizes poised promoters and enhancers, which regulate expression of key developmental genes. These findings implicate de novo point mutations in several hundreds of genes that collectively contribute to approximately 10% of severe CHD.

Published
2013

6. Genome of the Netherlands population-specific imputations identify an ABCA6 variant associated with cholesterol levels

Author

Van Leeuwen, Elisabeth M., Karssen, Lennart C., Deelen, Joris, Isaacs, Aaron, Medina-Gomez, Carolina, Mbarek, Hamdi, Kanterakis, Alexandros, Trompet, Stella, Postmus, Iris, Verweij, Niek, Van Enckevort, David J., Huffman, Jennifer E., White, Charles C., Feitosa, Mary F., Bartz, Traci M., Manichaikul, Ani, Joshi, Peter K., Peloso, Gina M., Deelen, Patrick, Van Dijk, Freerk, Willemsen, Gonneke, De Geus, Eco J., Milaneschi, Yuri, Penninx, Brenda W J H, Francioli, Laurent C., Menelaou, Androniki, Pulit, Sara L., Rivadeneira, Fernando, Hofman, Albert, Oostra, Ben A., Franco, Oscar H., Leach, Irene Mateo, Beekman, Marian, De Craen, Anton J M, Uh, Hae Won, Trochet, Holly, Hocking, Lynne J., Porteous, David J., Sattar, Naveed, Packard, Chris J., Buckley, Brendan M., Brody, Jennifer A., Bis, Joshua C., Rotter, Jerome I., Mychaleckyj, Josyf C., Campbell, Harry, Duan, Qing, Lange, Leslie A., Wilson, James F., Hayward, Caroline, Polasek, Ozren, Vitart, Veronique, Rudan, Igor, Wright, Alan F., Rich, Stephen S., Psaty, Bruce M., Borecki, Ingrid B., Kearney, Patricia M., Stott, David J., Cupples, L. Adrienne, Jukema, J. Wouter, Van Der Harst, Pim, Sijbrands, Eric J., Hottenga, Jouke Jan, Uitterlinden, Andre G., Swertz, Morris A., Van Ommen, Gert Jan B, De Bakker, Paul I W, Eline Slagboom, P., Boomsma, Dorret I., Wijmenga, Cisca, Van Duijn, Cornelia M., Neerincx, Pieter B T, Elbers, Clara C., Palamara, Pier Francesco, Peer, Itsik, Abdellaoui, Abdel, Kloosterman, Wigard P., Van Oven, Mannis, Vermaat, Martijn, Li, Mingkun, Laros, Jeroen F J, Stoneking, Mark, De Knijff, Peter, Kayser, Manfred, Veldink, Jan H., Van Den Berg, Leonard H., Byelas, Heorhiy, Den Dunnen, Johan T., Dijkstra, Martijn, Amin, Najaf, Van Der Velde, K. Joeri, Van Setten, Jessica, Kattenberg, Mathijs, Van Schaik, Barbera D C, Bot, Jan, Nijman, Isaäc J., Mei, Hailiang, Koval, Vyacheslav, Ye, Kai, Lameijer, Eric Wubbo, Moed, Matthijs H., Hehir-Kwa, Jayne Y., Handsaker, Robert E., Sunyaev, Shamil R., Sohail, Mashaal, Hormozdiari, Fereydoun, Marschall, Tobias, Schönhuth, Alexander, Guryev, Victor, Suchiman, H. Eka D, Wolffenbuttel, Bruce H., Platteel, Mathieu, Pitts, Steven J., Potluri, Shobha, Cox, David R., Li, Qibin, Li, Yingrui, Du, Yuanping, Chen, Ruoyan, Cao, Hongzhi, Li, Ning, Cao, Sujie, Wang, Jun, Bovenberg, Jasper A., Van Leeuwen, Elisabeth M., Karssen, Lennart C., Deelen, Joris, Isaacs, Aaron, Medina-Gomez, Carolina, Mbarek, Hamdi, Kanterakis, Alexandros, Trompet, Stella, Postmus, Iris, Verweij, Niek, Van Enckevort, David J., Huffman, Jennifer E., White, Charles C., Feitosa, Mary F., Bartz, Traci M., Manichaikul, Ani, Joshi, Peter K., Peloso, Gina M., Deelen, Patrick, Van Dijk, Freerk, Willemsen, Gonneke, De Geus, Eco J., Milaneschi, Yuri, Penninx, Brenda W J H, Francioli, Laurent C., Menelaou, Androniki, Pulit, Sara L., Rivadeneira, Fernando, Hofman, Albert, Oostra, Ben A., Franco, Oscar H., Leach, Irene Mateo, Beekman, Marian, De Craen, Anton J M, Uh, Hae Won, Trochet, Holly, Hocking, Lynne J., Porteous, David J., Sattar, Naveed, Packard, Chris J., Buckley, Brendan M., Brody, Jennifer A., Bis, Joshua C., Rotter, Jerome I., Mychaleckyj, Josyf C., Campbell, Harry, Duan, Qing, Lange, Leslie A., Wilson, James F., Hayward, Caroline, Polasek, Ozren, Vitart, Veronique, Rudan, Igor, Wright, Alan F., Rich, Stephen S., Psaty, Bruce M., Borecki, Ingrid B., Kearney, Patricia M., Stott, David J., Cupples, L. Adrienne, Jukema, J. Wouter, Van Der Harst, Pim, Sijbrands, Eric J., Hottenga, Jouke Jan, Uitterlinden, Andre G., Swertz, Morris A., Van Ommen, Gert Jan B, De Bakker, Paul I W, Eline Slagboom, P., Boomsma, Dorret I., Wijmenga, Cisca, Van Duijn, Cornelia M., Neerincx, Pieter B T, Elbers, Clara C., Palamara, Pier Francesco, Peer, Itsik, Abdellaoui, Abdel, Kloosterman, Wigard P., Van Oven, Mannis, Vermaat, Martijn, Li, Mingkun, Laros, Jeroen F J, Stoneking, Mark, De Knijff, Peter, Kayser, Manfred, Veldink, Jan H., Van Den Berg, Leonard H., Byelas, Heorhiy, Den Dunnen, Johan T., Dijkstra, Martijn, Amin, Najaf, Van Der Velde, K. Joeri, Van Setten, Jessica, Kattenberg, Mathijs, Van Schaik, Barbera D C, Bot, Jan, Nijman, Isaäc J., Mei, Hailiang, Koval, Vyacheslav, Ye, Kai, Lameijer, Eric Wubbo, Moed, Matthijs H., Hehir-Kwa, Jayne Y., Handsaker, Robert E., Sunyaev, Shamil R., Sohail, Mashaal, Hormozdiari, Fereydoun, Marschall, Tobias, Schönhuth, Alexander, Guryev, Victor, Suchiman, H. Eka D, Wolffenbuttel, Bruce H., Platteel, Mathieu, Pitts, Steven J., Potluri, Shobha, Cox, David R., Li, Qibin, Li, Yingrui, Du, Yuanping, Chen, Ruoyan, Cao, Hongzhi, Li, Ning, Cao, Sujie, Wang, Jun, and Bovenberg, Jasper A.

Abstract

Variants associated with blood lipid levels may be population-specific. To identify low-frequency variants associated with this phenotype, population-specific reference panels may be used. Here we impute nine large Dutch biobanks (∼35,000 samples) with the population-specific reference panel created by the Genome of the Netherlands Project and perform association testing with blood lipid levels. We report the discovery of five novel associations at four loci (P value -4), including a rare missense variant in ABCA6 (rs77542162, p.Cys1359Arg, frequency 0.034), which is predicted to be deleterious. The frequency of this ABCA6 variant is 3.65-fold increased in the Dutch and its effect (βLDL-C =0.135, βTC =0.140) is estimated to be very similar to those observed for single variants in well-known lipid genes, such as LDLR.

Published
2015

7. Genome of the Netherlands population-specific imputations identify an ABCA6 variant associated with cholesterol levels

Author

CMM Groep Kaaij, CMM Groep Kloosterman, Child Health, Cancer, ZL Neuromusculaire Ziekten Medisch, Experimentele Afd. Cardiologie 1, CMM Groep Cuppen, JC onderzoeksprogramma Methodologie, Van Leeuwen, Elisabeth M., Karssen, Lennart C., Deelen, Joris, Isaacs, Aaron, Medina-Gomez, Carolina, Mbarek, Hamdi, Kanterakis, Alexandros, Trompet, Stella, Postmus, Iris, Verweij, Niek, Van Enckevort, David J., Huffman, Jennifer E., White, Charles C., Feitosa, Mary F., Bartz, Traci M., Manichaikul, Ani, Joshi, Peter K., Peloso, Gina M., Deelen, Patrick, Van Dijk, Freerk, Willemsen, Gonneke, De Geus, Eco J., Milaneschi, Yuri, Penninx, Brenda W J H, Francioli, Laurent C., Menelaou, Androniki, Pulit, Sara L., Rivadeneira, Fernando, Hofman, Albert, Oostra, Ben A., Franco, Oscar H., Leach, Irene Mateo, Beekman, Marian, De Craen, Anton J M, Uh, Hae Won, Trochet, Holly, Hocking, Lynne J., Porteous, David J., Sattar, Naveed, Packard, Chris J., Buckley, Brendan M., Brody, Jennifer A., Bis, Joshua C., Rotter, Jerome I., Mychaleckyj, Josyf C., Campbell, Harry, Duan, Qing, Lange, Leslie A., Wilson, James F., Hayward, Caroline, Polasek, Ozren, Vitart, Veronique, Rudan, Igor, Wright, Alan F., Rich, Stephen S., Psaty, Bruce M., Borecki, Ingrid B., Kearney, Patricia M., Stott, David J., Cupples, L. Adrienne, Jukema, J. Wouter, Van Der Harst, Pim, Sijbrands, Eric J., Hottenga, Jouke Jan, Uitterlinden, Andre G., Swertz, Morris A., Van Ommen, Gert Jan B, De Bakker, Paul I W, Eline Slagboom, P., Boomsma, Dorret I., Wijmenga, Cisca, Van Duijn, Cornelia M., Neerincx, Pieter B T, Elbers, Clara C., Palamara, Pier Francesco, Peer, Itsik, Abdellaoui, Abdel, Kloosterman, Wigard P., Van Oven, Mannis, Vermaat, Martijn, Li, Mingkun, Laros, Jeroen F J, Stoneking, Mark, De Knijff, Peter, Kayser, Manfred, Veldink, Jan H., Van Den Berg, Leonard H., Byelas, Heorhiy, Den Dunnen, Johan T., Dijkstra, Martijn, Amin, Najaf, Van Der Velde, K. Joeri, Van Setten, Jessica, Kattenberg, Mathijs, Van Schaik, Barbera D C, Bot, Jan, Nijman, Isaäc J., Mei, Hailiang, Koval, Vyacheslav, Ye, Kai, Lameijer, Eric Wubbo, Moed, Matthijs H., Hehir-Kwa, Jayne Y., Handsaker, Robert E., Sunyaev, Shamil R., Sohail, Mashaal, Hormozdiari, Fereydoun, Marschall, Tobias, Schönhuth, Alexander, Guryev, Victor, Suchiman, H. Eka D, Wolffenbuttel, Bruce H., Platteel, Mathieu, Pitts, Steven J., Potluri, Shobha, Cox, David R., Li, Qibin, Li, Yingrui, Du, Yuanping, Chen, Ruoyan, Cao, Hongzhi, Li, Ning, Cao, Sujie, Wang, Jun, Bovenberg, Jasper A., de Bakker, Paul I W, CMM Groep Kaaij, CMM Groep Kloosterman, Child Health, Cancer, ZL Neuromusculaire Ziekten Medisch, Experimentele Afd. Cardiologie 1, CMM Groep Cuppen, JC onderzoeksprogramma Methodologie, Van Leeuwen, Elisabeth M., Karssen, Lennart C., Deelen, Joris, Isaacs, Aaron, Medina-Gomez, Carolina, Mbarek, Hamdi, Kanterakis, Alexandros, Trompet, Stella, Postmus, Iris, Verweij, Niek, Van Enckevort, David J., Huffman, Jennifer E., White, Charles C., Feitosa, Mary F., Bartz, Traci M., Manichaikul, Ani, Joshi, Peter K., Peloso, Gina M., Deelen, Patrick, Van Dijk, Freerk, Willemsen, Gonneke, De Geus, Eco J., Milaneschi, Yuri, Penninx, Brenda W J H, Francioli, Laurent C., Menelaou, Androniki, Pulit, Sara L., Rivadeneira, Fernando, Hofman, Albert, Oostra, Ben A., Franco, Oscar H., Leach, Irene Mateo, Beekman, Marian, De Craen, Anton J M, Uh, Hae Won, Trochet, Holly, Hocking, Lynne J., Porteous, David J., Sattar, Naveed, Packard, Chris J., Buckley, Brendan M., Brody, Jennifer A., Bis, Joshua C., Rotter, Jerome I., Mychaleckyj, Josyf C., Campbell, Harry, Duan, Qing, Lange, Leslie A., Wilson, James F., Hayward, Caroline, Polasek, Ozren, Vitart, Veronique, Rudan, Igor, Wright, Alan F., Rich, Stephen S., Psaty, Bruce M., Borecki, Ingrid B., Kearney, Patricia M., Stott, David J., Cupples, L. Adrienne, Jukema, J. Wouter, Van Der Harst, Pim, Sijbrands, Eric J., Hottenga, Jouke Jan, Uitterlinden, Andre G., Swertz, Morris A., Van Ommen, Gert Jan B, De Bakker, Paul I W, Eline Slagboom, P., Boomsma, Dorret I., Wijmenga, Cisca, Van Duijn, Cornelia M., Neerincx, Pieter B T, Elbers, Clara C., Palamara, Pier Francesco, Peer, Itsik, Abdellaoui, Abdel, Kloosterman, Wigard P., Van Oven, Mannis, Vermaat, Martijn, Li, Mingkun, Laros, Jeroen F J, Stoneking, Mark, De Knijff, Peter, Kayser, Manfred, Veldink, Jan H., Van Den Berg, Leonard H., Byelas, Heorhiy, Den Dunnen, Johan T., Dijkstra, Martijn, Amin, Najaf, Van Der Velde, K. Joeri, Van Setten, Jessica, Kattenberg, Mathijs, Van Schaik, Barbera D C, Bot, Jan, Nijman, Isaäc J., Mei, Hailiang, Koval, Vyacheslav, Ye, Kai, Lameijer, Eric Wubbo, Moed, Matthijs H., Hehir-Kwa, Jayne Y., Handsaker, Robert E., Sunyaev, Shamil R., Sohail, Mashaal, Hormozdiari, Fereydoun, Marschall, Tobias, Schönhuth, Alexander, Guryev, Victor, Suchiman, H. Eka D, Wolffenbuttel, Bruce H., Platteel, Mathieu, Pitts, Steven J., Potluri, Shobha, Cox, David R., Li, Qibin, Li, Yingrui, Du, Yuanping, Chen, Ruoyan, Cao, Hongzhi, Li, Ning, Cao, Sujie, Wang, Jun, Bovenberg, Jasper A., and de Bakker, Paul I W

Published
2015

8. Reorganization of corticostriatal circuits in healthy G2019S LRRK2 carriers

Author

Helmich, Rick C., primary, Thaler, Avner, additional, van Nuenen, Bart F.L., additional, Gurevich, Tanya, additional, Mirelman, Anat, additional, Marder, Karen S., additional, Bressman, Susan, additional, Orr-Urtreger, Avi, additional, Giladi, Nir, additional, Bloem, Bastiaan R., additional, Toni, Ivan, additional, Saunders-Pullman, Rachel, additional, Raymond, Deborah, additional, Ozelius, Laurie, additional, Shanker, Vicki, additional, Groves, Mark, additional, Palmese, Christina, additional, Iyer, Akhila, additional, Soto-Valencia, Jeannie, additional, Stanley, Kaili Maloy, additional, San Luciano, Marta, additional, Deik, Andres, additional, Barrett, Matthew James, additional, Cabassa, Jose, additional, Severt, Lawrence, additional, Hunt, Ann, additional, Lubarr, Naomi, additional, Sachdev, Rivka, additional, Miravite, Joan, additional, Lewis, Sara, additional, Clark, Lorraine N., additional, Alcalay, Roy, additional, Fahn, Stanley, additional, Cote, Lucien, additional, Greene, Paul, additional, Waters, Cheryl, additional, Mazzoni, Pietro, additional, Ford, Blair, additional, Louis, Elan, additional, Levy, Oren, additional, Tang, Ming Xin, additional, Rakitin, Brian C., additional, Mejia, Helen, additional, Roos, Ernest, additional, Riley, Martha Orbe, additional, Rosado, Llency, additional, Moskowitz, Carol, additional, Dorovski, Tsvyatko, additional, Clark, Lorraine, additional, Liu, Xinmin, additional, Kisselev, Sergey, additional, Peer, Itsik, additional, and Vacic, Vladimir, additional

Published
2015
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9. Whole-genome sequence variation, population structure and demographic history of the Dutch population

Author

Francioli, Laurent C., Menelaou, Andronild, Pulit, Sara L., Van Dijk, Freerk, Palamara, Pier Francesco, Elbers, Clara C., Neerincx, Pieter B. T., Ye, Kai, Guryev, Victor, Kloosterman, Wigard P., Deelen, Patrick, Abdellaoui, Abdel, Van Leeuwen, Elisabeth M., Van Oven, Mannis, Vermaat, Martijn, Li, Mingkun, Laros, Jeroen F. J., Karssen, Lennart C., Kanterakis, Alexandros, Amin, Najaf, Hottenga, Jouke Jan, Lameijer, Eric-Wubbo, Kattenberg, Mathijs, Dijkstra, Martijn, Byelas, Heorhiy, Van Settenl, Jessica, Van Schaik, Barbera D. C., Bot, Jan, Nijman, Isaac J., Renkens, Ivo, Marscha, Tobias, Schonhuth, Alexander, Hehir-Kwa, Jayne Y., Handsaker, Robert E., Polak, Paz, Sohail, Mashaal, Vuzman, Dana, Hormozdiari, Fereydoun, Van Enckevort, David, Mei, Hailiang, Koval, Vyacheslav, Moed, Ma-Tthijs H., Van der Velde, K. Joeri, Rivadeneira, Fernando, Estrada, Karol, Medina-Gomez, Carolina, Isaacs, Aaron, McCarroll, Steven A., Beekrnan, Marian, De Craen, Anton J. M., Suchiman, H. Eka D., Hofman, Albert, Oostra, Ben, Uitterlinden, Andre G., Willemsen, Gonneke, Plattee, Mathieu, Veldink, Jan H., Van den Berg, Leonard H., Pitts, Steven J., Potluri, Shobha, Sundar, Purnima, Cox, David R., Sunyaev, Shamil R., Den Dunnen, Johan T., Stoneking, Mark, De Knijff, Peter, Kayser, Manfred, Li, Qibin, Li, Yingrui, Du, Yuanping, Chen, Ruoyan, Cao, Hongzhi, Li, Ning, Cao, Sujie, Wang, Jun, Bovenberg, Jasper A., Peer, Itsik, Slagboom, P. Eline, Van Duijn, Cornelia M., Boomsma, Dorret I., Van Ommen, Gert-Jan B., De Bakker, Paul I. W., Swertz, Morris A., Wijmenga, Cisca, Francioli, Laurent C., Menelaou, Andronild, Pulit, Sara L., Van Dijk, Freerk, Palamara, Pier Francesco, Elbers, Clara C., Neerincx, Pieter B. T., Ye, Kai, Guryev, Victor, Kloosterman, Wigard P., Deelen, Patrick, Abdellaoui, Abdel, Van Leeuwen, Elisabeth M., Van Oven, Mannis, Vermaat, Martijn, Li, Mingkun, Laros, Jeroen F. J., Karssen, Lennart C., Kanterakis, Alexandros, Amin, Najaf, Hottenga, Jouke Jan, Lameijer, Eric-Wubbo, Kattenberg, Mathijs, Dijkstra, Martijn, Byelas, Heorhiy, Van Settenl, Jessica, Van Schaik, Barbera D. C., Bot, Jan, Nijman, Isaac J., Renkens, Ivo, Marscha, Tobias, Schonhuth, Alexander, Hehir-Kwa, Jayne Y., Handsaker, Robert E., Polak, Paz, Sohail, Mashaal, Vuzman, Dana, Hormozdiari, Fereydoun, Van Enckevort, David, Mei, Hailiang, Koval, Vyacheslav, Moed, Ma-Tthijs H., Van der Velde, K. Joeri, Rivadeneira, Fernando, Estrada, Karol, Medina-Gomez, Carolina, Isaacs, Aaron, McCarroll, Steven A., Beekrnan, Marian, De Craen, Anton J. M., Suchiman, H. Eka D., Hofman, Albert, Oostra, Ben, Uitterlinden, Andre G., Willemsen, Gonneke, Plattee, Mathieu, Veldink, Jan H., Van den Berg, Leonard H., Pitts, Steven J., Potluri, Shobha, Sundar, Purnima, Cox, David R., Sunyaev, Shamil R., Den Dunnen, Johan T., Stoneking, Mark, De Knijff, Peter, Kayser, Manfred, Li, Qibin, Li, Yingrui, Du, Yuanping, Chen, Ruoyan, Cao, Hongzhi, Li, Ning, Cao, Sujie, Wang, Jun, Bovenberg, Jasper A., Peer, Itsik, Slagboom, P. Eline, Van Duijn, Cornelia M., Boomsma, Dorret I., Van Ommen, Gert-Jan B., De Bakker, Paul I. W., Swertz, Morris A., and Wijmenga, Cisca

Published
2014

10. Lower cognitive performance in healthy G2019S LRRK2 mutation carriers

Author

Thaler, Avner, primary, Mirelman, Anat, additional, Gurevich, Tanya, additional, Simon, Ely, additional, Orr-Urtreger, Avi, additional, Marder, Karen, additional, Bressman, Susan, additional, Giladi, Nir, additional, Saunders-Pullman, Rachel, additional, Raymond, Deborah, additional, Ozelius, Laurie, additional, Shanker, Vicki, additional, Groves, Mark, additional, Palmese, Christina, additional, Iyer, Akhila, additional, Soto-Valencia, Jeannie, additional, Stanley, Kaili Maloy, additional, Luciano, Marta San, additional, Deik, Andres, additional, Barrett, Matthew James, additional, Cabassa, Jose, additional, Severt, Lawrence, additional, Hunt, Ann, additional, Lubarr, Naomi, additional, Sachdev, Rivka, additional, Miravite, Joan, additional, Lewis, Sara, additional, Clark, Lorraine N., additional, Alcalay, Roy, additional, Fahn, Stanley, additional, Cote, Lucien, additional, Greene, Paul, additional, Waters, Cheryl, additional, Mazzoni, Pietro, additional, Ford, Blair, additional, Louis, Elan, additional, Levy, Oren, additional, Tang, Ming Xin, additional, Rakitin, Brian C., additional, Mejia, Helen, additional, Roos, Ernest, additional, Riley, Martha Orbe, additional, Rosado, Llency, additional, Moskowitz, Carol, additional, Dorovski, Tsvyatko, additional, Clark, Lorraine, additional, Liu, Xinmin, additional, Kisselev, Sergey, additional, Peer, Itsik, additional, Vacic, Vladimir, additional, Balash, Yaacov, additional, Hertzel, Shabtai, additional, Gan Or, Ziv, additional, Shira, Anat Bar, additional, Weiss, Mali Gana, additional, Kobo, Hila, additional, Bregman, Noa, additional, Kestenbaum, Meir, additional, Hendler, Talma, additional, Lehrman, Hedva, additional, Sapir, Einat Even, additional, Levy, Shiran, additional, Yasinovsky, Kira, additional, Shkedy, Anat, additional, and Zelis, Maayan, additional

Published
2012
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