7 results on '"Gill, Michael"'
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2. Combined analysis from eleven linkage studies of bipolar disorder provides strong evidence of susceptibility loci on chromosomes 6q and 8q
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McQueen, Matthew B., Devlin, B., Faraone, Stephen V., Nimgaonkar, Vishwajit L., Sklar, Pamela, Smoller, Jordan W., Jamra, Rami Abou, Albus, Margot, Bacanu, Silviu-Alin, Baron, Miron, Barrett, Thomas B., Berrettini, Wade, Blacker, Deborah, Byerley, William, Cichon, Sven, Coryell, Willam, Craddock, Nick, Daly, Mark J., DePaulo, J. Raymond, Edenberg, Howard J., Foroud, Tatiana, Gill, Michael, Gilliam, T. Conrad, Hamshere, Marian, Jones, Ian, Jones, Lisa, Juo, Suh-Hang, Kelsoe, John R., Lambert, David, Lange, Christoph, Lerer, Bernard, Liu, Jianjun, Maier, Wolfgang, MacKinnon, James D., McInnis, Melvin G., McMahon, Francis J., Murphy, Dennis L., Nothen, Markus M., Nurnberger, John I., Jr., Pato, Carlos N., Pato, Michele T., Potash, James B., Propping, Peter, Pulver, Ann E., Rice, John P., Rietschel, Marcella, Scheftner, William, Schumacher, Johannes, Segurado, Ricardo, Van Steen, Kristel, Xie, Weiting, Zandi, Peter P., and Laird, Nan M.
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Suicide -- Research ,Bipolar disorder -- Research ,Bipolar disorder -- Genetic aspects ,Biological sciences - Published
- 2005
3. Joint analysis of the DRD5 marker concludes association with attention-deficit/hyperactivity disorder confined to the predominantly inattentive and combined subtypes
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Lowe, Naomi, Kirley, Aiveen, Hawi, Ziarih, Sham, Pak, Wickham, Harvey, Kratochvil, Christopher J., Smith, Shelley D., Lee, Saretta Y., Levy, Florence, Kent, Lindsey, Middle, Fiona, Rohde, Luis A., Roman, Tatiana, Tahir, Eda, Yazgan, Yanke, Asherson, Philip, Mill, Jonathan, Thapar, Anita, Payton, Antony, Todd, Richard D., Stephens, Timothy, Ebstein, Richard P., Manor, Iris, Barr, Cathy L., Wigg, Karen G., Sinke, Richard J., Buitelaar, Jan K., Smalley, Susan L., Nelson, Stan F., Biederman, Joseph, Faraone, Stephen V., and Gill, Michael
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Biological sciences - Published
- 2004
4. Genome scan meta-analysis of schizophrenia and bipolar disorder, Part III: bipolar disorder
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Segurado, Ricardo, Detera-Wadleigh, Sevilla D., Levinson, Douglas F., Lewis, Cathryn M., Gill, Michael, Nurnberger, John I., Jr., Craddock, Nick, DePaulo, J. Raymond, Baron, Miron, Gershon, Elliot S., Ekholm, Jenny, Cichon, Sven, Turecki, Gustavo, Claes, Stephan, Kelsoe, John R., Schofield, Peter R., Badenhop, Renee F., Morissette, J., Coon, Hilary, Blackwood, Douglas, McInnes, L. Alison, Foroud, Tatiana, Edenberg, Howard J., Reich, Theodore, Rice, John P., Goate, Alison, McInnis, Melvin G., McMahon, Francis J., Badner, Judith A., Goldin, Lynn R., Bennett, Phil, Willour, Virginia L., Zandi, Peter P., Liu, Jianjun, Gilliam, Conrad, Juo, Suh-Hang, Berrettini, Wade H., Yoshikawa, Takeo, Peltonen, Leena, Lonnqvist, Jouko, Nothen, Markus M., Schumacher, Johannes, Windemuth, Christine, Rietschel, Marcella, Propping, Peter, Maier, Wolfgang, Alda, Martin, Grof, Paul, Rouleau, Guy A., Del-Favero, Jurgen, Van Broeckhoven, Christine, Mendlewicz, Julien, Adolfsson, Rolf, Spence, M. Anne, Luebbert, Hermann, Adams, Linda J., Donald, Jennifer A., Mitchell, Philip B., Barden, Nicholas, Shink, Eric, Byerley, William, Muir, Walter, Visscher, Peter M., Macgregor, Stuart, Gurling, Hugh, Kalsi, Gursharan, McQuillin, Andrew, Escamilla, Michael A., Reus, Victor I., Leon, Pedro, Freimer, Nelson B., Ewald, Henrik, Kruse, Torben A., Mors, Ole, Radhakrishna, Uppala, Blouin, Jean-Louis, Antonarakis, Stylianos E., and Akarsu, Nurten
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Bipolar disorder -- Research ,Bipolar disorder -- Genetic aspects ,Schizophrenia -- Research ,Schizophrenia -- Genetic aspects ,Biological sciences - Published
- 2003
5. Reply to Joober and Sengupta.
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Segurado, Ricardo, Hawi, Ziarih, and Gill, Michael
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LETTERS to the editor , *ATTENTION-deficit hyperactivity disorder - Abstract
A letter to the editor is presented in response to the article "Parent-of-origin effect and risk for attention-deficit/hyperactivity disorder: Balancing the evidence against bias and chance findings," by Ridha Joober and Sarojini Sengupta in the present issue of the journal.
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- 2006
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6. Pleiotropic Meta-Analysis of Cognition, Education, and Schizophrenia Differentiates Roles of Early Neurodevelopmental and Adult Synaptic Pathways.
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Lam M, Hill WD, Trampush JW, Yu J, Knowles E, Davies G, Stahl E, Huckins L, Liewald DC, Djurovic S, Melle I, Sundet K, Christoforou A, Reinvang I, DeRosse P, Lundervold AJ, Steen VM, Espeseth T, Räikkönen K, Widen E, Palotie A, Eriksson JG, Giegling I, Konte B, Hartmann AM, Roussos P, Giakoumaki S, Burdick KE, Payton A, Ollier W, Chiba-Falek O, Attix DK, Need AC, Cirulli ET, Voineskos AN, Stefanis NC, Avramopoulos D, Hatzimanolis A, Arking DE, Smyrnis N, Bilder RM, Freimer NA, Cannon TD, London E, Poldrack RA, Sabb FW, Congdon E, Conley ED, Scult MA, Dickinson D, Straub RE, Donohoe G, Morris D, Corvin A, Gill M, Hariri AR, Weinberger DR, Pendleton N, Bitsios P, Rujescu D, Lahti J, Le Hellard S, Keller MC, Andreassen OA, Deary IJ, Glahn DC, Malhotra AK, and Lencz T
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- Adult, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Neurodevelopmental Disorders pathology, Cognition physiology, Cognition Disorders physiopathology, Educational Status, Neurodevelopmental Disorders etiology, Polymorphism, Single Nucleotide, Schizophrenia physiopathology, Synaptic Transmission
- Abstract
Susceptibility to schizophrenia is inversely correlated with general cognitive ability at both the phenotypic and the genetic level. Paradoxically, a modest but consistent positive genetic correlation has been reported between schizophrenia and educational attainment, despite the strong positive genetic correlation between cognitive ability and educational attainment. Here we leverage published genome-wide association studies (GWASs) in cognitive ability, education, and schizophrenia to parse biological mechanisms underlying these results. Association analysis based on subsets (ASSET), a pleiotropic meta-analytic technique, allowed jointly associated loci to be identified and characterized. Specifically, we identified subsets of variants associated in the expected ("concordant") direction across all three phenotypes (i.e., greater risk for schizophrenia, lower cognitive ability, and lower educational attainment); these were contrasted with variants that demonstrated the counterintuitive ("discordant") relationship between education and schizophrenia (i.e., greater risk for schizophrenia and higher educational attainment). ASSET analysis revealed 235 independent loci associated with cognitive ability, education, and/or schizophrenia at p < 5 × 10
-8 . Pleiotropic analysis successfully identified more than 100 loci that were not significant in the input GWASs. Many of these have been validated by larger, more recent single-phenotype GWASs. Leveraging the joint genetic correlations of cognitive ability, education, and schizophrenia, we were able to dissociate two distinct biological mechanisms-early neurodevelopmental pathways that characterize concordant allelic variation and adulthood synaptic pruning pathways-that were linked to the paradoxical positive genetic association between education and schizophrenia. Furthermore, genetic correlation analyses revealed that these mechanisms contribute not only to the etiopathogenesis of schizophrenia but also to the broader biological dimensions implicated in both general health outcomes and psychiatric illness., (Copyright © 2019. Published by Elsevier Inc.)- Published
- 2019
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7. Convergence of genes and cellular pathways dysregulated in autism spectrum disorders.
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Pinto D, Delaby E, Merico D, Barbosa M, Merikangas A, Klei L, Thiruvahindrapuram B, Xu X, Ziman R, Wang Z, Vorstman JA, Thompson A, Regan R, Pilorge M, Pellecchia G, Pagnamenta AT, Oliveira B, Marshall CR, Magalhaes TR, Lowe JK, Howe JL, Griswold AJ, Gilbert J, Duketis E, Dombroski BA, De Jonge MV, Cuccaro M, Crawford EL, Correia CT, Conroy J, Conceição IC, Chiocchetti AG, Casey JP, Cai G, Cabrol C, Bolshakova N, Bacchelli E, Anney R, Gallinger S, Cotterchio M, Casey G, Zwaigenbaum L, Wittemeyer K, Wing K, Wallace S, van Engeland H, Tryfon A, Thomson S, Soorya L, Rogé B, Roberts W, Poustka F, Mouga S, Minshew N, McInnes LA, McGrew SG, Lord C, Leboyer M, Le Couteur AS, Kolevzon A, Jiménez González P, Jacob S, Holt R, Guter S, Green J, Green A, Gillberg C, Fernandez BA, Duque F, Delorme R, Dawson G, Chaste P, Café C, Brennan S, Bourgeron T, Bolton PF, Bölte S, Bernier R, Baird G, Bailey AJ, Anagnostou E, Almeida J, Wijsman EM, Vieland VJ, Vicente AM, Schellenberg GD, Pericak-Vance M, Paterson AD, Parr JR, Oliveira G, Nurnberger JI, Monaco AP, Maestrini E, Klauck SM, Hakonarson H, Haines JL, Geschwind DH, Freitag CM, Folstein SE, Ennis S, Coon H, Battaglia A, Szatmari P, Sutcliffe JS, Hallmayer J, Gill M, Cook EH, Buxbaum JD, Devlin B, Gallagher L, Betancur C, and Scherer SW
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- Child, Female, Gene Regulatory Networks, Humans, Male, Multigene Family, Pedigree, Sequence Deletion, Child Development Disorders, Pervasive genetics, DNA Copy Number Variations, Metabolic Networks and Pathways genetics
- Abstract
Rare copy-number variation (CNV) is an important source of risk for autism spectrum disorders (ASDs). We analyzed 2,446 ASD-affected families and confirmed an excess of genic deletions and duplications in affected versus control groups (1.41-fold, p = 1.0 × 10(-5)) and an increase in affected subjects carrying exonic pathogenic CNVs overlapping known loci associated with dominant or X-linked ASD and intellectual disability (odds ratio = 12.62, p = 2.7 × 10(-15), ∼3% of ASD subjects). Pathogenic CNVs, often showing variable expressivity, included rare de novo and inherited events at 36 loci, implicating ASD-associated genes (CHD2, HDAC4, and GDI1) previously linked to other neurodevelopmental disorders, as well as other genes such as SETD5, MIR137, and HDAC9. Consistent with hypothesized gender-specific modulators, females with ASD were more likely to have highly penetrant CNVs (p = 0.017) and were also overrepresented among subjects with fragile X syndrome protein targets (p = 0.02). Genes affected by de novo CNVs and/or loss-of-function single-nucleotide variants converged on networks related to neuronal signaling and development, synapse function, and chromatin regulation., (Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.)
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- 2014
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