18 results on '"Pennington, B.F."'
Search Results
2. Hypothesis-driven genome-wide association studies provide novel insights into genetics of reading disabilities
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Price, K.M., Wigg, K.G., Eising, E., Feng, Y, Blokland, K., Wilkinson, M., Kerr, E.N., Guger, S.L., Abbondanza, F., Allegrini, A.G., Andlauer, T.F.M., Bates, T.C., Bernard, M., Bonte, M., Boomsma, D.I., Bourgeron, T., Brandeis, D., Carreiras, M., Ceroni, F., Csépe, V., Dale, P.S., DeFries, J.C., Jong, P.F. de, Démonet, J.F., Zeeuw, E.L. de, Franken, M.-C.J., Francks, C., Gerritse, M.L., Gialluisi, A., Gordon, S.D., Gruen, J.R., Hayiou-Thomas, M.E., Hernández-Cabrera, J., Hottenga, J.-J., Hulme, C., Jansen, P.R., Kere, J., Koomar, T., Landerl, K., Leonard, G.T., Liao, Z., Luciano, M., Lyytinen, H., Martin, N.G., Martinelli, A., Maurer, U., Michaelson, J.J., Mirza-Schreiber, N., Moll, K., Monaco, A.P., Morgan, A.T., Müller-Myhsok, B., Newbury, D.F., Nöthen, M.M., Olson, R.K., Paracchini, S., Paus, T., Pausova, Z., Pennell, C.E., Pennington, B.F., Plomin, R.J., Ramus, F., Reilly, S., Richer, L., Rimfeld, K., Schulte-Körne, G., Shapland, C.Y., Simpson, N.H., Smith, S.D., Snowling, M.J., St Pourcain, B., Stein, J.F., Talcott, J.B., Tiemeier, H., Tomblin, J.B., Truong, D.T., Bergen, E. van, Schroeff, M.P. van der, Donkelaar, M.M.J. van, Verhoef, E., Wang, C.A., Watkins, K.E., Whitehouse, A.J.O., Willcutt, E.G., Wright, M.J., Zhu, G., Fisher, S.E., Lovett, M.W., Strug, L.J., Barr, C.L., University of St Andrews. School of Medicine, University of St Andrews. Centre for Biophotonics, University of St Andrews. Biomedical Sciences Research Complex, University of St Andrews. Institute of Behavioural and Neural Sciences, University of St Andrews. St Andrews Bioinformatics Unit, University of St Andrews. Cellular Medicine Division, STEMM - Stem Cells and Metabolism Research Program, Juha Kere / Principal Investigator, Research Programs Unit, University of Helsinki, Consortium, Quantitative Trait Working Group of the GenLang, European Commission, Otorhinolaryngology and Head and Neck Surgery, Child and Adolescent Psychiatry / Psychology, RS: FPN CN 7, Language, Biological Psychology, Amsterdam Reproduction & Development, APH - Mental Health, APH - Methodology, APH - Health Behaviors & Chronic Diseases, APH - Personalized Medicine, Complex Trait Genetics, Amsterdam Neuroscience - Complex Trait Genetics, LEARN! - Educational neuroscience, learning and development, and Human genetics
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Neuroinformatics ,single nucleotide ,Candidate gene ,Autism Spectrum Disorder ,Developmental dyslexia ,autism spectrum disorder ,QH426 Genetics ,Polymorphism, Single Nucleotide ,Neuronal migration ,3124 Neurology and psychiatry ,polymorphism ,Dyslexia ,Cellular and Molecular Neuroscience ,All institutes and research themes of the Radboud University Medical Center ,problem solving ,SDG 3 - Good Health and Well-being ,dyslexia ,Humans ,Kiaa0319 ,Family ,humans ,Children ,QH426 ,Problem Solving ,Biological Psychiatry ,MCC ,Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7] ,genome-wide association study ,Dyx1c1 ,Plasma-membrane ,3rd-DAS ,Psychiatry and Mental health ,Susceptibility ,RC0321 ,SDG 4 - Quality Education ,RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry ,Genome-Wide Association Study ,Knockout mice - Abstract
Reading Disability (RD) is often characterized by difficulties in the phonology of the language. While the molecular mechanisms underlying it are largely undetermined, loci are being revealed by genome-wide association studies (GWAS). In a previous GWAS for word reading (Price, 2020), we observed that top single-nucleotide polymorphisms (SNPs) were located near to or in genes involved in neuronal migration/axon guidance (NM/AG) or loci implicated in autism spectrum disorder (ASD). A prominent theory of RD etiology posits that it involves disturbed neuronal migration, while potential links between RD-ASD have not been extensively investigated. To improve power to identify associated loci, we up-weighted variants involved in NM/AG or ASD, separately, and performed a new Hypothesis-Driven (HD)–GWAS. The approach was applied to a Toronto RD sample and a meta-analysis of the GenLang Consortium. For the Toronto sample (n = 624), no SNPs reached significance; however, by gene-set analysis, the joint contribution of ASD-related genes passed the threshold (p~1.45 × 10–2, threshold = 2.5 × 10–2). For the GenLang Cohort (n = 26,558), SNPs in DOCK7 and CDH4 showed significant association for the NM/AG hypothesis (sFDR q = 1.02 × 10–2). To make the GenLang dataset more similar to Toronto, we repeated the analysis restricting to samples selected for reading/language deficits (n = 4152). In this GenLang selected subset, we found significant association for a locus intergenic between BTG3-C21orf91 for both hypotheses (sFDR q < 9.00 × 10–4). This study contributes candidate loci to the genetics of word reading. Data also suggest that, although different variants may be involved, alleles implicated in ASD risk may be found in the same genes as those implicated in word reading. This finding is limited to the Toronto sample suggesting that ascertainment influences genetic associations., Translational Psychiatry, 12 (1), ISSN:2158-3188
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- 2022
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3. Genome-wide analyses of individual differences in quantitatively assessed reading- and language-related skills in up to 34,000 people
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Eising, E., Mirza-Schreiber, N., Zeeuw, E.L. de, Wang, C.A., Truong, D.T., Allegrini, A.G., Shapland, C.Y., Zhu, G., Wigg, K.G., Gerritse, M.L., Molz, B., Alagöz, G., Gialluisi, A., Abbondanza, F., Rimfeld, K., Donkelaar, M.M.J. van, Liao, Z., Jansen, P.R., Andlauer, T.F.M., Bates, T.C., Bernard, M., Blokland, K., Bonte, M., Børglum, A.D., Bourgeron, T., Brandeis, D., Ceroni, F., Csépe, V., Dale, P.S., Jong, P.F. de, DeFries, J.C., Démonet, J.F., Demontis, D., Feng, Yu, Gordon, S.D.S., Guger, S.L., Hayiou-Thomas, M.E., Hernández-Cabrera, J.A., Hottenga, J.J., Hulme, C., Kere, J., Kerr, E.N., Koomar, T., Landerl, K., Leonard, G.T., Lovett, M.W., Lyytinen, H., Martin, N.G., Martinelli, A., Maurer, U., Michaelson, J.J., Moll, K., Monaco, A.P., Morgan, A.T., Nöthen, M.M., Pausova, Z., Pennell, C.E., Pennington, B.F., Price, K.M., Rajagopal, V.M., Ramus, F., Richer, L., Simpson, N.H., Smith, S.D., Snowling, M.J., Stein, J., Strug, L.J., Talcott, J.B., Tiemeier, H., Schroeff, M.P. van der, Verhoef, E., Watkins, K.E., Wilkinson, M., Wright, M.J., Barr, C.L., Boomsma, D.I., Carreiras, M., Franken, M.J., Gruen, J.R., Luciano, M., Müller-Myhsok, B., Newbury, D.F., Olson, R.K., Paracchini, S., Paus, T., Plomin, R., Reilly, S., Schulte-Körne, G., Tomblin, J.B., Bergen, E. van, Whitehouse, A.J.O., Willcutt, E.G., Pourcain, B. St, Francks, C., Fisher, S.E., St Pourcain, B., Génétique humaine et fonctions cognitives - Human Genetics and Cognitive Functions (GHFC (UMR_3571 / U-Pasteur_1)), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Laboratoire de sciences cognitives et psycholinguistique (LSCP), Département d'Etudes Cognitives - ENS Paris (DEC), École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-École des hautes études en sciences sociales (EHESS)-Centre National de la Recherche Scientifique (CNRS), Human genetics, APH - Aging & Later Life, APH - Mental Health, Biological Psychology, Complex Trait Genetics, Amsterdam Neuroscience - Complex Trait Genetics, APH - Health Behaviors & Chronic Diseases, APH - Personalized Medicine, Amsterdam Reproduction & Development, APH - Methodology, LEARN! - Educational neuroscience, learning and development, Child and Adolescent Psychiatry / Psychology, Otorhinolaryngology and Head and Neck Surgery, STEMM - Stem Cells and Metabolism Research Program, Juha Kere / Principal Investigator, Research Programs Unit, University of Helsinki, Language, RS: FPN CN 7, The Royal Society, University of St Andrews. Cellular Medicine Division, University of St Andrews. School of Medicine, University of St Andrews. Centre for Biophotonics, University of St Andrews. Biomedical Sciences Research Complex, University of St Andrews. Institute of Behavioural and Neural Sciences, and University of St Andrews. St Andrews Bioinformatics Unit
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Neuroinformatics ,Adult ,kieli ja kielet ,Adolescent ,Individuality ,QH426 Genetics ,Polymorphism, Single Nucleotide ,lukeminen ,Language in Interaction ,Young Adult ,SDG 3 - Good Health and Well-being ,RA0421 ,reading ,RA0421 Public health. Hygiene. Preventive Medicine ,Humans ,Speech ,study ,Polymorphism ,Reading j ,Preschool ,Child ,QH426 ,perinnöllisyys ,Genome-wide Association Study ,Language ,Meta-analysis ,Reading ,MCC ,Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7] ,genome-wide association study ,language ,Multidisciplinary ,meta-analyysi ,1184 Genetics, developmental biology, physiology ,kielitaito ,[SDV.NEU.SC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Cognitive Sciences ,DAS ,Single Nucleotide ,meta-analysis ,Genetic Loci ,Child, Preschool ,Genome-Wide Association Study ,perimä ,lukutaito ,genome-wide association ,SDG 4 - Quality Education - Abstract
Published August 23, 2022 The use of spoken and written language is a fundamental human capacity. Individual differences in reading- and language-related skills are influenced by genetic variation, with twin-based heritability estimates of 30 to 80% depending on the trait. The genetic architecture is complex, heterogeneous, and multifactorial, but investigations of contributions of single-nucleotide polymorphisms (SNPs) were thus far underpowered. We present a multicohort genome-wide association study (GWAS) of five traits assessed individually using psychometric measures (word reading, nonword reading, spelling, phoneme awareness, and nonword repetition) in samples of 13,633 to 33,959 participants aged 5 to 26 y. We identified genome-wide significant association with word reading (rs11208009, P = 1.098 × 1028) at a locus that has not been associated with intelligence or educational attainment. All five reading-/language-related traits showed robust SNP heritability, accounting for 13 to 26% of trait variability. Genomic structural equation modeling revealed a shared genetic factor explaining most of the variation in word/nonword reading, spelling, and phoneme awareness, which only partially overlapped with genetic variation contributing to nonword repetition, intelligence, and educational attainment. A multivariate GWAS of word/nonword reading, spelling, and phoneme awareness maximized power for follow-up investigation. Genetic correlation analysis with neuroimaging traits identified an association with the surface area of the banks of the left superior temporal sulcus, a brain region linked to the processing of spoken and written language. Heritability was enriched for genomic elements regulating gene expression in the fetal brain and in chromosomal regions that are depleted of Neanderthal variants. Together, these results provide avenues for deciphering the biological underpinnings of uniquely human traits. We thank all the children, twins, families, and participants who took part and are taking part in the 22 cohorts whose data contributed to these GWAS meta-analyses; the staff working on the different cohorts, including volunteers, study coordinators, interviewers, teachers, nurses, research scientists, general practitioners, midwives, psychologists, psychometrists, computer and laboratory technicians, and colleagues who assisted in the quality control and preparation of the imputed GWAS data; and the pharmacies and hospitals that were involved. B.M., B.M.-M., B.S.P., C.F., E.E., E.V., G.A., M.v.D., and S.E.F. are supported by the Max Planck Society. A.G. and T.F.M.A. were supported by the Munich Cluster for Systems Neurology (SyNergy), and A.G. was supported by Fondazione Umberto Veronesi. A.T.M. is supported by National Health and Medical Research Council of Australia (NHMRC) Grants 1105008 and 1195955 and Centre of Research Excellence Grant 1116976. A.J.O.W. is supported by NHMRC Grant 1173896. B.S.P. is supported by Simons Foundation Autism Research Initiative Grant 514787. C.Y.S. works in the Medical Research Council Integrative Epidemiology Unit at the University of Bristol (MC_UU_00011/3). D.I.B. acknowledges Royal Netherlands Academy of Science Professor Award PAH/6635. E.E. is supported by NIH Grant R01DC016977. E.G.W. and J.R.G. are supported by National Institute of Child Health and Human Development (NICHD) Grant P50 HD 27802. F.R. is supported by Agence Nationale de la Recherche Grants ANR-06-NEURO-019-01, ANR-17-EURE-0017 IEC, ANR-10-IDEX-0001-02 PSL, and ANR-11-BSV4-014-01 and European Commission Grant LSHM-CT-2005-018696. H.T. is supported by the Netherlands Organization for Scientific Research (NWO) and Netherlands Organisation for Health Research and Development (ZonMW) Grant VICI 016.VICI.170.200. J.C.D. was supported by NICHD Grant P50 HD 27802. J.J.M., J.B.To., and T.K. were supported by NIH Grant R01 DC014489. K.M.P. was supported by the Hospital for Sick Children Research Training Program (Restracomp). K.R. is supported by a Sir Henry Wellcome Postdoctoral Fellowship (213514/Z/18/Z). M.J.S. is supported by Wellcome Trust Grant WT082032MA. S.P. and F.A. are supported by Royal Society Grants UF150663 and RGF\EA\180141. T.B. is supported by Institut Pasteur, the Bettencourt-Schueller Foundation, and Université de Paris. The Adolescent Brain Cognitive Development Study is supported by the NIH and additional federal partners (NIH Grants U01DA041048, U01DA050989, U01DA051016, U01DA041022, U01DA051018, U01DA051037, U01DA050987, U01DA041174, U01DA041106, U01DA041117, U01DA041028, U01DA041134, U01DA050988, U01DA051039, U01DA041156, U01DA041025, U01DA041120, U01DA051038, U01DA041148, U01DA041093, U01DA041089, U24DA041123, and U24DA041147). The Aston Cohort was supported by funding from European Union (EU) Horizon 2020 Programme 641652 and Waterloo Foundation Grant 797/17290. The St. Andrews Bioinformatics Unit is funded by Wellcome Trust Grants 105621/Z/14/Z and 204821/Z/16/Z. ALSPAC is supported by UK Medical Research Council and Wellcome Grant 217065/Z/19/Z and the University of Bristol. A comprehensive list of grant funding is available on the ALSPAC website (http://www.bristol.ac.uk/alspac/external/documents/grant-acknowledgements.pdf). The Basque Center on Cognition, Brain and Language (BCBL) cohort was supported by the Basque Government through the Basic Excellence Research Centre program and the Agencia Estatal de Investigación through BCBL Severo Ochoa excellence accreditation. The Brisbane Adolescent Twin Sample was supported by Australian Research Council Grants A7960034, A79906588, A79801419, DP0212016, and DP0343921, with genotyping funded by the NHMRC Grant 389891. The Colorado Learning Disabilities Research Center cohort was supported by NICHD Grant P50 HD 27802. The Early Language in Victoria Study was supported by NHMRC Grant 436958. The Familial Influences on Literacy Abilities cohort is supported by the University of Amsterdam, the Max Planck Institue Nijmegen, and NWO Grants Rubicon 446-12-005 and VENI 451-15-017. The GRaD study was funded by the Manton Foundation, NIH Grants P50-HD027802 and K99-HD094902, and the Lambert Family. NeuroDys was funded by an EU Sixth Framework Program grant to the NeuroDys Consortium, Swiss National Science Foundation Grant 32-108130, and Austrian Science Fund Grant 18351-B02. The Netherlands Twin Register is funded by NWO Grants 480-04-004, 481-08-011, 056-32-010, 024.001.003, 480-15-001/674, 184.021.007, 184.033.111, and 56-464-14192; ZonMW Grants 911-09-032 and 912-10-020; the Amsterdam Public Health and Amsterdam Reproduction and Development Research Institutes; European Science Council Grant ERC Advanced 230374; EU Seventh Framework Program (FP7) Grant FP7/2007-2013: 602768; National Institute of Mental Health (NIMH) Grants U24 MH068457-06, R01 MH58799-03, and 1RC2 MH089995; and the Avera Institute for Human Genetics. The Pediatric Imaging, Neurocognition, and Genetics cohort is funded by NIH Grant RC2DA029475, the National Institute on Drug Abuse, and the Eunice Kennedy Shriver NICHD. The Philadelphia Neurodevelopmental Cohort is funded by NIH Grants RC2MH089983 and RC2MH089924, an institutional development award to the Center for Applied Genomics from The Children’s Hospital of Philadelphia, and a donation from Adele and Daniel Kubert and thanks the NIH data repository. The Raine study was supported by long-term funding from NHMRC Grants 572613, 403981, and 1059711 and Canadian Institutes of Health Research (CIHR) Grant MOP-82893. Funding was also provided by the University of Western Australia, Curtin University, the Women and Infants Research Foundation, the Telethon Kids Institute, Edith Cowan University, Murdoch University, the University of Notre Dame Australia, and the Raine Medical Research Foundation. The Raine study analyses were supported by the Pawsey Supercomputing Centre with funding from the Australian Government and the Government of Western Australia. The Saguenay Youth Study is supported by the CIHR, the Heart and Stroke Foundation of Quebec, and the Canadian Foundation for Innovation. The SLI Consortium was funded by Wellcome Trust Grant 076566 and UK Medical Research Council Grant G1000569. The Twins Early Development Study is supported by UK Medical Research Council Grants MR/V012878/1 and MR/M021475/1, NIH Grant AG046938, and the EU FP7 grant FP7/2007-2013/: 602768. Toronto was supported by CIHR Grant MOP-133440. UK Dyslexia was supported by Wellcome Trust Grants 076566/Z/05/Z and 075491/Z/04, Waterloo Foundation Grant 797–1720, EU Grant 018696, and Royal Society Grant UF100463. The York cohort was funded by Wellcome Trust Grant 082036/B/07/Z. We acknowledge iPSYCH for sharing their summary statistics. The iPSYCH team was supported by Lundbeck Foundation Grants R102-A9118, R155-2014-1724, and R248-2017-2003; NIMH Grant 1U01MH109514-01; and the Universities and University Hospitals of Aarhus and Copenhagen. The Danish National Biobank resource was supported by the Novo Nordisk Foundation. High-performance computer capacity was provided by the Center for Genomics and Personalized Medicine and the Centre for Integrative Sequencing, Aarhus University, Denmark.
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- 2022
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4. Discovery of 42 genome-wide significant loci associated with dyslexia
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Doust, C., Fontanillas, P., Eising, E., Gordon, S.D., Wang, Z, Alagoz, G., Molz, B., St Pourcain, B., Francks, C., Marioni, R.E., Zhao, J, Paracchini, S., Talcott, J.B., Monaco, A.P., Stein, J.F., Gruen, J.R., Olson, R.K., Willcutt, E.G., DeFries, J.C., Pennington, B.F., Smith, S.D., Wright, M.J., Martin, N.G., Auton, A., Bates, T.C., Fisher, S.E., Luciano, M., Doust, C., Fontanillas, P., Eising, E., Gordon, S.D., Wang, Z, Alagoz, G., Molz, B., St Pourcain, B., Francks, C., Marioni, R.E., Zhao, J, Paracchini, S., Talcott, J.B., Monaco, A.P., Stein, J.F., Gruen, J.R., Olson, R.K., Willcutt, E.G., DeFries, J.C., Pennington, B.F., Smith, S.D., Wright, M.J., Martin, N.G., Auton, A., Bates, T.C., Fisher, S.E., and Luciano, M.
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Contains fulltext : 284950.pdf (Publisher’s version ) (Open Access)
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- 2022
5. Dyslexia and Related Communication Disorders
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Friend, A., primary, Pennington, B.F., additional, Smith, S.D., additional, and Gilger, J.W., additional
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- 2014
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6. Evidence for linkage and association with reading disability, on 6p21.3-22
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Kaplan, D.E., Gayan, J., Ahn, J., Won, T.-W., Pauls, D., Olson, R.K., DeFries, J.C, Wood, F., Pennington, B.F., Page, G.P., Smith, S.D., and Gruen, J.R.
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Genetic research -- Analysis ,Reading disability -- Causes of ,Dyslexia -- Causes of ,Chromosomes -- Genetic aspects ,Chromosome mapping -- Genetic aspects ,Phenotype -- Genetic aspects ,Biological sciences - Published
- 2002
7. Dyslexia, Genetics of
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Pennington, B.F., primary
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- 2001
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8. Bivariate linkage scan for reading disability and attention-deficit/hyperactivity disorder localizes pleiotropic loci
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Gayan, J., Willcutt, E.G., Fisher, S.E., Francks, C., Cardon, L.R., DeFries, J.C., Monaco, A.P., Smith, S.D., Pennington, B.F., and Olson, R.K.
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Psychology and mental health - Abstract
The established genetic correlation between reading disability (RD) and attention-deficit/hyperactivity disorder suggests that their comorbidity is due at least in part to genes that have an impact on several phenotypes, a phenomenon known as pleiotropy. A bivariate linkage test employed for selected samples to help identifying these pleiotropic loci highlights the utility of the linkage method to study pleitropy.
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- 2005
9. Investigating the effects of copy number variants on reading and language performance
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Gialluisi, A., Visconti, A., Willcutt, E.G., Smith, S.D., Pennington, B.F., Falchi, M., DeFries, J.C., Olson, R.K., Francks, C., Fisher, S.E., Gialluisi, A., Visconti, A., Willcutt, E.G., Smith, S.D., Pennington, B.F., Falchi, M., DeFries, J.C., Olson, R.K., Francks, C., and Fisher, S.E.
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Contains fulltext : 162007.pdf (publisher's version ) (Open Access)
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- 2016
10. Linkage of an ADHD phenotype to 6p21.3 in a population with reading disability
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Smith, S.D., Pennington, B.F., Willcutt, E., Deffenbacherr, K., Hoover, D., Smolen, A., Moyzis, R., Olson, R.K., and DeFries, J.C.
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Genetic research -- Analysis ,Human genetics -- Research ,Attention-deficit hyperactivity disorder -- Genetic aspects ,Dyslexia -- Genetic aspects ,Biological sciences - Published
- 2000
11. Genome-wide screening for DNA variants associated with reading and language traits
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Gialluisi, A., Newbury, D.F., Wilcutt, E.G., Olson, R.K., DeFries, J.C., Brandler, W.M., Pennington, B.F., Smith, S.D., Scerri, T.S., Simpson, N.H., Luciano, M., Evans, D.M., Bates, T.C., Stein, J.F., Talcott, J.B., Monaco, A.P., Paracchini, S., Francks, C., Fisher, S.E., Consortium, S.L.I., Gialluisi, A., Newbury, D.F., Wilcutt, E.G., Olson, R.K., DeFries, J.C., Brandler, W.M., Pennington, B.F., Smith, S.D., Scerri, T.S., Simpson, N.H., Luciano, M., Evans, D.M., Bates, T.C., Stein, J.F., Talcott, J.B., Monaco, A.P., Paracchini, S., Francks, C., Fisher, S.E., and Consortium, S.L.I.
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Item does not contain fulltext
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- 2014
12. Differential genetic etiology of reading disability as a function of mathematics performance
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Institute for Social Research, University of Michigan, Ann Arbor, Michigan, USA, Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado, USA, Department of Psychology, University of Denver, Denver, Colorado, USA, Ann Arbor, Casto, S.D., Pennington, B.F., Light, J.G., DeFries, J.C., Institute for Social Research, University of Michigan, Ann Arbor, Michigan, USA, Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado, USA, Department of Psychology, University of Denver, Denver, Colorado, USA, Ann Arbor, Casto, S.D., Pennington, B.F., Light, J.G., and DeFries, J.C.
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In order to assess the etiology of reading disability as a function of mathematics performance, data from 168 monozygotic (MZ) and 127 same-sex dizygotic (DZ) twin pairs in which at least one member of each pair was reading-disabled were subjected to quantitative genetic analyses. MZ and DZ concordance rates for reading disability were computed for different levels of mathematics performance, and reading performance data were fitted to an extension of the basic multiple regression model for the analysis of selected twin data. Results of these analyses suggest that genetic factors may be especially salient as a cause of reading disability in children with borderline deficits in mathematics performance: thus, mathematics performance may be a valid dimension for diagnosing subtypes of reading disability.
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- 2006
13. Brain morphometry in reading-disabled twins
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Pennington, B.F., primary, Filipek, P.A., additional, Lefly, D., additional, Churchwell, J., additional, Kennedy, D.N., additional, Simon, J.H., additional, Filley, C.M., additional, Galaburda, A., additional, Alarcon, M., additional, and DeFries, J.C., additional
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- 1999
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14. Why Associations Among Traits Do Not Necessarily Indicate Their Common Etiology - Comment
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Gilger, J.W., primary and Pennington, B.F., additional
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- 1995
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15. The neuropsychology of Down syndrome: evidence for hippocampal dysfunction.
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Pennington, B.F., Moon, J., Edgin, J., Stedron, J., Nadel, L., Pennington, Bruce F, Moon, Jennifer, Edgin, Jamie, Stedron, Jennifer, and Nadel, Lynn
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DOWN syndrome , *NEUROPSYCHOLOGICAL tests for children , *COGNITION disorders diagnosis , *FRONTAL lobe , *COGNITION disorders , *COMPARATIVE studies , *HIPPOCAMPUS (Brain) , *NEUROPSYCHOLOGICAL tests , *RESEARCH methodology , *MEDICAL cooperation , *RESEARCH , *EVALUATION research , *SEVERITY of illness index , *DISEASE complications , *PHYSIOLOGY - Abstract
This study tested prefrontal and hippocampal functions in a sample of 28 school-aged (M = 14.7 years, SD = 2.7) individuals with Down syndrome (DS) compared with 28 (M = 4.9 years, SD = .75) typically developing children individually matched on mental age (MA). Both neuropsychological domains were tested with multiple behavioral measures. Benchmark measures of verbal and spatial function demonstrated that this DS sample was similar to others in the literature. The main finding was a significant Group x Domain interaction effect indicating differential hippocampal dysfunction in the group with DS. However, there was a moderate partial correlation (r = .54, controlling for chronological age) between hippocampal and prefrontal composite scores in the DS group, and both composites contributed unique variance to the prediction of MA and adaptive behavior in that group. In sum, these results indicate a particular weakness in hippocampal functions in DS in the context of overall cognitive dysfunction. It is interesting that these results are similar to what has been found in a mouse model of DS. Such a model will make it easier to understand the neurobiological mechanisms that lead to the development of hippocampal dysfunction in DS. [ABSTRACT FROM AUTHOR]
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- 2003
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16. Word identification in reading and the promise of subsymbolic psycholinguistics.
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Van Orden, G.C. and Pennington, B.F.
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PHONETICS - Abstract
Criticizes of dual-process theory, and argues that it has misconstrued the correspondence between words' spellings and their phonology. Describes a subsymbolic alternative to dual-process theory; The decline of dual-process theory; The GPC hypothesis; The delayed-phonology hypothesis; The independent-processes hypothesis; More.
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- 1990
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17. Interfacial Tension of the Methane-Normal Decane System
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Stegemeier, G.L., primary, Pennington, B.F., additional, Brauer, E.B., additional, and Hough, E.W., additional
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- 1962
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18. Dyslexia, Genetics of
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Pennington, B.F.
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