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Your search keyword '"Crowley, P."' showing total 17 results
Start Over Author "Crowley, P." Journal molecular psychiatry
17 results on '"Crowley, P."'

1. Neurocognitive profiles of 22q11.2 and 16p11.2 deletions and duplications

Author

Gur, Ruben C., Bearden, Carrie E., Jacquemont, Sebastien, Swillen, Ann, van Amelsvoort, Therese, van den Bree, Marianne, Vorstman, Jacob, Sebat, Jonathan, Ruparel, Kosha, Gallagher, Robert Sean, McClellan, Emily, White, Lauren, Crowley, Terrence Blaine, Giunta, Victoria, Kushan, Leila, O’Hora, Kathleen, Verbesselt, Jente, Vandensande, Ans, Vingerhoets, Claudia, van Haelst, Mieke, Hall, Jessica, Harwood, Janet, Chawner, Samuel J.R.A., Patel, Nishi, Palad, Katrina, Hong, Oanh, Guevara, James, Martin, Charles Olivier, Jizi, Khadije, Bélanger, Anne-Marie, Scherer, Stephen W., Bassett, Anne S., McDonald-McGinn, Donna M., and Gur, Raquel E.

Published
2025
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2. A burden of rare copy number variants in obsessive-compulsive disorder

Author

Halvorsen, Matthew W., de Schipper, Elles, Bäckman, Julia, Strom, Nora I., Hagen, Kristen, Lindblad-Toh, Kerstin, Karlsson, Elinor K., Pedersen, Nancy L., Wallert, John, Bulik, Cynthia M., Fundín, Bengt, Landén, Mikael, Kvale, Gerd, Hansen, Bjarne, Haavik, Jan, Mattheisen, Manuel, Rück, Christian, Mataix-Cols, David, and Crowley, James J.

Published
2024
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3. Genome-Wide Association Study of Obsessive-Compulsive Symptoms including 33,943 individuals from the general population

Author

Strom, Nora I., Burton, Christie L., Iyegbe, Conrad, Silzer, Talisa, Antonyan, Lilit, Pool, René, Lemire, Mathieu, Crowley, James J., Hottenga, Jouke-Jan, Ivanov, Volen Z., Larsson, Henrik, Lichtenstein, Paul, Magnusson, Patrik, Rück, Christian, Schachar, Russell, Wu, Hei Man, Cath, Danielle, Crosbie, Jennifer, Mataix-Cols, David, Boomsma, Dorret I., Mattheisen, Manuel, Meier, Sandra M., Smit, Dirk J. A., and Arnold, Paul D.

Published
2024
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4. Genetic contributors to risk of schizophrenia in the presence of a 22q11.2 deletion.

Author

Cleynen, Isabelle, Engchuan, Worrawat, Hestand, Matthew S, Heung, Tracy, Holleman, Aaron M, Johnston, H Richard, Monfeuga, Thomas, McDonald-McGinn, Donna M, Gur, Raquel E, Morrow, Bernice E, Swillen, Ann, Vorstman, Jacob AS, Bearden, Carrie E, Chow, Eva WC, van den Bree, Marianne, Emanuel, Beverly S, Vermeesch, Joris R, Warren, Stephen T, Owen, Michael J, Chopra, Pankaj, Cutler, David J, Duncan, Richard, Kotlar, Alex V, Mulle, Jennifer G, Voss, Anna J, Zwick, Michael E, Diacou, Alexander, Golden, Aaron, Guo, Tingwei, Lin, Jhih-Rong, Wang, Tao, Zhang, Zhengdong, Zhao, Yingjie, Marshall, Christian, Merico, Daniele, Jin, Andrea, Lilley, Brenna, Salmons, Harold I, Tran, Oanh, Holmans, Peter, Pardinas, Antonio, Walters, James TR, Demaerel, Wolfram, Boot, Erik, Butcher, Nancy J, Costain, Gregory A, Lowther, Chelsea, Evers, Rens, van Amelsvoort, Therese AMJ, van Duin, Esther, Vingerhoets, Claudia, Breckpot, Jeroen, Devriendt, Koen, Vergaelen, Elfi, Vogels, Annick, Crowley, T Blaine, McGinn, Daniel E, Moss, Edward M, Sharkus, Robert J, Unolt, Marta, Zackai, Elaine H, Calkins, Monica E, Gallagher, Robert S, Gur, Ruben C, Tang, Sunny X, Fritsch, Rosemarie, Ornstein, Claudia, Repetto, Gabriela M, Breetvelt, Elemi, Duijff, Sasja N, Fiksinski, Ania, Moss, Hayley, Niarchou, Maria, Murphy, Kieran C, Prasad, Sarah E, Daly, Eileen M, Gudbrandsen, Maria, Murphy, Clodagh M, Murphy, Declan G, Buzzanca, Antonio, Fabio, Fabio Di, Digilio, Maria C, Pontillo, Maria, Marino, Bruno, Vicari, Stefano, Coleman, Karlene, Cubells, Joseph F, Ousley, Opal Y, Carmel, Miri, Gothelf, Doron, Mekori-Domachevsky, Ehud, Michaelovsky, Elena, Weinberger, Ronnie, Weizman, Abraham, Kushan, Leila, Jalbrzikowski, Maria, Armando, Marco, Eliez, Stéphan, Sandini, Corrado, and Schneider, Maude

Subjects
International 22q11.2DS Brain and Behavior Consortium, Prevention, Serious Mental Illness, Genetics, Human Genome, Schizophrenia, Neurosciences, Mental Health, Clinical Research, Pediatric, Brain Disorders, 2.1 Biological and endogenous factors, Mental health, Psychiatry, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences
Abstract

Schizophrenia occurs in about one in four individuals with 22q11.2 deletion syndrome (22q11.2DS). The aim of this International Brain and Behavior 22q11.2DS Consortium (IBBC) study was to identify genetic factors that contribute to schizophrenia, in addition to the ~20-fold increased risk conveyed by the 22q11.2 deletion. Using whole-genome sequencing data from 519 unrelated individuals with 22q11.2DS, we conducted genome-wide comparisons of common and rare variants between those with schizophrenia and those with no psychotic disorder at age ≥25 years. Available microarray data enabled direct comparison of polygenic risk for schizophrenia between 22q11.2DS and independent population samples with no 22q11.2 deletion, with and without schizophrenia (total n = 35,182). Polygenic risk for schizophrenia within 22q11.2DS was significantly greater for those with schizophrenia (padj = 6.73 × 10-6). Novel reciprocal case-control comparisons between the 22q11.2DS and population-based cohorts showed that polygenic risk score was significantly greater in individuals with psychotic illness, regardless of the presence of the 22q11.2 deletion. Within the 22q11.2DS cohort, results of gene-set analyses showed some support for rare variants affecting synaptic genes. No common or rare variants within the 22q11.2 deletion region were significantly associated with schizophrenia. These findings suggest that in addition to the deletion conferring a greatly increased risk to schizophrenia, the risk is higher when the 22q11.2 deletion and common polygenic risk factors that contribute to schizophrenia in the general population are both present.

Published
2021

5. Examination of the shared genetic basis of anorexia nervosa and obsessive–compulsive disorder

Author

Yilmaz, Zeynep, Halvorsen, Matthew, Bryois, Julien, Yu, Dongmei, Thornton, Laura M, Zerwas, Stephanie, Micali, Nadia, Moessner, Rainald, Burton, Christie L, Zai, Gwyneth, Erdman, Lauren, Kas, Martien J, Arnold, Paul D, Davis, Lea K, Knowles, James A, Breen, Gerome, Scharf, Jeremiah M, Nestadt, Gerald, Mathews, Carol A, Bulik, Cynthia M, Mattheisen, Manuel, and Crowley, James J

Subjects
Biological Psychology, Clinical and Health Psychology, Psychology, Genetics, Serious Mental Illness, Nutrition, Brain Disorders, Anorexia, Human Genome, Prevention, Mental Health, Eating Disorders, 2.1 Biological and endogenous factors, Aetiology, Mental health, Anorexia Nervosa, Body Mass Index, Comorbidity, Genome-Wide Association Study, Humans, Obsessive-Compulsive Disorder, Phenotype, Eating Disorders Working Group of the Psychiatric Genomics Consortium, Tourette Syndrome/Obsessive–Compulsive Disorder Working Group of the Psychiatric Genomics Consortium, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry, Clinical sciences, Biological psychology, Clinical and health psychology
Abstract

Anorexia nervosa (AN) and obsessive-compulsive disorder (OCD) are often comorbid and likely to share genetic risk factors. Hence, we examine their shared genetic background using a cross-disorder GWAS meta-analysis of 3495 AN cases, 2688 OCD cases, and 18,013 controls. We confirmed a high genetic correlation between AN and OCD (rg = 0.49 ± 0.13, p = 9.07 × 10-7) and a sizable SNP heritability (SNP h2 = 0.21 ± 0.02) for the cross-disorder phenotype. Although no individual loci reached genome-wide significance, the cross-disorder phenotype showed strong positive genetic correlations with other psychiatric phenotypes (e.g., rg = 0.36 with bipolar disorder and 0.34 with neuroticism) and negative genetic correlations with metabolic phenotypes (e.g., rg = -0.25 with body mass index and -0.20 with triglycerides). Follow-up analyses revealed that although AN and OCD overlap heavily in their shared risk with other psychiatric phenotypes, the relationship with metabolic and anthropometric traits is markedly stronger for AN than for OCD. We further tested whether shared genetic risk for AN/OCD was associated with particular tissue or cell-type gene expression patterns and found that the basal ganglia and medium spiny neurons were most enriched for AN-OCD risk, consistent with neurobiological findings for both disorders. Our results confirm and extend genetic epidemiological findings of shared risk between AN and OCD and suggest that larger GWASs are warranted.

Published
2020

9. Genetics of response to cognitive behavior therapy in adults with major depression: a preliminary report

Author

Andersson, Evelyn, Crowley, James J., Lindefors, Nils, Ljótsson, Brjánn, Hedman-Lagerlöf, Erik, Boberg, Julia, El Alaoui, Samir, Karlsson, Robert, Lu, Yi, Mattheisen, Manuel, Kähler, Anna K., Svanborg, Cecilia, Mataix-Cols, David, Mattsson, Simon, Forsell, Erik, Kaldo, Viktor, Schalling, Martin, Lavebratt, Catharina, Sullivan, Patrick F., and Rück, Christian

Published
2019
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10. Common-variant associations with fragile X syndrome

Author

Crowley, James J., Szatkiewicz, Jin, Kähler, Anna K., Giusti-Rodriguez, Paola, Ancalade, NaEshia, Booker, Jessica K., Carr, Jennifer L., Crawford, Greg E., Losh, Molly, Stockmeier, Craig A., Taylor, Annette K., Piven, Joseph, and Sullivan, Patrick F.

Published
2019
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12. Correction: Common-variant associations with fragile X syndrome

Author

Crowley, James J., Szatkiewicz, Jin, Kähler, Anna K., Giusti-Rodriguez, Paola, Ancalade, NaEshia, Booker, Jessica K., Carr, Jennifer L., Giamberardino, Stephanie N., Crawford, Greg E., Losh, Molly, Stockmeier, Craig A., Taylor, Annette K., Piven, Joseph, and Sullivan, Patrick F.

Published
2020
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13. Neurocognitive profiles of 22q11.2 and 16p11.2 deletions and duplications

Author

Gur, Ruben C., Bearden, Carrie E., Jacquemont, Sebastien, Swillen, Ann, van Amelsvoort, Therese, van den Bree, Marianne, Vorstman, Jacob, Sebat, Jonathan, Ruparel, Kosha, Gallagher, Robert Sean, McClellan, Emily, White, Lauren, Crowley, Terrence Blaine, Giunta, Victoria, Kushan, Leila, O’Hora, Kathleen, Verbesselt, Jente, Vandensande, Ans, Vingerhoets, Claudia, van Haelst, Mieke, Hall, Jessica, Harwood, Janet, Chawner, Samuel J.R.A., Patel, Nishi, Palad, Katrina, Hong, Oanh, Guevara, James, Martin, Charles Olivier, Jizi, Khadije, Bélanger, Anne-Marie, Scherer, Stephen W., Bassett, Anne S., McDonald-McGinn, Donna M., and Gur, Raquel E.

Abstract

Rare recurrent copy number variants (CNVs) at chromosomal loci 22q11.2 and 16p11.2 are genetic disorders with lifespan risk for neuropsychiatric disorders. Microdeletions and duplications are associated with neurocognitive deficits, yet few studies compared these groups using the same measures to address confounding measurement differences. We report a prospective international collaboration applying the same computerized neurocognitive assessment, the Penn Computerized Neurocognitive Battery (CNB), administered in a multi-site study on rare genomic disorders: 22q11.2 deletions (n= 492); 22q11.2 duplications (n= 106); 16p11.2 deletion (n= 117); and 16p11.2 duplications (n= 46). Domains examined include executive functions, episodic memory, complex cognition, social cognition, and psychomotor speed. Accuracy and speed for each domain were included as dependent measures in a mixed-model repeated measures analysis. Locus (22q11.2, 16p11.2) and Copy number (deletion/duplication) were grouping factors and Measure (accuracy, speed) and neurocognitive domain were repeated measures factors, with Sex and Site as covariates. We also examined correlation with IQ. We found a significant Locus × Copy number × Domain × Measure interaction (p= 0.0004). 22q11.2 deletions were associated with greater performance accuracy deficits than 22q11.2 duplications, while 16p11.2 duplications were associated with greater specific deficits than 16p11.2 deletions. Duplications at both loci were associated with reduced speed compared to deletions. Performance profiles differed among the groups with particularly poor memory performance of the 22q11.2 deletion group while the 16p11.2 duplication group had greatest deficits in complex cognition. Average accuracy on the CNB was moderately correlated with Full Scale IQ. Deletions and duplications of 22q11.2 and 16p11.2 have differential effects on accuracy and speed of neurocognition indicating locus specificity of performance profiles. These profile differences can help inform mechanistic substrates to heterogeneity in presentation and outcome, and can only be established in large-scale international consortia using the same neurocognitive assessment. Future studies could aim to link performance profiles to clinical features and brain function.

Published
2024
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14. Copy number variation in schizophrenia in Sweden

Author

Szatkiewicz, J P, O'Dushlaine, C, Chen, G, Chambert, K, Moran, J L, Neale, B M, Fromer, M, Ruderfer, D, Akterin, S, Bergen, S E, Kähler, A, Magnusson, P K E, Kim, Y, Crowley, J J, Rees, E, Kirov, G, O'Donovan, M C, Owen, M J, Walters, J, Scolnick, E, Sklar, P, Purcell, S, Hultman, C M, McCarroll, S A, and Sullivan, P F

Published
2014
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16. Comparative genomic evidence for the involvement of schizophrenia risk genes in antipsychotic effects

Author

Kim, Y, Giusti-Rodriguez, P, Crowley, J J, Bryois, J, Nonneman, R J, Ryan, A K, Quackenbush, C R, Iglesias-Ussel, M D, Lee, P H, Sun, W, de Villena, F P-M, and Sullivan, P F

Abstract

Genome-wide association studies (GWAS) for schizophrenia have identified over 100 loci encoding >500 genes. It is unclear whether any of these genes, other than dopamine receptor D2, are immediately relevant to antipsychotic effects or represent novel antipsychotic targets. We applied an in vivo molecular approach to this question by performing RNA sequencing of brain tissue from mice chronically treated with the antipsychotic haloperidol or vehicle. We observed significant enrichments of haloperidol-regulated genes in schizophrenia GWAS loci and in schizophrenia-associated biological pathways. Our findings provide empirical support for overlap between genetic variation underlying the pathophysiology of schizophrenia and the molecular effects of a prototypical antipsychotic.

Published
2018
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17. Improved ethical guidance for the return of results from psychiatric genomics research

Author

Lázaro-Muñoz, G, Farrell, M S, Crowley, J J, Filmyer, D M, Shaughnessy, R A, Josiassen, R C, and Sullivan, P F

Abstract

There is an emerging consensus that genomic researchers should, at a minimum, offer to return to individual participants clinically valid, medically important and medically actionable genomic findings (for example, pathogenic variants in BRCA1) identified in the course of research. However, this is not a common practice in psychiatric genetics research. Furthermore, psychiatry researchers often generate findings that do not meet all of these criteria, yet there may be ethically compelling arguments to offer selected results. Here, we review the return of results debate in genomics research and propose that, as for genomic studies of other medical conditions, psychiatric genomics researchers should offer findings that meet the minimum criteria stated above. Additionally, if resources allow, psychiatry researchers could consider offering to return pre-specified ‘clinically valuable’ findings even if not medically actionable—for instance, findings that help corroborate a psychiatric diagnosis, and findings that indicate important health risks. Similarly, we propose offering ‘likely clinically valuable’ findings, specifically, variants of uncertain significance potentially related to a participant’s symptoms. The goal of this Perspective is to initiate a discussion that can help identify optimal ways of managing the return of results from psychiatric genomics research.

Published
2018
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