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1. Latin American Trans‐ancestry INitiative for OCD genomics (LATINO): Study protocol

Author

Crowley, James J., Cappi, Carolina, Ochoa‐Panaifo, Marcos E., Frederick, Renee M., Kook, Minjee, Wiese, Andrew D., Rancourt, Diana, Atkinson, Elizabeth G., Giusti‐Rodriguez, Paola, Anderberg, Jacey L., Abramowitz, Jonathan S, Adorno, Victor R, Aguirre, Cinthia, Alves, Gilberto S, Alves, Gustavo S, Ancalade, NaEshia, Anderberg, Jacey L, Arellano Espinosa, Alejandro A, Arnold, Paul D, Atkinson, Elizabeth G, Ayton, Daphne M, Barbosa, Izabela G, Castano, Laura Marcela Barón, Barrera, Cynthia N, Berardo, María Celeste, Berrones, Dayan, Best, John R, Bigdeli, Tim B, Borda, Tania, Burton, Christie L, Buxbaum, Joseph D, Callahan, Jennifer L, Cappi, Carolina, Carneiro, Maria Cecília B, Cepeda, Sandra L, Chazelle, Evelyn, Chire, Jessica M, Munoz, Macarena Churruca, Quiroz, Pamela Claisse, Cobite, Journa, Comer, Jonathan S, Costa, Daniel L, Crosbie, Jennifer, Crowley, James J, Cruz, Victor O, Dager, Guillermo, Daza, Luisa F, Rosa‐Gómez, Anabel, Río, Daniela, Delage, Fernanda Z, Dreher, Carolina B, Fay, Lucila, Fazio, Tomas, Ferrão, Ygor A, Ferreira, Gabriela M, Figueroa, Edith G, Fontenelle, Leonardo F, Forero, Diego A, Fragoso, Daniele TH, Frederick, Renee M, Gadad, Bharathi S, Garrison, Sheldon R, Giusti‐Rodriguez, Paola, Gonzalez, Laura D, González, Andres, González, Marco A, Gonzalez‐Barrios, Polaris, Goodman, Wayne, Grice, Dorothy E, Guintivano, Jerry, Guttfreund, Daniel G, Guzick, Andrew G, Halvorsen, Matthew W, Hovey, Joseph D, Huang, Hailiang, Irreño‐Sotomonte, Jonathan, Janssen‐Aguilar, Reinhard, Jensen, Matias, Jimenez Reynolds, Alexandra Z, Lujambio, Joali Alexandra Juárez, Khalfe, Nasim, Knutsen, Madison A, Kook, Minjee, Lack, Caleb, Lanzagorta, Nuria, Lázaro‐Muñoz, Gabriel, Lima, Monicke O, Longhurst, Melanie O, Lozada Martinez, David A, Luna, Elba S, Marques, Andrea H, Martinez, Molly, Martinez Mallen, Mayra C, Martinez‐Gonzalez, Karen G, Los Angeles Matos, Maria, Mattheisen, Manuel, Maye, Caitlyn E, McGuire, Joseph F, Menezes, Gabriela, Miguel, Euripedes C, Minaya, Charlene, Miño, Tomás, Mithani, Sara M, Oca, Circe Montes, Morales‐Rivero, Alonso, Moreira‐de‐Oliveira, Maria E, Morris, Olivia J, Moya, Pablo R, Moyano, María Beatriz, Muñoz, Sandra I, Naqqash, Zainab, Nicolini, Humberto, Núñez Bracho, Ambar A, Núñez Bracho, Belinda E, Rojas, Maria Corina Ochoa, Ochoa‐Panaifo, Marcos E, Olavarria Castaman, Luis A, Balmaceda, Trinidad Olivos, Ortega, Iliana, Patel, Darpan I, Pato, Michele T, Patrick, Ainsley K, Mino, Mariel Paz y, Perales Orellana, Jose L, Stumpf, Bárbara Perdigão, Peregrina, Tamara, Pereira, Stacey, Duarte, Tania Pérez, Piacsek, Kelly L, Placencia, Maritza, Prieto, María Belén, Quarantini, Lucas C, Quarantini‐Alvim, Yana, Ramos, Iaroslava C, Ramos, Renato T, Ramos, Vanessa R, Ramsey, Kesley A, Rancourt, Diana, Ray, Elise V, Richter, Margaret A, Riemann, Bradley C, Rivas, Juan C, Rodriguez, Carolyn I, Rosario, Maria C, Ruggero, Camilo J, Ruiz‐Chow, Angel A, Ruiz‐Velasco, Alejandra, Sagarnaga, Melisa N, Sampaio, Aline S, Saraiva, Leonardo C, Schachar, Russell J, Schneider, Sophie C, Schweissing, Ethan J, Seligman, Laura D, Shavitt, Roseli G, Soileau, Keaton J, Stewart, S. Evelyn, Storch, Eric A, Storch, Shaina B, Strouphauer, Emily R, Cuevas, Vissente Tapia, Timpano, Kiara R, Garza, Beatriz Treviño‐de, Vallejo‐Silva, Alexie, Vargas‐Medrano, Javier, Vásquez, María I, Martinez, Guadalupe Vidal, Weinzimmer, Saira A, Wiese, Andrew D, Yanez, Mauricio A, Zai, Gwyneth, Zapata‐Restrepo, Lina M, Zappa, Luz M, Zepeda‐Burgos, Raquel M, Zoghbi, Anthony W, Sampaio, Aline Santos, Hounie, Ana Gabriela, Ribeiro, Ana Paula, Souza e Silva, Angela Rodrigues, Martinho, Ariane Fadel, Stumpf, Bárbara Luciane Perdigão, Melo Fadel, Bianca Torres Mendonça, Porto, Camila Vale, Chacur, Carina Freitas, Loureiro, Carla Pereira, Dreher, Carolina Blaya, Cappi, Carolina, Bortoncello, Cristiane Flôres, Conceição Costa, Daniel Lucas, Fragoso, Daniele Tamae Hashimoto, Miguel, Euripedes Constantino, Delage, Fernanda Zetola, Cervone, Flávia, Menezes, Gabriela Bezerra, Souza Barros, Gabriela Cirqueira, Ferreira, Gabriela Mourão, Alves, Gilberto Sousa, Alves, Gustavo Santiago, Caminha, Hugo, Barbosa, Izabela Guimarães, Cenci, Jaqueline, Muhlbauer, Julia Fernandes Eigenheer, Silva, Juliana Rigue, Saraiva, Leonardo Cardoso, Costa Fontenelle, Leonardo Franklin, Camba Lopez, Lígia S., Faro, Livi Ferreira Testoni, Moreira, Luan Pinheiro Domingues, Laurito, Luana Dumans, Castro Quarantini, Lucas, Samezima, Luciana Midori, Santos Martins, Luiz Felipe Guimarães, Oliveira, Marcos Vinícius Sousa, Mathis, Maria Alice, Lopes, Maria Carolina Paraíso, Carneiro, Maria Cecília, Rosário, Maria Conceição, Oliveira, Maria Eduarda Ismerio Moreira, Pinho, Marina Martorelli, Oliveira Lima, Monicke, Nagano, Nádia, Danna, Patrycia Chedid, Silva, Pedro Pereira Fortes, Jesus Cardoso, Raquel Fernandes, Christo, Renan Barbosa, Avila, Richard Chuquel Silveira, Radins, Rodrigo Bolsson, Shavitt, Roseli Gedanke, Santos Ribeiro, Samara, Silveira Meirelles, Tatiane Veríssimo, Aguiar, Thays Mendes, Silva Sousa, Theresa Kerolayne, Vieira, Thiago Blanco, Ramos, Vanessa Rogério, Vasconcellos, Veronica Huhne, Alvim, Yana Quarantini, Ferrão, Ygor Arzeno, Abramowitz, Jonathan S., Adorno, Victor R., Aguirre, Cinthia, Alves, Gilberto S., Alves, Gustavo S., Ancalade, NaEshia, Arellano Espinosa, Alejandro A., Arnold, Paul D., Ayton, Daphne M., Barbosa, Izabela G., Castano, Laura Marcela Barón, Barrera, Cynthia N., Berardo, María Celeste, Berrones, Dayan, Best, John R., Bigdeli, Tim B., Burton, Christie L., Buxbaum, Joseph D., Callahan, Jennifer L., Carneiro, Maria Cecília B., Cepeda, Sandra L., Chazelle, Evelyn, Chire, Jessica M., Munoz, Macarena Churruca, Quiroz, Pamela Claisse, Cobite, Journa, Comer, Jonathan S., Costa, Daniel L., Crosbie, Jennifer, Cruz, Victor O., Dager, Guillermo, Daza, Luisa F., Rosa‐Gómez, Anabel, Río, Daniela, Delage, Fernanda Z., Dreher, Carolina B., Fay, Lucila, Fazio, Tomas, Ferrão, Ygor A., Ferreira, Gabriela M., Figueroa, Edith G., Fontenelle, Leonardo F., Forero, Diego A., Fragoso, Daniele T. H., Gadad, Bharathi S., Garrison, Sheldon R., González, Andres, Gonzalez, Laura D., González, Marco A., Gonzalez‐Barrios, Polaris, Goodman, Wayne K., Grice, Dorothy E., Guintivano, Jerry, Guttfreund, Daniel G., Guzick, Andrew G., Halvorsen, Matthew W., Hovey, Joseph D., Huang, Hailiang, Irreño‐Sotomonte, Jonathan, Janssen‐Aguilar, Reinhard, Jensen, Matias, Jimenez Reynolds, Alexandra Z., Lujambio, Joali Alexandra Juárez, Khalfe, Nasim, Knutsen, Madison A., Lack, Caleb, Lanzagorta, Nuria, Lima, Monicke O., Longhurst, Melanie O., Lozada Martinez, David A., Luna, Elba S., Marques, Andrea H., Martinez, Molly S., Los Angeles Matos, Maria, Maye, Caitlyn E., McGuire, Joseph F., Menezes, Gabriela, Minaya, Charlene, Miño, Tomás, Mithani, Sara M., Oca, Circe Montes, Morales‐Rivero, Alonso, Moreira‐de‐Oliveira, Maria E., Morris, Olivia J., Muñoz, Sandra I., Naqqash, Zainab, Núñez Bracho, Ambar A., Núñez Bracho, Belinda E., Rojas, Maria Corina Ochoa, Olavarria Castaman, Luis A., Balmaceda, Trinidad Olivos, Ortega, Iliana, Patel, Darpan I., Patrick, Ainsley K., Paz y Mino, Mariel, Perales Orellana, Jose L., Stumpf, Bárbara Perdigão, Peregrina, Tamara, Duarte, Tania Pérez, Piacsek, Kelly L., Placencia, Maritza, Prieto, María Belén, Quarantini, Lucas C., Quarantini‐Alvim, Yana, Ramos, Renato T., Ramos, Iaroslava C., Ramos, Vanessa R., Ramsey, Kesley A., Ray, Elise V., Richter, Margaret A., Riemann, Bradley C., Rivas, Juan C., Rosario, Maria C., Ruggero, Camilo J., Ruiz‐Chow, Angel A., Ruiz‐Velasco, Alejandra, Sagarnaga, Melisa N., Sampaio, Aline S., Saraiva, Leonardo C., Schachar, Russell J., Schneider, Sophie C., Schweissing, Ethan J., Seligman, Laura D., Shavitt, Roseli G., Soileau, Keaton J., Stewart, S. Evelyn, Storch, Shaina B., Strouphauer, Emily R., Cuevas, Vissente Tapia, Timpano, Kiara R., Garza, Beatriz Treviño‐de, Vallejo‐Silva, Alexie, Vargas‐Medrano, Javier, Vásquez, María I., Martinez, Guadalupe Vidal, Weinzimmer, Saira A., Yanez, Mauricio A., Zai, Gwyneth, Zapata‐Restrepo, Lina M., Zappa, Luz M., Zepeda‐Burgos, Raquel M., Zoghbi, Anthony W., Miguel, Euripedes C., Rodriguez, Carolyn I., Martinez Mallen, Mayra C., Moya, Pablo R., Borda, Tania, Moyano, María Beatriz, Mattheisen, Manuel, Pereira, Stacey, Lázaro‐Muñoz, Gabriel, Martinez‐Gonzalez, Karen G., Pato, Michele T., Nicolini, Humberto, and Storch, Eric A.

Abstract

Obsessive‐compulsive disorder (OCD) is a debilitating psychiatric disorder. Worldwide, its prevalence is ~2% and its etiology is mostly unknown. Identifying biological factors contributing to OCD will elucidate underlying mechanisms and might contribute to improved treatment outcomes. Genomic studies of OCD are beginning to reveal long‐sought risk loci, but >95% of the cases currently in analysis are of homogenous European ancestry. If not addressed, this Eurocentric bias will result in OCD genomic findings being more accurate for individuals of European ancestry than other ancestries, thereby contributing to health disparities in potential future applications of genomics. In this study protocol paper, we describe the Latin American Trans‐ancestry INitiative for OCD genomics (LATINO, https://www.latinostudy.org). LATINO is a new network of investigators from across Latin America, the United States, and Canada who have begun to collect DNA and clinical data from 5000 richly phenotyped OCD cases of Latin American ancestry in a culturally sensitive and ethical manner. In this project, we will utilize trans‐ancestry genomic analyses to accelerate the identification of OCD risk loci, fine‐map putative causal variants, and improve the performance of polygenic risk scores in diverse populations. We will also capitalize on rich clinical data to examine the genetics of treatment response, biologically plausible OCD subtypes, and symptom dimensions. Additionally, LATINO will help elucidate the diversity of the clinical presentations of OCD across cultures through various trainings developed and offered in collaboration with Latin American investigators. We believe this study will advance the important goal of global mental health discovery and equity.

Published
2024
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2. Rare tandem repeat expansions associate with genes involved in synaptic and neuronal signaling functions in schizophrenia

Author

Wen, Jia, Trost, Brett, Engchuan, Worrawat, Halvorsen, Matthew, Pallotto, Linda M., Mitina, Aleksandra, Ancalade, NaEshia, Farrell, Martilias, Backstrom, Ian, Guo, Keyi, Pellecchia, Giovanna, Thiruvahindrapuram, Bhooma, Giusti-Rodriguez, Paola, Rosen, Jonathan David, Li, Yun, Won, Hyejung, Magnusson, Patrik K. E., Gyllensten, Ulf, Bassett, Anne S., Hultman, Christina M., Sullivan, Patrick F., Yuen, Ryan K. C., and Szatkiewicz, Jin P.

Abstract

Tandem repeat expansions (TREs) are associated with over 60 monogenic disorders and have recently been implicated in complex disorders such as cancer and autism spectrum disorder. The role of TREs in schizophrenia is now emerging. In this study, we have performed a genome-wide investigation of TREs in schizophrenia. Using genome sequence data from 1154 Swedish schizophrenia cases and 934 ancestry-matched population controls, we have detected genome-wide rare (<0.1% population frequency) TREs that have motifs with a length of 2–20 base pairs. We find that the proportion of individuals carrying rare TREs is significantly higher in the schizophrenia group. There is a significantly higher burden of rare TREs in schizophrenia cases than in controls in genic regions, particularly in postsynaptic genes, in genes overlapping brain expression quantitative trait loci, and in brain-expressed genes that are differentially expressed between schizophrenia cases and controls. We demonstrate that TRE-associated genes are more constrained and primarily impact synaptic and neuronal signaling functions. These results have been replicated in an independent Canadian sample that consisted of 252 schizophrenia cases of European ancestry and 222 ancestry-matched controls. Our results support the involvement of rare TREs in schizophrenia etiology.

Published
2022
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3. Gene expression changes following chronic antipsychotic exposure in single cells from mouse striatum

Author

Abrantes, Anthony, Giusti-Rodriguez, Paola, Ancalade, NaEshia, Sekle, Shadia, Basiri, Marcus L., Stuber, Garret D., Sullivan, Patrick F., and Hultman, Rainbo

Abstract

Schizophrenia is an idiopathic psychiatric disorder with a high degree of polygenicity. Evidence from genetics, single-cell transcriptomics, and pharmacological studies suggest an important, but untested, overlap between genes involved in the etiology of schizophrenia and the cellular mechanisms of action of antipsychotics. To directly compare genes with antipsychotic-induced differential expression to genes involved in schizophrenia, we applied single-cell RNA-sequencing to striatal samples from male C57BL/6 J mice chronically exposed to a typical antipsychotic (haloperidol), an atypical antipsychotic (olanzapine), or placebo. We identified differentially expressed genes in three cell populations identified from the single-cell RNA-sequencing (medium spiny neurons [MSNs], microglia, and astrocytes) and applied multiple analysis pipelines to contextualize these findings, including comparison to GWAS results for schizophrenia. In MSNs in particular, differential expression analysis showed that there was a larger share of differentially expressed genes (DEGs) from mice treated with olanzapine compared with haloperidol. DEGs were enriched in loci implicated by genetic studies of schizophrenia, and we highlighted nine genes with convergent evidence. Pathway analyses of gene expression in MSNs highlighted neuron/synapse development, alternative splicing, and mitochondrial function as particularly engaged by antipsychotics. In microglia, we identified pathways involved in microglial activation and inflammation as part of the antipsychotic response. In conclusion, single-cell RNA sequencing may provide important insights into antipsychotic mechanisms of action and links to findings from psychiatric genomic studies.

Published
2022
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4. 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.

Abstract

Fragile X syndrome is rare but a prominent cause of intellectual disability. It is usually caused by a de novo mutation that occurs on multiple haplotypes and thus would not be expected to be detectible using genome-wide association (GWA). We conducted GWA in 89 male FXS cases and 266 male controls, and detected multiple genome-wide significant signals near FMR1 (odds ratio?=?8.10, P?=?2.5?×?10-10). These findings withstood robust attempts at falsification. Fine-mapping yielded a minimum P?=?1.13?×?10-14, but did not narrow the interval. Comprehensive functional genomic integration did not provide a mechanistic hypothesis. Controls carrying a risk haplotype had significantly longer FMR1 CGG repeats than controls with the protective haplotype (P?=?4.75?×?10-5), which may predispose toward increases in CGG number to the premutation range over many generations. This is a salutary reminder of the complexity of even “simple” monogenetic disorders.

Published
2019
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5. Exploration of large, rare copy number variants associated with psychiatric and neurodevelopmental disorders in individuals with anorexia nervosa

Author

Yilmaz, Zeynep, Szatkiewicz, Jin P., Crowley, James J., Ancalade, NaEshia, Brandys, Marek K., van Elburg, Annemarie, de Kovel, Carolien G.F., Adan, Roger A.H., Hinney, Anke, Hebebrand, Johannes, Gratacos, Monica, Fernandez-Aranda, Fernando, Escaramis, Georgia, Gonzalez, Juan R., Estivill, Xavier, Zeggini, Eleftheria, Sullivan, Patrick F., and Bulik, Cynthia M.

Abstract

Supplemental Digital Content is available in the text.Anorexia nervosa (AN) is a serious and heritable psychiatric disorder. To date, studies of copy number variants (CNVs) have been limited and inconclusive because of small sample sizes. We conducted a case-only genome-wide CNV survey in 1983 female AN cases included in the Genetic Consortium for Anorexia Nervosa. Following stringent quality control procedures, we investigated whether pathogenic CNVs in regions previously implicated in psychiatric and neurodevelopmental disorders were present in AN cases. We observed two instances of the well-established pathogenic CNVs in AN cases. In addition, one case had a deletion in the 13q12 region, overlapping with a deletion reported previously in two AN cases. As a secondary aim, we also examined our sample for CNVs over 1 Mbp in size. Out of the 40 instances of such large CNVs that were not implicated previously for AN or neuropsychiatric phenotypes, two of them contained genes with previous neuropsychiatric associations, and only five of them had no associated reports in public CNV databases. Although ours is the largest study of its kind in AN, larger datasets are needed to comprehensively assess the role of CNVs in the etiology of AN.

Published
2017
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6. 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.

Abstract

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Published
2020
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