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1. X-chromosome and kidney function: evidence from a multi-trait genetic analysis of 908,697 individuals reveals sex-specific and sex-differential findings in genes regulated by androgen response elements.

Author

Scholz, Markus, Horn, Katrin, Pott, Janne, Wuttke, Matthias, Kühnapfel, Andreas, Nasr, M, Kirsten, Holger, Li, Yong, Hoppmann, Anselm, Gorski, Mathias, Ghasemi, Sahar, Li, Man, Tin, Adrienne, Chai, Jin-Fang, Cocca, Massimiliano, Wang, Judy, Nutile, Teresa, Akiyama, Masato, Åsvold, Bjørn, Bansal, Nisha, Biggs, Mary, Boutin, Thibaud, Brenner, Hermann, Brumpton, Ben, Burkhardt, Ralph, Cai, Jianwen, Campbell, Archie, Campbell, Harry, Chalmers, John, Chasman, Daniel, Chee, Miao, Chen, Xu, Cheng, Ching-Yu, Cifkova, Renata, Daviglus, Martha, Delgado, Graciela, Dittrich, Katalin, Edwards, Todd, Endlich, Karlhans, Michael Gaziano, J, Giri, Ayush, Giulianini, Franco, Gordon, Scott, Gudbjartsson, Daniel, Hallan, Stein, Hamet, Pavel, Hartman, Catharina, Hayward, Caroline, Heid, Iris, Hellwege, Jacklyn, Holleczek, Bernd, Holm, Hilma, Hutri-Kähönen, Nina, Hveem, Kristian, Isermann, Berend, Jonas, Jost, Joshi, Peter, Kamatani, Yoichiro, Kanai, Masahiro, Kastarinen, Mika, Khor, Chiea, Kiess, Wieland, Kleber, Marcus, Körner, Antje, Kovacs, Peter, Krajcoviechova, Alena, Kramer, Holly, Krämer, Bernhard, Kuokkanen, Mikko, Kähönen, Mika, Lange, Leslie, Lash, James, Lehtimäki, Terho, Li, Hengtong, Lin, Bridget, Liu, Jianjun, Loeffler, Markus, Lyytikäinen, Leo-Pekka, Magnusson, Patrik, Martin, Nicholas, Matsuda, Koichi, Milaneschi, Yuri, Mishra, Pashupati, Mononen, Nina, Montgomery, Grant, Mook-Kanamori, Dennis, Mychaleckyj, Josyf, März, Winfried, Nauck, Matthias, Nikus, Kjell, Nolte, Ilja, Noordam, Raymond, Okada, Yukinori, Olafsson, Isleifur, Oldehinkel, Albertine, Penninx, Brenda, Perola, Markus, Pirastu, Nicola, and Polasek, Ozren

Subjects
Humans, Male, Female, Androgens, Genome-Wide Association Study, Kidney, Chromosomes, Human, X, Response Elements, Polymorphism, Single Nucleotide, Genetic Predisposition to Disease, Tetraspanins
Abstract

X-chromosomal genetic variants are understudied but can yield valuable insights into sexually dimorphic human traits and diseases. We performed a sex-stratified cross-ancestry X-chromosome-wide association meta-analysis of seven kidney-related traits (n = 908,697), identifying 23 loci genome-wide significantly associated with two of the traits: 7 for uric acid and 16 for estimated glomerular filtration rate (eGFR), including four novel eGFR loci containing the functionally plausible prioritized genes ACSL4, CLDN2, TSPAN6 and the female-specific DRP2. Further, we identified five novel sex-interactions, comprising male-specific effects at FAM9B and AR/EDA2R, and three sex-differential findings with larger genetic effect sizes in males at DCAF12L1 and MST4 and larger effect sizes in females at HPRT1. All prioritized genes in loci showing significant sex-interactions were located next to androgen response elements (ARE). Five ARE genes showed sex-differential expressions. This study contributes new insights into sex-dimorphisms of kidney traits along with new prioritized gene targets for further molecular research.

Published
2024

3. Prioritization of Kidney Cell Types Highlights Myofibroblast Cells in Regulating Human Blood Pressure

Author

Evangelou, Evangelos, Warren, Helen R., Gao, He, Ntritsos, Georgios, Dimou, Niki, Esko, Tonu, Mägi, Reedik, Milani, Lili, Almgren, Peter, Boutin, Thibaud, Debette, Stéphanie, Ding, Jun, Giulianini, Franco, Holliday, Elizabeth G., Jackson, Anne U., Li -Gao, Ruifang, Lin, Wei -Yu, Luan, Jian'an, Mangino, Massimo, Oldmeadow, Christopher, Prins, Bram Peter, Qian, Yong, Sargurupremraj, Muralidharan, Shah, Nabi, Surendran, Praveen, Thériault, Sébastien, Verweij, Niek, Willems, Sara M., Zhao, Jing -Hua, Amouyel, Philippe, Connell, John, de Mutsert, Renée, Doney, Alex S.F., Farrall, Martin, Menni, Cristina, Morris, Andrew D., Noordam, Raymond, Paré, Guillaume, Poulter, Neil R., Shields, Denis C., Stanton, Alice, Thom, Simon, Abecasis, Gonçalo, Amin, Najaf, Arking, Dan E., Ayers, Kristin L., Barbieri, Caterina M., Batini, Chiara, Bis, Joshua C., Blake, Tineka, Bochud, Murielle, Boehnke, Michael, Boerwinkle, Eric, Boomsma, Dorret I., Bottinger, Erwin P., Braund, Peter S., Brumat, Marco, Campbell, Archie, Campbell, Harry, Chakravarti, Aravinda, Chambers, John C., Chauhan, Ganesh, Ciullo, Marina, Cocca, Massimiliano, Collins, Francis, Cordell, Heather J., Davies, Gail, de Borst, Martin H., de Geus, Eco J., Deary, Ian J., Deelen, Joris, Del Greco M, Fabiola, Demirkale, Cumhur Yusuf, Dörr, Marcus, Ehret, Georg B., Elosua, Roberto, Enroth, Stefan, Erzurumluoglu, A. Mesut, Ferreira, Teresa, Frånberg, Mattias, Franco, Oscar H., Gandin, Ilaria, Gasparini, Paolo, Giedraitis, Vilmantas, Gieger, Christian, Girotto, Giorgia, Goel, Anuj, Gow, Alan J., Gudnason, Vilmundur, Guo, Xiuqing, Gyllensten, Ulf, Hamsten, Anders, Harris, Tamara B., Harris, Sarah E., Hartman, Catharina A., Havulinna, Aki S., Hicks, Andrew A., Hofer, Edith, Hofman, Albert, Hottenga, Jouke-Jan, Huffman, Jennifer E., Hwang, Shih-Jen, Ingelsson, Erik, James, Alan, Jansen, Rick, Jarvelin, Marjo -Riitta, Joehanes, Roby, Johansson, Åsa, Johnson, Andrew D., Joshi, Peter K., Jousilahti, Pekka, Jukema, J. Wouter, Jula, Antti, Kähönen, Mika, Kathiresan, Sekar, Keavney, Bernard D., Khaw, Kay-Tee, Knekt, Paul, Knight, Joanne, Kolcic, Ivana, Kooner, Jaspal S., Koskinen, Seppo, Kristiansson, Kati, Kutalik, Zoltan, Laan, Maris, Larson, Marty, Launer, Lenore J., Lehne, Benjamin, Lehtimäki, Terho, Liewald, David C.M., Lin, Li, Lind, Lars, Lindgren, Cecilia M., Liu, YongMei, Loos, Ruth J.F., Lopez, Lorna M., Lu, Yingchang, Lyytikäinen, Leo-Pekka, Mahajan, Anubha, Mamasoula, Chrysovalanto, Marrugat, Jaume, Marten, Jonathan, Milaneschi, Yuri, Morgan, Anna, Morris, Andrew P., Morrison, Alanna C., Munson, Peter J., Nalls, Mike A., Nandakumar, Priyanka, Nelson, Christopher P., Niiranen, Teemu, Nolte, Ilja M., Nutile, Teresa, Oldehinkel, Albertine J., Oostra, Ben A., O'Reilly, Paul F., Org, Elin, Padmanabhan, Sandosh, Palmas, Walter, Palotie, Aarno, Pattie, Alison, Penninx, Brenda W.J.H., Perola, Markus, Peters, Annette, Polasek, Ozren, Pramstaller, Peter P., Nguyen, Quang Tri, Raitakari, Olli T., Rettig, Rainer, Rice, Kenneth, Ridker, Paul M., Ried, Janina S., Riese, Harriëtte, Ripatti, Samuli, Robino, Antonietta, Rose, Lynda M., Rotter, Jerome I., Rudan, Igor, Ruggiero, Daniela, Saba, Yasaman, Sala, Cinzia F., Salomaa, Veikko, Samani, Nilesh J., Sarin, Antti-Pekka, Schmidt, Reinhold, Schmidt, Helena, Shrine, Nick, Siscovick, David, Smith, Albert V., Snieder, Harold, Sõber, Siim, Sorice, Rossella, Starr, John M., Stott, David J., Strachan, David P., Strawbridge, Rona J., Sundström, Johan, Swertz, Morris A., Taylor, Kent D., Teumer, Alexander, Tobin, Martin D., Tomaszewski, Maciej, Toniolo, Daniela, Traglia, Michela, Trompet, Stella, Tuomilehto, Jaakko, Tzourio, Christophe, Uitterlinden, André G., Vaez, Ahmad, van der Most, Peter J., van Duijn, Cornelia M., Verwoert, Germaine C., Vitart, Veronique, Völker, Uwe, Vollenweider, Peter, Vuckovic, Dragana, Watkins, Hugh, Wild, Sarah H., Willemsen, Gonneke, Wilson, James F., Wright, Alan F., Yao, Jie, Zemunik, Tatijana, Zhang, Weihua, Attia, John R., Butterworth, Adam S., Chasman, Daniel I., Conen, David, Cucca, Francesco, Danesh, John, Hayward, Caroline, Howson, Joanna M.M., Laakso, Markku, Lakatta, Edward G., Langenberg, Claudia, Melander, Olle, Mook-Kanamori, Dennis O., Palmer, Colin N.A., Risch, Lorenz, Scott, Robert A., Scott, Rodney J., Sever, Peter, Spector, Tim D., van der Harst, Pim, Wareham, Nicholas J., Zeggini, Eleftheria, Levy, Daniel, Munroe, Patricia B., Newton-Cheh, Christopher, Brown, Morris J., Metspalu, Andres, Psaty, Bruce M., Wain, Louise V., Elliott, Paul, Caulfield, Mark J., Ganji-Arjenaki, Mahboube, Kamali, Zoha, Sardari, Soroush, and de Borst, Martin

Published
2024
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4. Polymorphisms in ERBB4 and TACR1 associated with dry mouth in clozapine-treated patients.

Author

Puolakka, Hanna, Solismaa, Anssi, Lyytikäinen, Leo-Pekka, Viikki, Merja, Seppälä, Niko, Mononen, Nina, Lehtimäki, Terho, and Kampman, Olli

Subjects
DROOLING, XEROSTOMIA, GENETIC variation, GENETIC polymorphisms, GENETIC regulation
Abstract

Background: Sialorrhea is a common and uncomfortable adverse effect of clozapine, and its severity varies between patients. The aim of the study was to select broadly genes related to the regulation of salivation and study associations between sialorrhea and dry mouth and polymorphisms in the selected genes. Methods: The study population consists of 237 clozapine-treated patients, of which 172 were genotyped. Associations between sialorrhea and dry mouth with age, sex, BMI, smoking, clozapine dose, clozapine and norclozapine serum levels, and other comedication were studied. Genetic associations were analyzed with linear and logistic regression models explaining sialorrhea and dry mouth with each SNP added separately to the model as coefficients. Results: Clozapine dose, clozapine or norclozapine concentration and their ratio were not associated with sialorrhea or dryness of mouth. Valproate use (p = 0.013) and use of other antipsychotics (p = 0.015) combined with clozapine were associated with excessive salivation. No associations were found between studied polymorphisms and sialorrhea. In analyses explaining dry mouth with logistic regression with age and sex as coefficients, two proxy-SNPs were associated with dry mouth: epidermal growth factor receptor 4 (ERBB4) rs3942465 (adjusted p = 0.025) and tachykinin receptor 1 (TACR1) rs58933792 (adjusted p = 0.029). Conclusion: Use of valproate or antipsychotic polypharmacy may increase the risk of sialorrhea. Genetic variations in ERBB4 and TACR1 might contribute to experienced dryness of mouth among patients treated with clozapine. [ABSTRACT FROM AUTHOR]

Published
2024
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7. Prioritization of Kidney Cell Types Highlights Myofibroblast Cells in Regulating Human Blood Pressure

Author

Ganji-Arjenaki, Mahboube, primary, Kamali, Zoha, additional, Evangelou, Evangelos, additional, Warren, Helen R., additional, Gao, He, additional, Ntritsos, Georgios, additional, Dimou, Niki, additional, Esko, Tonu, additional, Mägi, Reedik, additional, Milani, Lili, additional, Almgren, Peter, additional, Boutin, Thibaud, additional, Debette, Stéphanie, additional, Ding, Jun, additional, Giulianini, Franco, additional, Holliday, Elizabeth G., additional, Jackson, Anne U., additional, Li -Gao, Ruifang, additional, Lin, Wei -Yu, additional, Luan, Jian'an, additional, Mangino, Massimo, additional, Oldmeadow, Christopher, additional, Prins, Bram Peter, additional, Qian, Yong, additional, Sargurupremraj, Muralidharan, additional, Shah, Nabi, additional, Surendran, Praveen, additional, Thériault, Sébastien, additional, Verweij, Niek, additional, Willems, Sara M., additional, Zhao, Jing -Hua, additional, Amouyel, Philippe, additional, Connell, John, additional, de Mutsert, Renée, additional, Doney, Alex S.F., additional, Farrall, Martin, additional, Menni, Cristina, additional, Morris, Andrew D., additional, Noordam, Raymond, additional, Paré, Guillaume, additional, Poulter, Neil R., additional, Shields, Denis C., additional, Stanton, Alice, additional, Thom, Simon, additional, Abecasis, Gonçalo, additional, Amin, Najaf, additional, Arking, Dan E., additional, Ayers, Kristin L., additional, Barbieri, Caterina M., additional, Batini, Chiara, additional, Bis, Joshua C., additional, Blake, Tineka, additional, Bochud, Murielle, additional, Boehnke, Michael, additional, Boerwinkle, Eric, additional, Boomsma, Dorret I., additional, Bottinger, Erwin P., additional, Braund, Peter S., additional, Brumat, Marco, additional, Campbell, Archie, additional, Campbell, Harry, additional, Chakravarti, Aravinda, additional, Chambers, John C., additional, Chauhan, Ganesh, additional, Ciullo, Marina, additional, Cocca, Massimiliano, additional, Collins, Francis, additional, Cordell, Heather J., additional, Davies, Gail, additional, de Borst, Martin H., additional, de Geus, Eco J., additional, Deary, Ian J., additional, Deelen, Joris, additional, Del Greco M, Fabiola, additional, Demirkale, Cumhur Yusuf, additional, Dörr, Marcus, additional, Ehret, Georg B., additional, Elosua, Roberto, additional, Enroth, Stefan, additional, Erzurumluoglu, A. Mesut, additional, Ferreira, Teresa, additional, Frånberg, Mattias, additional, Franco, Oscar H., additional, Gandin, Ilaria, additional, Gasparini, Paolo, additional, Giedraitis, Vilmantas, additional, Gieger, Christian, additional, Girotto, Giorgia, additional, Goel, Anuj, additional, Gow, Alan J., additional, Gudnason, Vilmundur, additional, Guo, Xiuqing, additional, Gyllensten, Ulf, additional, Hamsten, Anders, additional, Harris, Tamara B., additional, Harris, Sarah E., additional, Hartman, Catharina A., additional, Havulinna, Aki S., additional, Hicks, Andrew A., additional, Hofer, Edith, additional, Hofman, Albert, additional, Hottenga, Jouke-Jan, additional, Huffman, Jennifer E., additional, Hwang, Shih-Jen, additional, Ingelsson, Erik, additional, James, Alan, additional, Jansen, Rick, additional, Jarvelin, Marjo -Riitta, additional, Joehanes, Roby, additional, Johansson, Åsa, additional, Johnson, Andrew D., additional, Joshi, Peter K., additional, Jousilahti, Pekka, additional, Jukema, J. Wouter, additional, Jula, Antti, additional, Kähönen, Mika, additional, Kathiresan, Sekar, additional, Keavney, Bernard D., additional, Khaw, Kay-Tee, additional, Knekt, Paul, additional, Knight, Joanne, additional, Kolcic, Ivana, additional, Kooner, Jaspal S., additional, Koskinen, Seppo, additional, Kristiansson, Kati, additional, Kutalik, Zoltan, additional, Laan, Maris, additional, Larson, Marty, additional, Launer, Lenore J., additional, Lehne, Benjamin, additional, Lehtimäki, Terho, additional, Liewald, David C.M., additional, Lin, Li, additional, Lind, Lars, additional, Lindgren, Cecilia M., additional, Liu, YongMei, additional, Loos, Ruth J.F., additional, Lopez, Lorna M., additional, Lu, Yingchang, additional, Lyytikäinen, Leo-Pekka, additional, Mahajan, Anubha, additional, Mamasoula, Chrysovalanto, additional, Marrugat, Jaume, additional, Marten, Jonathan, additional, Milaneschi, Yuri, additional, Morgan, Anna, additional, Morris, Andrew P., additional, Morrison, Alanna C., additional, Munson, Peter J., additional, Nalls, Mike A., additional, Nandakumar, Priyanka, additional, Nelson, Christopher P., additional, Niiranen, Teemu, additional, Nolte, Ilja M., additional, Nutile, Teresa, additional, Oldehinkel, Albertine J., additional, Oostra, Ben A., additional, O'Reilly, Paul F., additional, Org, Elin, additional, Padmanabhan, Sandosh, additional, Palmas, Walter, additional, Palotie, Aarno, additional, Pattie, Alison, additional, Penninx, Brenda W.J.H., additional, Perola, Markus, additional, Peters, Annette, additional, Polasek, Ozren, additional, Pramstaller, Peter P., additional, Nguyen, Quang Tri, additional, Raitakari, Olli T., additional, Rettig, Rainer, additional, Rice, Kenneth, additional, Ridker, Paul M., additional, Ried, Janina S., additional, Riese, Harriëtte, additional, Ripatti, Samuli, additional, Robino, Antonietta, additional, Rose, Lynda M., additional, Rotter, Jerome I., additional, Rudan, Igor, additional, Ruggiero, Daniela, additional, Saba, Yasaman, additional, Sala, Cinzia F., additional, Salomaa, Veikko, additional, Samani, Nilesh J., additional, Sarin, Antti-Pekka, additional, Schmidt, Reinhold, additional, Schmidt, Helena, additional, Shrine, Nick, additional, Siscovick, David, additional, Smith, Albert V., additional, Snieder, Harold, additional, Sõber, Siim, additional, Sorice, Rossella, additional, Starr, John M., additional, Stott, David J., additional, Strachan, David P., additional, Strawbridge, Rona J., additional, Sundström, Johan, additional, Swertz, Morris A., additional, Taylor, Kent D., additional, Teumer, Alexander, additional, Tobin, Martin D., additional, Tomaszewski, Maciej, additional, Toniolo, Daniela, additional, Traglia, Michela, additional, Trompet, Stella, additional, Tuomilehto, Jaakko, additional, Tzourio, Christophe, additional, Uitterlinden, André G., additional, Vaez, Ahmad, additional, van der Most, Peter J., additional, van Duijn, Cornelia M., additional, Verwoert, Germaine C., additional, Vitart, Veronique, additional, Völker, Uwe, additional, Vollenweider, Peter, additional, Vuckovic, Dragana, additional, Watkins, Hugh, additional, Wild, Sarah H., additional, Willemsen, Gonneke, additional, Wilson, James F., additional, Wright, Alan F., additional, Yao, Jie, additional, Zemunik, Tatijana, additional, Zhang, Weihua, additional, Attia, John R., additional, Butterworth, Adam S., additional, Chasman, Daniel I., additional, Conen, David, additional, Cucca, Francesco, additional, Danesh, John, additional, Hayward, Caroline, additional, Howson, Joanna M.M., additional, Laakso, Markku, additional, Lakatta, Edward G., additional, Langenberg, Claudia, additional, Melander, Olle, additional, Mook-Kanamori, Dennis O., additional, Palmer, Colin N.A., additional, Risch, Lorenz, additional, Scott, Robert A., additional, Scott, Rodney J., additional, Sever, Peter, additional, Spector, Tim D., additional, van der Harst, Pim, additional, Wareham, Nicholas J., additional, Zeggini, Eleftheria, additional, Levy, Daniel, additional, Munroe, Patricia B., additional, Newton-Cheh, Christopher, additional, Brown, Morris J., additional, Metspalu, Andres, additional, Psaty, Bruce M., additional, Wain, Louise V., additional, Elliott, Paul, additional, Caulfield, Mark J., additional, Sardari, Soroush, additional, and de Borst, Martin, additional

Published
2024
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8. Polygenic risk for schizophrenia predicting social trajectories in a general population sample.

Author

Saarinen, Aino, Hietala, Jarmo, Lyytikäinen, Leo-Pekka, Hamal Mishra, Binisha, Sormunen, Elina, Lavonius, Veikka, Kähönen, Mika, Raitakari, Olli, Lehtimäki, Terho, and Keltikangas-Järvinen, Liisa

Subjects
MENTAL illness risk factors, SCHIZOPHRENIA risk factors, GENETICS of schizophrenia, RISK assessment, PSYCHOLOGICAL resilience, PREDICTION models, SOCIAL factors, DESCRIPTIVE statistics, REPORTING of diseases, PARENTHOOD, AGE distribution, GENETIC risk score, EXPERIENCE, SOCIAL networks, FAMILY structure, MARITAL status, SOCIAL support, MENTAL depression
Abstract

Background: We investigated (a) whether polygenic risk for schizophrenia predicts different trajectories of social development among those who have not developed psychoses and (b) whether possible associations are PRSSCZ-specific or evident also for any polygenic risk for mental disorders, e.g. for major depression. Methods: Participants came from the population-based Young Finns Study (n = 2377). We calculated a polygenic risk score for schizophrenia (PRSSCZ) and for major depression (PRSDEP). Diagnoses of psychotic disorders were derived from the hospital care register. Social development from adolescence to middle age was measured by (a) perceived social support from friends, family, and a close other, (b) perceived sociability, and (c) family structure (partnership status, number of children, age of first-time parenthood). Results: Among those without manifest psychoses, high PRSSCZ predicted lower experienced support from friends (B = −0.04, p = 0.009–0.035) and family (B = −0.04, p = 0.009–0.035) especially after early adulthood, and also lower perceived sociability (B = −0.05, p = 0.010–0.026). PRSSCZ was not related to family structure. PRSDEP did not predict any domain of social development. Conclusions: Individuals at high PRSSCZ (not converted to psychosis) seem to experience a lower preference to be with others over being alone. Individuals with high (v. low) PRSSCZ seem to have a similar family structure in terms of partnership status or number of children but, nevertheless, they experience less support from their family. Among those not converted to psychosis in a typical age period, high PRSSCZ may predict a 'later risk phase' and reduced functional resilience when approaching middle age. [ABSTRACT FROM AUTHOR]

Published
2024
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10. Polygenic risk for schizophrenia, social dispositions, and pace of epigenetic aging: Results from the Young Finns Study.

Author

Saarinen, Aino, Marttila, Saara, Mishra, Pashupati P., Lyytikäinen, Leo‐Pekka, Raitoharju, Emma, Mononen, Nina, Sormunen, Elina, Kähönen, Mika, Raitakari, Olli, Hietala, Jarmo, Keltikangas‐Järvinen, Liisa, and Lehtimäki, Terho

Subjects
MONOGENIC & polygenic inheritance (Genetics), REWARD (Psychology), EPIGENETICS, AGING, PREMATURE aging (Medicine)
Abstract

Schizophrenia is often regarded as a disorder of premature aging. We investigated (a) whether polygenic risk for schizophrenia (PRSsch) relates to pace of epigenetic aging and (b) whether personal dispositions toward active and emotionally close relationships protect against accelerated epigenetic aging in individuals with high PRSsch. The sample came from the population‐based Young Finns Study (n = 1348). Epigenetic aging was measured with DNA methylation aging algorithms such as AgeAccelHannum, EEAAHannum, IEAAHannum, IEAAHorvath, AgeAccelHorvath, AgeAccelPheno, AgeAccelGrim, and DunedinPACE. A PRSsch was calculated using summary statistics from the most comprehensive genome‐wide association study of schizophrenia to date. Social dispositions were assessed in terms of extraversion, sociability, reward dependence, cooperativeness, and attachment security. We found that PRSsch did not have a statistically significant effect on any studied indicator of epigenetic aging. Instead, PRSsch had a significant interaction with reward dependence (p = 0.001–0.004), cooperation (p = 0.009–0.020), extraversion (p = 0.019–0.041), sociability (p = 0.003–0.016), and attachment security (p = 0.007–0.014) in predicting AgeAccelHannum, EEAAHannum, or IEAAHannum. Specifically, participants with high PRSsch appeared to display accelerated epigenetic aging at higher (vs. lower) levels of extraversion, sociability, attachment security, reward dependence, and cooperativeness. A rather opposite pattern was evident for those with low PRSsch. No such interactions were evident when predicting the other indicators of epigenetic aging. In conclusion, against our hypothesis, frequent social interactions may relate to accelerated epigenetic aging in individuals at risk for psychosis. We speculate that this may be explained by social‐cognitive impairments (perceiving social situations as overwhelming or excessively arousing) or ending up in less supportive or deviant social groups. [ABSTRACT FROM AUTHOR]

Published
2024
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11. Genetic risk scores associated with temperament clusters in Finnish depression patients.

Author

Salminen, Simo-Pekko, Solismaa, Anssi, Lyytikäinen, Leo-Pekka, Paavonen, Vesa, Mononen, Nina, Lehtimäki, Terho, Leinonen, Esa, and Kampman, Olli

Subjects
GENETIC risk score, CATECHOL-O-methyltransferase gene, MENTAL depression, TEMPERAMENT, REWARD (Psychology)
Abstract

Objective: Cloninger's temperament dimensions have been studied widely in relation to genetics. In this study, we examined Cloninger's temperament dimensions grouped with cluster analyses and their association with single nucleotide polymorphisms (SNPs). This study included 212 genotyped Finnish patients from the Ostrobothnia Depression Study. Methods: The temperament clusters were analysed at baseline and at six weeks from the beginning of the depression intervention study. We selected depression-related catecholamine and serotonin genes based on a literature search, and 59 SNPs from ten different genes were analysed. The associations of single SNPs with temperament clusters were studied. Using the selected genes, genetic risk score (GRS) analyses were conducted considering appropriate confounding factors. Results: No single SNP had a significant association with the temperament clusters. Associations between GRSs and temperament clusters were observed in multivariate models that were significant after permutation analyses. Two SNPs from the DRD3 gene, two SNPs from the SLC6A2 gene, one SNP from the SLC6A4 gene, and one SNP from the HTR2A gene associated with the HHA/LRD/LP (high harm avoidance, low reward dependence, low persistence) cluster at baseline. Two SNPs from the HTR2A gene were associated with the HHA/LRD/LP cluster at six weeks. Two SNPs from the HTR2A gene and two SNPs from the COMT gene were associated with the HP (high persistence) cluster at six weeks. Conclusion: GRSs seem to associate with an individual's temperament profile, which can be observed in the clusters used. Further research needs to be conducted on these types of clusters and their clinical applicability. [ABSTRACT FROM AUTHOR]

Published
2024
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12. Multi-ancestry genome-wide gene–sleep interactions identify novel loci for blood pressure

Author

Wang, Heming, Noordam, Raymond, Cade, Brian E., Schwander, Karen, Winkler, Thomas W., Lee, Jiwon, Sung, Yun Ju, Bentley, Amy R., Manning, Alisa K., Aschard, Hugues, Kilpeläinen, Tuomas O., Ilkov, Marjan, Brown, Michael R., Horimoto, Andrea R., Richard, Melissa, Bartz, Traci M., Vojinovic, Dina, Lim, Elise, Nierenberg, Jovia L., Liu, Yongmei, Chitrala, Kumaraswamynaidu, Rankinen, Tuomo, Musani, Solomon K., Franceschini, Nora, Rauramaa, Rainer, Alver, Maris, Zee, Phyllis C., Harris, Sarah E., van der Most, Peter J., Nolte, Ilja M., Munroe, Patricia B., Palmer, Nicholette D., Kühnel, Brigitte, Weiss, Stefan, Wen, Wanqing, Hall, Kelly A., Lyytikäinen, Leo-Pekka, O’Connell, Jeff, Eiriksdottir, Gudny, Launer, Lenore J., de Vries, Paul S., Arking, Dan E., Chen, Han, Boerwinkle, Eric, Krieger, Jose E., Schreiner, Pamela J., Sidney, Stephen, Shikany, James M., Rice, Kenneth, Chen, Yii-Der Ida, Gharib, Sina A., Bis, Joshua C., Luik, Annemarie I., Ikram, M. Arfan, Uitterlinden, André G., Amin, Najaf, Xu, Hanfei, Levy, Daniel, He, Jiang, Lohman, Kurt K., Zonderman, Alan B., Rice, Treva K., Sims, Mario, Wilson, Gregory, Sofer, Tamar, Rich, Stephen S., Palmas, Walter, Yao, Jie, Guo, Xiuqing, Rotter, Jerome I., Biermasz, Nienke R., Mook-Kanamori, Dennis O., Martin, Lisa W., Barac, Ana, Wallace, Robert B., Gottlieb, Daniel J., Komulainen, Pirjo, Heikkinen, Sami, Mägi, Reedik, Milani, Lili, Metspalu, Andres, Starr, John M., Milaneschi, Yuri, Waken, R. J., Gao, Chuan, Waldenberger, Melanie, Peters, Annette, Strauch, Konstantin, Meitinger, Thomas, Roenneberg, Till, Völker, Uwe, Dörr, Marcus, Shu, Xiao-Ou, Mukherjee, Sutapa, Hillman, David R., Kähönen, Mika, Wagenknecht, Lynne E., Gieger, Christian, Grabe, Hans J., Zheng, Wei, Palmer, Lyle J., Lehtimäki, Terho, Gudnason, Vilmundur, Morrison, Alanna C., Pereira, Alexandre C., Fornage, Myriam, Psaty, Bruce M., van Duijn, Cornelia M., Liu, Ching-Ti, Kelly, Tanika N., Evans, Michele K., Bouchard, Claude, Fox, Ervin R., Kooperberg, Charles, Zhu, Xiaofeng, Lakka, Timo A., Esko, Tõnu, North, Kari E., Deary, Ian J., Snieder, Harold, Penninx, Brenda W. J. H., Gauderman, W. James, Rao, Dabeeru C., Redline, Susan, and van Heemst, Diana

Abstract

Long and short sleep duration are associated with elevated blood pressure (BP), possibly through effects on molecular pathways that influence neuroendocrine and vascular systems. To gain new insights into the genetic basis of sleep-related BP variation, we performed genome-wide gene by short or long sleep duration interaction analyses on four BP traits (systolic BP, diastolic BP, mean arterial pressure, and pulse pressure) across five ancestry groups in two stages using 2 degree of freedom (df) joint test followed by 1df test of interaction effects. Primary multi-ancestry analysis in 62,969 individuals in stage 1 identified three novel gene by sleep interactions that were replicated in an additional 59,296 individuals in stage 2 (stage 1 + 2 Pjoint< 5 × 10−8), including rs7955964 (FIGNL2/ANKRD33) that increases BP among long sleepers, and rs73493041 (SNORA26/C9orf170) and rs10406644 (KCTD15/LSM14A) that increase BP among short sleepers (Pint< 5 × 10−8). Secondary ancestry-specific analysis identified another novel gene by long sleep interaction at rs111887471 (TRPC3/KIAA1109) in individuals of African ancestry (Pint= 2 × 10−6). Combined stage 1 and 2 analyses additionally identified significant gene by long sleep interactions at 10 loci including MKLN1and RGL3/ELAVL3previously associated with BP, and significant gene by short sleep interactions at 10 loci including C2orf43 previously associated with BP (Pint< 10−3). 2df test also identified novel loci for BP after modeling sleep that has known functions in sleep–wake regulation, nervous and cardiometabolic systems. This study indicates that sleep and primary mechanisms regulating BP may interact to elevate BP level, suggesting novel insights into sleep-related BP regulation.

Published
2024
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13. A Large-Scale Genome-Wide Study of Gene-Sleep Duration Interactions for Blood Pressure in 811,405 Individuals from Diverse Populations.

Author

Wang H, Nagarajan P, Winkler T, Bentley A, Miller C, Kraja A, Schwander K, Lee S, Wang W, Brown M, Morrison J, Giri A, O'Connell J, Bartz T, de las Fuentes L, Gudmundsdottir V, Guo X, Harris S, Huang Z, Kals M, Kho M, Lefevre C, Luan J, Lyytikäinen LP, Mangino M, Milaneschi Y, Palmer N, Rao V, Rauramaa R, Shen B, Stadler S, Sun Q, Tang J, Thériault S, van der Graaf A, van der Most P, Wang Y, Weiss S, Westerman K, Yang Q, Yasuharu T, Zhao W, Zhu W, Altschul D, Ansari MAY, Anugu P, Argoty-Pantoja A, Arzt M, Aschard H, Attia J, Bazzano L, Breyer M, Brody J, Cade B, Chen HH, Chen YI, Chen Z, de Vries P, Dimitrov L, Do A, Du J, Dupont C, Edwards T, Evans M, Faquih T, Felix S, Fisher-Hoch S, Floyd J, Graff M, Charles Gu C, Gu D, Hairston K, Hanley A, Heid I, Heikkinen S, Highland H, Hood M, Kähönen M, Karvonen-Gutierrez C, Kawaguchi T, Kazuya S, Tanika K, Komulainen P, Levy D, Lin H, Liu P, Marques-Vidal P, McCormick J, Mei H, Meigs J, Menni C, Nam K, Nolte I, Pacheco N, Petty L, Polikowsky H, Province M, Psaty B, Raffield L, Raitakari O, Rich S, Riha R, Risch L, Risch M, Ruiz-Narvaez E, Scott R, Sitlani C, Smith J, Sofer T, Teder-Laving M, Völker U, Vollenweider P, Wang G, van Dijk KW, Wilson O, Xia R, Yao J, Young K, Zhang R, Zhu X, Below J, Böger C, Conen D, Cox S, Dörr M, Feitosa M, Fox E, Franceschini N, Gharib S, Gudnason V, Harlow S, He J, Holliday E, Kutalik Z, Lakka T, Lawlor D, Lee S, Lehtimäki T, Li C, Liu CT, Mägi R, Matsuda F, Morrison A, Penninx BWJH, Peyser P, Rotter J, Snieder H, Spector T, Wagenknecht L, Wareham N, Zonderman A, North K, Fornage M, Hung A, Manning A, Gauderman W, Chen H, Munroe P, Rao D, van Heemst D, Redline S, and Noordam R

Abstract

Although both short and long sleep duration are associated with elevated hypertension risk, our understanding of their interplay with biological pathways governing blood pressure remains limited. To address this, we carried out genome-wide cross-population gene-by-short-sleep and long-sleep duration interaction analyses for three blood pressure traits (systolic, diastolic, and pulse pressure) in 811,405 individuals from diverse population groups. We discover 22 novel gene-sleep duration interaction loci for blood pressure, mapped to 23 genes. Investigating these genes' functional implications shed light on neurological, thyroidal, bone metabolism, and hematopoietic pathways that necessitate future investigation for blood pressure management that caters to sleep health lifestyle. Non-overlap between short sleep (12) and long sleep (10) interactions underscores the plausible nature of distinct influences of both sleep duration extremes in cardiovascular health. Several of our loci are specific towards a particular population background or sex, emphasizing the importance of addressing heterogeneity entangled in gene-environment interactions, when considering precision medicine design approaches for blood pressure management., Competing Interests: Declarations CONFLICT OF INTEREST C.L.M. has received funding from AstraZeneca not related to the current study. B.M.P. serves on the steering committee of the Yale Open Data Access Project funded by Johnson & Johnson. D.C. receives consultancy fees from Roche Diagnostics and Trimedics and speaker fees from Servier. D.A.L. has received support from Medtronic LTD and Roche Diagnostics for biomarker research not related to the current study. The remaining authors declare no competing interests.

Published
2024
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14. A Large-Scale Genome-Wide Study of Gene-Sleep Duration Interactions for Blood Pressure in 811,405 Individuals from Diverse Populations.

Author

Nagarajan P, Winkler TW, Bentley AR, Miller CL, Kraja AT, Schwander K, Lee S, Wang W, Brown MR, Morrison JL, Giri A, O'Connell JR, Bartz TM, de las Fuentes L, Gudmundsdottir V, Guo X, Harris SE, Huang Z, Kals M, Kho M, Lefevre C, Luan J, Lyytikäinen LP, Mangino M, Milaneschi Y, Palmer ND, Rao V, Rauramaa R, Shen B, Stadler S, Sun Q, Tang J, Thériault S, van der Graaf A, van der Most PJ, Wang Y, Weiss S, Westerman KE, Yang Q, Yasuharu T, Zhao W, Zhu W, Altschul D, Ansari MAY, Anugu P, Argoty-Pantoja AD, Arzt M, Aschard H, Attia JR, Bazzanno L, Breyer MA, Brody JA, Cade BE, Chen HH, Ida Chen YD, Chen Z, de Vries PS, Dimitrov LM, Do A, Du J, Dupont CT, Edwards TL, Evans MK, Faquih T, Felix SB, Fisher-Hoch SP, Floyd JS, Graff M, Gu C, Gu D, Hairston KG, Hanley AJ, Heid IM, Heikkinen S, Highland HM, Hood MM, Kähönen M, Karvonen-Gutierrez CA, Kawaguchi T, Kazuya S, Kelly TN, Komulainen P, Levy D, Lin HJ, Liu PY, Marques-Vidal P, McCormick JB, Mei H, Meigs JB, Menni C, Nam K, Nolte IM, Pacheco NL, Petty LE, Polikowsky HG, Province MA, Psaty BM, Raffield LM, Raitakari OT, Rich SS, Riha RL, Risch L, Risch M, Ruiz-Narvaez EA, Scott RJ, Sitlani CM, Smith JA, Sofer T, Teder-Laving M, Völker U, Vollenweider P, Wang G, van Dijk KW, Wilson OD, Xia R, Yao J, Young KL, Zhang R, Zhu X, Below JE, Böger CA, Conen D, Cox SR, Dörr M, Feitosa MF, Fox ER, Franceschini N, Gharib SA, Gudnason V, Harlow SD, He J, Holliday EG, Kutalik Z, Lakka TA, Lawlor DA, Lee S, Lehtimäki T, Li C, Liu CT, Mägi R, Matsuda F, Morrison AC, Penninx BW, Peyser PA, Rotter JI, Snieder H, Spector TD, Wagenknecht LE, Wareham NJ, Zonderman AB, North KE, Fornage M, Hung AM, Manning AK, Gauderman J, Chen H, Munroe PB, Rao DC, van Heemst D, Redline S, Noordam R, and Wang H

Abstract

Although both short and long sleep duration are associated with elevated hypertension risk, our understanding of their interplay with biological pathways governing blood pressure remains limited. To address this, we carried out genome-wide cross-population gene-by-short-sleep and long-sleep duration interaction analyses for three blood pressure traits (systolic, diastolic, and pulse pressure) in 811,405 individuals from diverse population groups. We discover 22 novel gene-sleep duration interaction loci for blood pressure, mapped to genes involved in neurological, thyroidal, bone metabolism, and hematopoietic pathways. Non-overlap between short sleep (12) and long sleep (10) interactions underscores the plausibility of distinct influences of both sleep duration extremes in cardiovascular health. With several of our loci reflecting specificity towards population background or sex, our discovery sheds light on the importance of embracing granularity when addressing heterogeneity entangled in gene-environment interactions, and in therapeutic design approaches for blood pressure management., Competing Interests: Conflict of Interest/Disclosures: C.L.M. has received funding from AstraZeneca not related to the current study. B.M.P. serves on the steering committee of the Yale Open Data Access Project funded by Johnson & Johnson. D.C. receives consultancy fees from Roche Diagnostics and Trimedics and speaker fees from Servier. D.A.L. has received support from Medtronic LTD and Roche Diagnostics for biomarker research not related to the current study. The remaining authors declare no competing interests.

Published
2024
Full Text
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