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2. Virtual Ontogeny of Cortical Growth Preceding Mental Illness

Author

Patel, Y., Shin, J., Abé, C., Agartz, I., Alloza, C., Alnæs, D., Ambrogi, S., Antonucci, L.A., Arango, C., Arolt, V., Auzias, G., Ayesa-Arriola, R., Banaj, N., Banaschewski, T., Bandeira, C., Başgöze, Z., Cupertino, R.B., Bau, C.H.D., Bauer, J., Baumeister, S., Bernardoni, F., Bertolino, A., Bonnin, C.D.M., Brandeis, D., Brem, S., Bruggemann, J., Bülow, R., Bustillo, J.R., Calderoni, S., Calvo, R., Canales-Rodríguez, E.J., Cannon, D.M., Carmona, S., Carr, V.J., Catts, S.V., Chenji, S., Chew, Q.H., Coghill, D., Connolly, C.G., Conzelmann, A., Craven, A.R., Crespo-Facorro, B., Cullen, K., Dahl, A., Dannlowski, U., Davey, C.G., Deruelle, C., Díaz-Caneja, C.M., Dohm, K., Ehrlich, S., Epstein, J., Erwin-Grabner, T., Eyler, L.T., Fedor, J., Fitzgerald, J., Foran, W., Ford, J.M., Fortea, L., Fuentes-Claramonte, P., Fullerton, J., Furlong, L., Gallagher, L., Gao, B., Gao, S., Goikolea, J.M., Gotlib, I., Goya-Maldonado, R., Grabe, H.J., Green, M., Grevet, E.H., Groenewold, N.A., Grotegerd, D., Gruber, O., Haavik, J., Hahn, T., Harrison, B.J., Heindel, W., Henskens, F., Heslenfeld, D.J., Hilland, E., Hoekstra, P.J., Hohmann, S., Holz, N., Howells, F.M., Ipser, J.C., Jahanshad, N., Jakobi, B., Jansen, A, Janssen, J., Jonassen, R., Kaiser, A., Kaleda, V., Karantonis, J., King, J.A., Kircher, T., Kochunov, P., Koopowitz, S.M., Landén, M., Landrø, N.I., Hoogman, M., Lawrie, S., Franke, B., Rooij, D. van, Buitelaar, J.K., Thompson, P., Paus, T., Patel, Y., Shin, J., Abé, C., Agartz, I., Alloza, C., Alnæs, D., Ambrogi, S., Antonucci, L.A., Arango, C., Arolt, V., Auzias, G., Ayesa-Arriola, R., Banaj, N., Banaschewski, T., Bandeira, C., Başgöze, Z., Cupertino, R.B., Bau, C.H.D., Bauer, J., Baumeister, S., Bernardoni, F., Bertolino, A., Bonnin, C.D.M., Brandeis, D., Brem, S., Bruggemann, J., Bülow, R., Bustillo, J.R., Calderoni, S., Calvo, R., Canales-Rodríguez, E.J., Cannon, D.M., Carmona, S., Carr, V.J., Catts, S.V., Chenji, S., Chew, Q.H., Coghill, D., Connolly, C.G., Conzelmann, A., Craven, A.R., Crespo-Facorro, B., Cullen, K., Dahl, A., Dannlowski, U., Davey, C.G., Deruelle, C., Díaz-Caneja, C.M., Dohm, K., Ehrlich, S., Epstein, J., Erwin-Grabner, T., Eyler, L.T., Fedor, J., Fitzgerald, J., Foran, W., Ford, J.M., Fortea, L., Fuentes-Claramonte, P., Fullerton, J., Furlong, L., Gallagher, L., Gao, B., Gao, S., Goikolea, J.M., Gotlib, I., Goya-Maldonado, R., Grabe, H.J., Green, M., Grevet, E.H., Groenewold, N.A., Grotegerd, D., Gruber, O., Haavik, J., Hahn, T., Harrison, B.J., Heindel, W., Henskens, F., Heslenfeld, D.J., Hilland, E., Hoekstra, P.J., Hohmann, S., Holz, N., Howells, F.M., Ipser, J.C., Jahanshad, N., Jakobi, B., Jansen, A, Janssen, J., Jonassen, R., Kaiser, A., Kaleda, V., Karantonis, J., King, J.A., Kircher, T., Kochunov, P., Koopowitz, S.M., Landén, M., Landrø, N.I., Hoogman, M., Lawrie, S., Franke, B., Rooij, D. van, Buitelaar, J.K., Thompson, P., and Paus, T.

Abstract

Contains fulltext : 281502.pdf (Publisher’s version ) (Closed access), BACKGROUND: Morphology of the human cerebral cortex differs across psychiatric disorders, with neurobiology and developmental origins mostly undetermined. Deviations in the tangential growth of the cerebral cortex during pre/perinatal periods may be reflected in individual variations in cortical surface area later in life. METHODS: Interregional profiles of group differences in surface area between cases and controls were generated using T1-weighted magnetic resonance imaging from 27,359 individuals including those with attention-deficit/hyperactivity disorder, autism spectrum disorder, bipolar disorder, major depressive disorder, schizophrenia, and high general psychopathology (through the Child Behavior Checklist). Similarity of interregional profiles of group differences in surface area and prenatal cell-specific gene expression was assessed. RESULTS: Across the 11 cortical regions, group differences in cortical area for attention-deficit/hyperactivity disorder, schizophrenia, and Child Behavior Checklist were dominant in multimodal association cortices. The same interregional profiles were also associated with interregional profiles of (prenatal) gene expression specific to proliferative cells, namely radial glia and intermediate progenitor cells (greater expression, larger difference), as well as differentiated cells, namely excitatory neurons and endothelial and mural cells (greater expression, smaller difference). Finally, these cell types were implicated in known pre/perinatal risk factors for psychosis. Genes coexpressed with radial glia were enriched with genes implicated in congenital abnormalities, birth weight, hypoxia, and starvation. Genes coexpressed with endothelial and mural genes were enriched with genes associated with maternal hypertension and preterm birth. CONCLUSIONS: Our findings support a neurodevelopmental model of vulnerability to mental illness whereby prenatal risk factors acting through cell-specific processes lead to deviations from t

Published
2022

3. Virtual Ontogeny of Cortical Growth Preceding Mental Illness

Author

Patel, Y, Shin, J, Abe, C, Agartz, I, Alloza, C, Alnaes, D, Ambrogi, S, Antonucci, LA, Arango, C, Arolt, V, Auzias, G, Ayesa-Arriola, R, Banaj, N, Banaschewski, T, Bandeira, C, Basgoze, Z, Cupertino, RB, Bau, CHD, Bauer, J, Baumeister, S, Bernardoni, F, Bertolino, A, del Mar Bonnin, C, Brandeis, D, Brem, S, Bruggemann, J, Bulow, R, Bustillo, JR, Calderoni, S, Calvo, R, Canales-Rodriguez, EJ, Cannon, DM, Carmona, S, Carr, VJ, Catts, SV, Chenji, S, Chew, QH, Coghill, D, Connolly, CG, Conzelmann, A, Craven, AR, Crespo-Facorro, B, Cullen, K, Dahl, A, Dannlowski, U, Davey, CG, Deruelle, C, Diaz-Caneja, CM, Dohm, K, Ehrlich, S, Epstein, J, Erwin-Grabner, T, Eyler, LT, Fedor, J, Fitzgerald, J, Foran, W, Ford, JM, Fortea, L, Fuentes-Claramonte, P, Fullerton, J, Furlong, L, Gallagher, L, Gao, B, Gao, S, Goikolea, JM, Gotlib, I, Goya-Maldonado, R, Grabe, HJ, Green, M, Grevet, EH, Groenewold, NA, Grotegerd, D, Gruber, O, Haavik, J, Hahn, T, Harrison, BJ, Heindel, W, Henskens, F, Heslenfeld, DJ, Hilland, E, Hoekstra, PJ, Hohmann, S, Holz, N, Howells, FM, Ipser, JC, Jahanshad, N, Jakobi, B, Jansen, A, Janssen, J, Jonassen, R, Kaiser, A, Kaleda, V, Karantonis, J, King, JA, Kircher, T, Kochunov, P, Koopowitz, S-M, Landen, M, Landro, NI, Lawrie, S, Lebedeva, I, Luna, B, Lundervold, AJ, MacMaster, FP, Maglanoc, LA, Mathalon, DH, McDonald, C, McIntosh, A, Meinert, S, Michie, PT, Mitchell, P, Moreno-Alcazar, A, Mowry, B, Muratori, F, Nabulsi, L, Nenadic, I, Tuura, RO, Oosterlaan, J, Overs, B, Pantelis, C, Parellada, M, Pariente, JC, Pauli, P, Pergola, G, Piarulli, FM, Picon, F, Piras, F, Pomarol-Clotet, E, Pretus, C, Quide, Y, Radua, J, Ramos-Quiroga, JA, Rasser, PE, Reif, A, Retico, A, Roberts, G, Rossell, S, Rovaris, DL, Rubia, K, Sacchet, M, Salavert, J, Salvador, R, Sarro, S, Sawa, A, Schall, U, Scott, R, Selvaggi, P, Silk, T, Sim, K, Skoch, A, Spalletta, G, Spaniel, F, Stein, DJ, Steinstrater, O, Stolicyn, A, Takayanagi, Y, Tamm, L, Tavares, M, Teumer, A, Thiel, K, Thomopoulos, SI, Tomecek, D, Tomyshev, AS, Tordesillas-Gutierrez, D, Tosetti, M, Uhlmann, A, Van Rheenen, T, Vazquez-Bourgon, J, Vernooij, MW, Vieta, E, Vilarroya, O, Weickert, C, Weickert, T, Westlye, LT, Whalley, H, Willinger, D, Winter, A, Wittfeld, K, Yang, TT, Yoncheva, Y, Zijlmans, JL, Hoogman, M, Franke, B, van Rooij, D, Buitelaar, J, Ching, CRK, Andreassen, OA, Pozzi, E, Veltman, D, Schmaal, L, van Erp, TGM, Turner, J, Castellanos, FX, Pausova, Z, Thompson, P, Paus, T, Patel, Y, Shin, J, Abe, C, Agartz, I, Alloza, C, Alnaes, D, Ambrogi, S, Antonucci, LA, Arango, C, Arolt, V, Auzias, G, Ayesa-Arriola, R, Banaj, N, Banaschewski, T, Bandeira, C, Basgoze, Z, Cupertino, RB, Bau, CHD, Bauer, J, Baumeister, S, Bernardoni, F, Bertolino, A, del Mar Bonnin, C, Brandeis, D, Brem, S, Bruggemann, J, Bulow, R, Bustillo, JR, Calderoni, S, Calvo, R, Canales-Rodriguez, EJ, Cannon, DM, Carmona, S, Carr, VJ, Catts, SV, Chenji, S, Chew, QH, Coghill, D, Connolly, CG, Conzelmann, A, Craven, AR, Crespo-Facorro, B, Cullen, K, Dahl, A, Dannlowski, U, Davey, CG, Deruelle, C, Diaz-Caneja, CM, Dohm, K, Ehrlich, S, Epstein, J, Erwin-Grabner, T, Eyler, LT, Fedor, J, Fitzgerald, J, Foran, W, Ford, JM, Fortea, L, Fuentes-Claramonte, P, Fullerton, J, Furlong, L, Gallagher, L, Gao, B, Gao, S, Goikolea, JM, Gotlib, I, Goya-Maldonado, R, Grabe, HJ, Green, M, Grevet, EH, Groenewold, NA, Grotegerd, D, Gruber, O, Haavik, J, Hahn, T, Harrison, BJ, Heindel, W, Henskens, F, Heslenfeld, DJ, Hilland, E, Hoekstra, PJ, Hohmann, S, Holz, N, Howells, FM, Ipser, JC, Jahanshad, N, Jakobi, B, Jansen, A, Janssen, J, Jonassen, R, Kaiser, A, Kaleda, V, Karantonis, J, King, JA, Kircher, T, Kochunov, P, Koopowitz, S-M, Landen, M, Landro, NI, Lawrie, S, Lebedeva, I, Luna, B, Lundervold, AJ, MacMaster, FP, Maglanoc, LA, Mathalon, DH, McDonald, C, McIntosh, A, Meinert, S, Michie, PT, Mitchell, P, Moreno-Alcazar, A, Mowry, B, Muratori, F, Nabulsi, L, Nenadic, I, Tuura, RO, Oosterlaan, J, Overs, B, Pantelis, C, Parellada, M, Pariente, JC, Pauli, P, Pergola, G, Piarulli, FM, Picon, F, Piras, F, Pomarol-Clotet, E, Pretus, C, Quide, Y, Radua, J, Ramos-Quiroga, JA, Rasser, PE, Reif, A, Retico, A, Roberts, G, Rossell, S, Rovaris, DL, Rubia, K, Sacchet, M, Salavert, J, Salvador, R, Sarro, S, Sawa, A, Schall, U, Scott, R, Selvaggi, P, Silk, T, Sim, K, Skoch, A, Spalletta, G, Spaniel, F, Stein, DJ, Steinstrater, O, Stolicyn, A, Takayanagi, Y, Tamm, L, Tavares, M, Teumer, A, Thiel, K, Thomopoulos, SI, Tomecek, D, Tomyshev, AS, Tordesillas-Gutierrez, D, Tosetti, M, Uhlmann, A, Van Rheenen, T, Vazquez-Bourgon, J, Vernooij, MW, Vieta, E, Vilarroya, O, Weickert, C, Weickert, T, Westlye, LT, Whalley, H, Willinger, D, Winter, A, Wittfeld, K, Yang, TT, Yoncheva, Y, Zijlmans, JL, Hoogman, M, Franke, B, van Rooij, D, Buitelaar, J, Ching, CRK, Andreassen, OA, Pozzi, E, Veltman, D, Schmaal, L, van Erp, TGM, Turner, J, Castellanos, FX, Pausova, Z, Thompson, P, and Paus, T

Abstract

BACKGROUND: Morphology of the human cerebral cortex differs across psychiatric disorders, with neurobiology and developmental origins mostly undetermined. Deviations in the tangential growth of the cerebral cortex during pre/perinatal periods may be reflected in individual variations in cortical surface area later in life. METHODS: Interregional profiles of group differences in surface area between cases and controls were generated using T1-weighted magnetic resonance imaging from 27,359 individuals including those with attention-deficit/hyperactivity disorder, autism spectrum disorder, bipolar disorder, major depressive disorder, schizophrenia, and high general psychopathology (through the Child Behavior Checklist). Similarity of interregional profiles of group differences in surface area and prenatal cell-specific gene expression was assessed. RESULTS: Across the 11 cortical regions, group differences in cortical area for attention-deficit/hyperactivity disorder, schizophrenia, and Child Behavior Checklist were dominant in multimodal association cortices. The same interregional profiles were also associated with interregional profiles of (prenatal) gene expression specific to proliferative cells, namely radial glia and intermediate progenitor cells (greater expression, larger difference), as well as differentiated cells, namely excitatory neurons and endothelial and mural cells (greater expression, smaller difference). Finally, these cell types were implicated in known pre/perinatal risk factors for psychosis. Genes coexpressed with radial glia were enriched with genes implicated in congenital abnormalities, birth weight, hypoxia, and starvation. Genes coexpressed with endothelial and mural genes were enriched with genes associated with maternal hypertension and preterm birth. CONCLUSIONS: Our findings support a neurodevelopmental model of vulnerability to mental illness whereby prenatal risk factors acting through cell-specific processes lead to deviations from t

Published
2022

6. Virtual Histology of Cortical Thickness and Shared Neurobiology in 6 Psychiatric Disorders

Author

Patel, Y, Parker, N, Shin, J, Howard, D, French, L, Thomopoulos, SI, Pozzi, E, Abe, Y, Abe, C, Anticevic, A, Alda, M, Aleman, A, Alloza, C, Alonso-Lana, S, Ameis, SH, Anagnostou, E, McIntosh, AA, Arango, C, Arnold, PD, Asherson, P, Assogna, F, Auzias, G, Ayesa-Arriola, R, Bakker, G, Banaj, N, Banaschewski, T, Bandeira, CE, Baranov, A, Bargallo, N, Bau, CHD, Baumeister, S, Baune, BT, Bellgrove, MA, Benedetti, F, Bertolino, A, Boedhoe, PSW, Boks, M, Bollettini, I, del Mar Bonnin, C, Borgers, T, Borgwardt, S, Brandeis, D, Brennan, BP, Bruggemann, JM, Bulow, R, Busatto, GF, Calderoni, S, Calhoun, VD, Calvo, R, Canales-Rodriguez, EJ, Cannon, DM, Carr, VJ, Cascella, N, Cercignani, M, Chaim-Avancini, TM, Christakou, A, Coghill, D, Conzelmann, A, Crespo-Facorro, B, Cubillo, AI, Cullen, KR, Cupertino, RB, Daly, E, Dannlowski, U, Davey, CG, Denys, D, Deruelle, C, Di Giorgio, A, Dickie, EW, Dima, D, Dohm, K, Ehrlich, S, Ely, BA, Erwin-Grabner, T, Ethofer, T, Fair, DA, Fallgatter, AJ, Faraone, SV, Fatjo-Vilas, M, Fedor, JM, Fitzgerald, KD, Ford, JM, Frodl, T, Fu, CHY, Fullerton, JM, Gabel, MC, Glahn, DC, Roberts, G, Gogberashvili, T, Goikolea, JM, Gotlib, IH, Goya-Maldonado, R, Grabe, HJ, Green, MJ, Grevet, EH, Groenewold, NA, Grotegerd, D, Gruber, O, Gruner, P, Guerrero-Pedraza, A, Gur, RE, Gur, RC, Haar, S, Haarman, BCM, Haavik, J, Hahn, T, Hajek, T, Harrison, BJ, Harrison, NA, Hartman, CA, Whalley, HC, Heslenfeld, DJ, Hibar, DP, Hilland, E, Hirano, Y, Ho, TC, Hoekstra, PJ, Hoekstra, L, Hohmann, S, Hong, LE, Hoschl, C, Hovik, MF, Howells, FM, Nenadic, I, Jalbrzikowski, M, James, AC, Janssen, J, Jaspers-Fayer, F, Xu, J, Jonassen, R, Karkashadze, G, King, JA, Kircher, T, Kirschner, M, Koch, K, Kochunov, P, Kohls, G, Konrad, K, Kramer, B, Krug, A, Kuntsi, J, Kwon, JS, Landen, M, Landro, NI, Lazaro, L, Lebedeva, IS, Leehr, EJ, Lera-Miguel, S, Lesch, K-P, Lochner, C, Louza, MR, Luna, B, Lundervold, AJ, MacMaster, FP, Maglanoc, LA, Malpas, CB, Portella, MJ, Marsh, R, Martyn, FM, Mataix-Cols, D, Mathalon, DH, McCarthy, H, McDonald, C, McPhilemy, G, Meinert, S, Menchon, JM, Minuzzi, L, Mitchell, PB, Moreno, C, Morgado, P, Muratori, F, Murphy, CM, Murphy, D, Mwangi, B, Nabulsi, L, Nakagawa, A, Nakamae, T, Namazova, L, Narayanaswamy, J, Jahanshad, N, Nguyen, DD, Nicolau, R, O'Gorman Tuura, RL, O'Hearn, K, Oosterlaan, J, Opel, N, Ophoff, RA, Oranje, B, Garcia de la Foz, VO, Overs, BJ, Paloyelis, Y, Pantelis, C, Parellada, M, Pauli, P, Pico-Perez, M, Picon, FA, Piras, F, Plessen, KJ, Pomarol-Clotet, E, Preda, A, Puig, O, Quide, Y, Radua, J, Ramos-Quiroga, JA, Rasser, PE, Rauer, L, Reddy, J, Redlich, R, Reif, A, Reneman, L, Repple, J, Retico, A, Richarte, V, Richter, A, Rosa, PGP, Rubia, KK, Hashimoto, R, Sacchet, MD, Salvador, R, Santonja, J, Sarink, K, Sarro, S, Satterthwaite, TD, Sawa, A, Schall, U, Schofield, PR, Schrantee, A, Seitz, J, Serpa, MH, Setien-Suero, E, Shaw, P, Shook, D, Silk, TJ, Sim, K, Simon, S, Simpson, HB, Singh, A, Skoch, A, Skokauskas, N, Soares, JC, Soreni, N, Soriano-Mas, C, Spalletta, G, Spaniel, F, Lawrie, SM, Stern, ER, Stewart, SE, Takayanagi, Y, Temmingh, HS, Tolin, DF, Tomecek, D, Tordesillas-Gutierrez, D, Tosetti, M, Uhlmann, A, van Amelsvoort, T, van der Wee, NJA, van der Werff, SJA, van Haren, NEM, van Wingen, GA, Vance, A, Vazquez-Bourgon, J, Vecchio, D, Venkatasubramanian, G, Vieta, E, Vilarroya, O, Vives-Gilabert, Y, Voineskos, AN, Volzke, H, von Polier, GG, Walton, E, Weickert, TW, Weickert, CS, Weideman, AS, Wittfeld, K, Wolf, DH, Wu, M-J, Yang, TT, Yang, K, Yoncheva, Y, Yun, J-Y, Cheng, Y, Zanetti, MV, Ziegler, GC, Franke, B, Hoogman, M, Buitelaar, JK, van Rooij, D, Andreassen, OA, Ching, CRK, Veltman, DJ, Schmaal, L, Stein, DJ, van den Heuvel, OA, Turner, JA, van Erp, TGM, Pausova, Z, Thompson, PM, Paus, T, Patel, Y, Parker, N, Shin, J, Howard, D, French, L, Thomopoulos, SI, Pozzi, E, Abe, Y, Abe, C, Anticevic, A, Alda, M, Aleman, A, Alloza, C, Alonso-Lana, S, Ameis, SH, Anagnostou, E, McIntosh, AA, Arango, C, Arnold, PD, Asherson, P, Assogna, F, Auzias, G, Ayesa-Arriola, R, Bakker, G, Banaj, N, Banaschewski, T, Bandeira, CE, Baranov, A, Bargallo, N, Bau, CHD, Baumeister, S, Baune, BT, Bellgrove, MA, Benedetti, F, Bertolino, A, Boedhoe, PSW, Boks, M, Bollettini, I, del Mar Bonnin, C, Borgers, T, Borgwardt, S, Brandeis, D, Brennan, BP, Bruggemann, JM, Bulow, R, Busatto, GF, Calderoni, S, Calhoun, VD, Calvo, R, Canales-Rodriguez, EJ, Cannon, DM, Carr, VJ, Cascella, N, Cercignani, M, Chaim-Avancini, TM, Christakou, A, Coghill, D, Conzelmann, A, Crespo-Facorro, B, Cubillo, AI, Cullen, KR, Cupertino, RB, Daly, E, Dannlowski, U, Davey, CG, Denys, D, Deruelle, C, Di Giorgio, A, Dickie, EW, Dima, D, Dohm, K, Ehrlich, S, Ely, BA, Erwin-Grabner, T, Ethofer, T, Fair, DA, Fallgatter, AJ, Faraone, SV, Fatjo-Vilas, M, Fedor, JM, Fitzgerald, KD, Ford, JM, Frodl, T, Fu, CHY, Fullerton, JM, Gabel, MC, Glahn, DC, Roberts, G, Gogberashvili, T, Goikolea, JM, Gotlib, IH, Goya-Maldonado, R, Grabe, HJ, Green, MJ, Grevet, EH, Groenewold, NA, Grotegerd, D, Gruber, O, Gruner, P, Guerrero-Pedraza, A, Gur, RE, Gur, RC, Haar, S, Haarman, BCM, Haavik, J, Hahn, T, Hajek, T, Harrison, BJ, Harrison, NA, Hartman, CA, Whalley, HC, Heslenfeld, DJ, Hibar, DP, Hilland, E, Hirano, Y, Ho, TC, Hoekstra, PJ, Hoekstra, L, Hohmann, S, Hong, LE, Hoschl, C, Hovik, MF, Howells, FM, Nenadic, I, Jalbrzikowski, M, James, AC, Janssen, J, Jaspers-Fayer, F, Xu, J, Jonassen, R, Karkashadze, G, King, JA, Kircher, T, Kirschner, M, Koch, K, Kochunov, P, Kohls, G, Konrad, K, Kramer, B, Krug, A, Kuntsi, J, Kwon, JS, Landen, M, Landro, NI, Lazaro, L, Lebedeva, IS, Leehr, EJ, Lera-Miguel, S, Lesch, K-P, Lochner, C, Louza, MR, Luna, B, Lundervold, AJ, MacMaster, FP, Maglanoc, LA, Malpas, CB, Portella, MJ, Marsh, R, Martyn, FM, Mataix-Cols, D, Mathalon, DH, McCarthy, H, McDonald, C, McPhilemy, G, Meinert, S, Menchon, JM, Minuzzi, L, Mitchell, PB, Moreno, C, Morgado, P, Muratori, F, Murphy, CM, Murphy, D, Mwangi, B, Nabulsi, L, Nakagawa, A, Nakamae, T, Namazova, L, Narayanaswamy, J, Jahanshad, N, Nguyen, DD, Nicolau, R, O'Gorman Tuura, RL, O'Hearn, K, Oosterlaan, J, Opel, N, Ophoff, RA, Oranje, B, Garcia de la Foz, VO, Overs, BJ, Paloyelis, Y, Pantelis, C, Parellada, M, Pauli, P, Pico-Perez, M, Picon, FA, Piras, F, Plessen, KJ, Pomarol-Clotet, E, Preda, A, Puig, O, Quide, Y, Radua, J, Ramos-Quiroga, JA, Rasser, PE, Rauer, L, Reddy, J, Redlich, R, Reif, A, Reneman, L, Repple, J, Retico, A, Richarte, V, Richter, A, Rosa, PGP, Rubia, KK, Hashimoto, R, Sacchet, MD, Salvador, R, Santonja, J, Sarink, K, Sarro, S, Satterthwaite, TD, Sawa, A, Schall, U, Schofield, PR, Schrantee, A, Seitz, J, Serpa, MH, Setien-Suero, E, Shaw, P, Shook, D, Silk, TJ, Sim, K, Simon, S, Simpson, HB, Singh, A, Skoch, A, Skokauskas, N, Soares, JC, Soreni, N, Soriano-Mas, C, Spalletta, G, Spaniel, F, Lawrie, SM, Stern, ER, Stewart, SE, Takayanagi, Y, Temmingh, HS, Tolin, DF, Tomecek, D, Tordesillas-Gutierrez, D, Tosetti, M, Uhlmann, A, van Amelsvoort, T, van der Wee, NJA, van der Werff, SJA, van Haren, NEM, van Wingen, GA, Vance, A, Vazquez-Bourgon, J, Vecchio, D, Venkatasubramanian, G, Vieta, E, Vilarroya, O, Vives-Gilabert, Y, Voineskos, AN, Volzke, H, von Polier, GG, Walton, E, Weickert, TW, Weickert, CS, Weideman, AS, Wittfeld, K, Wolf, DH, Wu, M-J, Yang, TT, Yang, K, Yoncheva, Y, Yun, J-Y, Cheng, Y, Zanetti, MV, Ziegler, GC, Franke, B, Hoogman, M, Buitelaar, JK, van Rooij, D, Andreassen, OA, Ching, CRK, Veltman, DJ, Schmaal, L, Stein, DJ, van den Heuvel, OA, Turner, JA, van Erp, TGM, Pausova, Z, Thompson, PM, and Paus, T

Abstract

IMPORTANCE: Large-scale neuroimaging studies have revealed group differences in cortical thickness across many psychiatric disorders. The underlying neurobiology behind these differences is not well understood. OBJECTIVE: To determine neurobiologic correlates of group differences in cortical thickness between cases and controls in 6 disorders: attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), bipolar disorder (BD), major depressive disorder (MDD), obsessive-compulsive disorder (OCD), and schizophrenia. DESIGN, SETTING, AND PARTICIPANTS: Profiles of group differences in cortical thickness between cases and controls were generated using T1-weighted magnetic resonance images. Similarity between interregional profiles of cell-specific gene expression and those in the group differences in cortical thickness were investigated in each disorder. Next, principal component analysis was used to reveal a shared profile of group difference in thickness across the disorders. Analysis for gene coexpression, clustering, and enrichment for genes associated with these disorders were conducted. Data analysis was conducted between June and December 2019. The analysis included 145 cohorts across 6 psychiatric disorders drawn from the ENIGMA consortium. The numbers of cases and controls in each of the 6 disorders were as follows: ADHD: 1814 and 1602; ASD: 1748 and 1770; BD: 1547 and 3405; MDD: 2658 and 3572; OCD: 2266 and 2007; and schizophrenia: 2688 and 3244. MAIN OUTCOMES AND MEASURES: Interregional profiles of group difference in cortical thickness between cases and controls. RESULTS: A total of 12 721 cases and 15 600 controls, ranging from ages 2 to 89 years, were included in this study. Interregional profiles of group differences in cortical thickness for each of the 6 psychiatric disorders were associated with profiles of gene expression specific to pyramidal (CA1) cells, astrocytes (except for BD), and microglia (except for OCD); collectively, gene

Published
2021

7. Virtual Histology of Cortical Thickness and Shared Neurobiology in 6 Psychiatric Disorders

Author

Patel, Y., Parker, N., Shin, J., Howard, D., French, L., Thomopoulos, S.I., Pozzi, E., Abe, Y., Abé, C., Anticevic, A., Alda, M., Aleman, A., Alloza, C., Alonso-Lana, S., Ameis, S.H., Anagnostou, E., McIntosh, A.A., Arango, C., Arnold, P.D., Asherson, P., Assogna, F., Auzias, G., Ayesa-Arriola, R., Bakker, G., Banaj, N., Banaschewski, T., Bandeira, C.E., Baranov, A., Bargalló, N., Bau, C.H.D., Baumeister, S., Baune, B.T., Bellgrove, M.A., Benedetti, F., Bertolino, A., Boedhoe, P.S.W., Boks, M., Bollettini, I., Del Mar Bonnin, C., Borgers, T., Borgwardt, S., Brandeis, D., Brennan, B.P., Bruggemann, J.M., Bülow, R., Busatto, G.F., Calderoni, S., Calhoun, V.D., Calvo, R., Canales-Rodríguez, E.J., Cannon, D.M., Carr, V.J., Cascella, N., Cercignani, M., Chaim-Avancini, T.M., Christakou, A., Coghill, D., Conzelmann, A., Crespo-Facorro, B., Cubillo, A.I., Cullen, K.R., Cupertino, R.B., Daly, E., Dannlowski, U., Davey, C.G., Denys, D., Deruelle, C., Di Giorgio, A., Dickie, E.W., Dima, D., Dohm, K., Ehrlich, S., Ely, B.A., Erwin-Grabner, T., Ethofer, T., Fair, D.A., Fallgatter, A.J., Faraone, S.V., Fatjó-Vilas, M., Fedor, J.M., Fitzgerald, K.D., Ford, J.M., Frodl, T., Fu, C.H.Y., Fullerton, J.M., Gabel, M.C., Glahn, D.C., Roberts, G., Gogberashvili, T., Goikolea, J.M., Gotlib, I.H., Goya-Maldonado, R., Grabe, H.J., Green, M.J., Grevet, E.H., Groenewold, N.A., Grotegerd, D., Gruber, O., Gruner, P., Guerrero-Pedraza, A., Gur, R.E., Gur, R.C., Haar, S., Haarman, B.C.M., Haavik, J., Hahn, T., Hajek, T., Harrison, B.J., Harrison, N.A., Hartman, C.A., Whalley, H.C., Heslenfeld, D.J., Hibar, D.P., Hilland, E., Hirano, Y., Ho, T.C., Hoekstra, P.J., Hoekstra, L., Hohmann, S., Hong, L.E., Höschl, C., Høvik, M.F., Howells, F.M., Nenadic, I., Jalbrzikowski, M., James, A.C., Janssen, J., Jaspers-Fayer, F., Xu, J., Jonassen, R., Karkashadze, G., King, J.A., Kircher, T., Kirschner, M., Koch, K., Kochunov, P., Kohls, G., Konrad, K., Krämer, B., Krug, A., Kuntsi, J., Kwon, J.S., Landén, M., Landrø, N.I., Lazaro, L., Lebedeva, I.S., Leehr, E.J., Lera-Miguel, S., Lesch, K.-P., Lochner, C., Louza, M.R., Luna, B., Lundervold, A.J., Macmaster, F.P., Maglanoc, L.A., Malpas, C.B., Portella, M.J., Marsh, R., Martyn, F.M., Mataix-Cols, D., Mathalon, D.H., McCarthy, H., McDonald, C., McPhilemy, G., Meinert, S., Menchón, J.M., Minuzzi, L., Mitchell, P.B., Moreno, C., Morgado, P., Muratori, F., Murphy, C.M., Murphy, D., Mwangi, B., Nabulsi, L., Nakagawa, A., Nakamae, T., Namazova, L., Narayanaswamy, J., Jahanshad, N., Nguyen, D.D., Nicolau, R., O'Gorman Tuura, R.L., O'Hearn, K., Oosterlaan, J., Opel, N., Ophoff, R.A., Oranje, B., García De La Foz, V.O., Overs, B.J., Paloyelis, Y., Pantelis, C., Parellada, M., Pauli, P., Picó-Pérez, M., Picon, F.A., Piras, F., Plessen, K.J., Pomarol-Clotet, E., Preda, A., Puig, O., Quidé, Y., Radua, J., Ramos-Quiroga, J.A., Rasser, P.E., Rauer, L., Reddy, J., Redlich, R., Reif, A., Reneman, L., Repple, J., Retico, A., Richarte, V., Richter, A., Rosa, P.G.P., Rubia, K.K., Hashimoto, R., Sacchet, M.D., Salvador, R., Santonja, J., Sarink, K., Sarró, S., Satterthwaite, T.D., Sawa, A., Schall, U., Schofield, P.R., Schrantee, A., Seitz, J., Serpa, M.H., Setién-Suero, E., Shaw, P., Shook, D., Silk, T.J., Sim, K., Simon, S., Simpson, H.B., Singh, A., Skoch, A., Skokauskas, N., Soares, J.C., Soreni, N., Soriano-Mas, C., Spalletta, G., Spaniel, F., Lawrie, S.M., Stern, E.R., Stewart, S.E., Takayanagi, Y., Temmingh, H.S., Tolin, D.F., Tomecek, D., Tordesillas-Gutiérrez, D., Tosetti, M., Uhlmann, A., Van Amelsvoort, T., Van Der Wee, N.J.A., Van Der Werff, S.J.A., Van Haren, N.E.M., Van Wingen, G.A., Vance, A., Vázquez-Bourgon, J., Vecchio, D., Venkatasubramanian, G., Vieta, E., Vilarroya, O., Vives-Gilabert, Y., Voineskos, A.N., Völzke, H., Von Polier, G.G., Walton, E., Weickert, T.W., Weickert, C.S., Weideman, A.S., Wittfeld, K., Wolf, D.H., Wu, M.-J., Yang, T.T., Yang, K., Yoncheva, Y., Yun, J.-Y., Cheng, Y., Zanetti, M.V., Ziegler, G.C., Franke, B., Hoogman, M., Buitelaar, J.K., Van Rooij, D., Andreassen, O.A., Ching, C.R.K., Veltman, D.J., Schmaal, L., Stein, D.J., Van Den Heuvel, O.A., Turner, J.A., Van Erp, T.G.M., Pausova, Z., Thompson, P.M., Paus, T., Patel, Y., Parker, N., Shin, J., Howard, D., French, L., Thomopoulos, S.I., Pozzi, E., Abe, Y., Abé, C., Anticevic, A., Alda, M., Aleman, A., Alloza, C., Alonso-Lana, S., Ameis, S.H., Anagnostou, E., McIntosh, A.A., Arango, C., Arnold, P.D., Asherson, P., Assogna, F., Auzias, G., Ayesa-Arriola, R., Bakker, G., Banaj, N., Banaschewski, T., Bandeira, C.E., Baranov, A., Bargalló, N., Bau, C.H.D., Baumeister, S., Baune, B.T., Bellgrove, M.A., Benedetti, F., Bertolino, A., Boedhoe, P.S.W., Boks, M., Bollettini, I., Del Mar Bonnin, C., Borgers, T., Borgwardt, S., Brandeis, D., Brennan, B.P., Bruggemann, J.M., Bülow, R., Busatto, G.F., Calderoni, S., Calhoun, V.D., Calvo, R., Canales-Rodríguez, E.J., Cannon, D.M., Carr, V.J., Cascella, N., Cercignani, M., Chaim-Avancini, T.M., Christakou, A., Coghill, D., Conzelmann, A., Crespo-Facorro, B., Cubillo, A.I., Cullen, K.R., Cupertino, R.B., Daly, E., Dannlowski, U., Davey, C.G., Denys, D., Deruelle, C., Di Giorgio, A., Dickie, E.W., Dima, D., Dohm, K., Ehrlich, S., Ely, B.A., Erwin-Grabner, T., Ethofer, T., Fair, D.A., Fallgatter, A.J., Faraone, S.V., Fatjó-Vilas, M., Fedor, J.M., Fitzgerald, K.D., Ford, J.M., Frodl, T., Fu, C.H.Y., Fullerton, J.M., Gabel, M.C., Glahn, D.C., Roberts, G., Gogberashvili, T., Goikolea, J.M., Gotlib, I.H., Goya-Maldonado, R., Grabe, H.J., Green, M.J., Grevet, E.H., Groenewold, N.A., Grotegerd, D., Gruber, O., Gruner, P., Guerrero-Pedraza, A., Gur, R.E., Gur, R.C., Haar, S., Haarman, B.C.M., Haavik, J., Hahn, T., Hajek, T., Harrison, B.J., Harrison, N.A., Hartman, C.A., Whalley, H.C., Heslenfeld, D.J., Hibar, D.P., Hilland, E., Hirano, Y., Ho, T.C., Hoekstra, P.J., Hoekstra, L., Hohmann, S., Hong, L.E., Höschl, C., Høvik, M.F., Howells, F.M., Nenadic, I., Jalbrzikowski, M., James, A.C., Janssen, J., Jaspers-Fayer, F., Xu, J., Jonassen, R., Karkashadze, G., King, J.A., Kircher, T., Kirschner, M., Koch, K., Kochunov, P., Kohls, G., Konrad, K., Krämer, B., Krug, A., Kuntsi, J., Kwon, J.S., Landén, M., Landrø, N.I., Lazaro, L., Lebedeva, I.S., Leehr, E.J., Lera-Miguel, S., Lesch, K.-P., Lochner, C., Louza, M.R., Luna, B., Lundervold, A.J., Macmaster, F.P., Maglanoc, L.A., Malpas, C.B., Portella, M.J., Marsh, R., Martyn, F.M., Mataix-Cols, D., Mathalon, D.H., McCarthy, H., McDonald, C., McPhilemy, G., Meinert, S., Menchón, J.M., Minuzzi, L., Mitchell, P.B., Moreno, C., Morgado, P., Muratori, F., Murphy, C.M., Murphy, D., Mwangi, B., Nabulsi, L., Nakagawa, A., Nakamae, T., Namazova, L., Narayanaswamy, J., Jahanshad, N., Nguyen, D.D., Nicolau, R., O'Gorman Tuura, R.L., O'Hearn, K., Oosterlaan, J., Opel, N., Ophoff, R.A., Oranje, B., García De La Foz, V.O., Overs, B.J., Paloyelis, Y., Pantelis, C., Parellada, M., Pauli, P., Picó-Pérez, M., Picon, F.A., Piras, F., Plessen, K.J., Pomarol-Clotet, E., Preda, A., Puig, O., Quidé, Y., Radua, J., Ramos-Quiroga, J.A., Rasser, P.E., Rauer, L., Reddy, J., Redlich, R., Reif, A., Reneman, L., Repple, J., Retico, A., Richarte, V., Richter, A., Rosa, P.G.P., Rubia, K.K., Hashimoto, R., Sacchet, M.D., Salvador, R., Santonja, J., Sarink, K., Sarró, S., Satterthwaite, T.D., Sawa, A., Schall, U., Schofield, P.R., Schrantee, A., Seitz, J., Serpa, M.H., Setién-Suero, E., Shaw, P., Shook, D., Silk, T.J., Sim, K., Simon, S., Simpson, H.B., Singh, A., Skoch, A., Skokauskas, N., Soares, J.C., Soreni, N., Soriano-Mas, C., Spalletta, G., Spaniel, F., Lawrie, S.M., Stern, E.R., Stewart, S.E., Takayanagi, Y., Temmingh, H.S., Tolin, D.F., Tomecek, D., Tordesillas-Gutiérrez, D., Tosetti, M., Uhlmann, A., Van Amelsvoort, T., Van Der Wee, N.J.A., Van Der Werff, S.J.A., Van Haren, N.E.M., Van Wingen, G.A., Vance, A., Vázquez-Bourgon, J., Vecchio, D., Venkatasubramanian, G., Vieta, E., Vilarroya, O., Vives-Gilabert, Y., Voineskos, A.N., Völzke, H., Von Polier, G.G., Walton, E., Weickert, T.W., Weickert, C.S., Weideman, A.S., Wittfeld, K., Wolf, D.H., Wu, M.-J., Yang, T.T., Yang, K., Yoncheva, Y., Yun, J.-Y., Cheng, Y., Zanetti, M.V., Ziegler, G.C., Franke, B., Hoogman, M., Buitelaar, J.K., Van Rooij, D., Andreassen, O.A., Ching, C.R.K., Veltman, D.J., Schmaal, L., Stein, D.J., Van Den Heuvel, O.A., Turner, J.A., Van Erp, T.G.M., Pausova, Z., Thompson, P.M., and Paus, T.

Abstract

Importance Large-scale neuroimaging studies have revealed group differences in cortical thickness across many psychiatric disorders. The underlying neurobiology behind these differences is not well understood. Objective To determine neurobiologic correlates of group differences in cortical thickness between cases and controls in 6 disorders: attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), bipolar disorder (BD), major depressive disorder (MDD), obsessive-compulsive disorder (OCD), and schizophrenia. Design, Setting, and Participants Profiles of group differences in cortical thickness between cases and controls were generated using T1-weighted magnetic resonance images. Similarity between interregional profiles of cell-specific gene expression and those in the group differences in cortical thickness were investigated in each disorder. Next, principal component analysis was used to reveal a shared profile of group difference in thickness across the disorders. Analysis for gene coexpression, clustering, and enrichment for genes associated with these disorders were conducted. Data analysis was conducted between June and December 2019. The analysis included 145 cohorts across 6 psychiatric disorders drawn from the ENIGMA consortium. The numbers of cases and controls in each of the 6 disorders were as follows: ADHD: 1814 and 1602; ASD: 1748 and 1770; BD: 1547 and 3405; MDD: 2658 and 3572; OCD: 2266 and 2007; and schizophrenia: 2688 and 3244. Main Outcomes and Measures Interregional profiles of group difference in cortical thickness between cases and controls. Results A total of 12 721 cases and 15 600 controls, ranging from ages 2 to 89 years, were included in this study. Interregional profiles of group differences in cortical thickness for each of the 6 psychiatric disorders were associated with profiles of gene expression specific to pyramidal (CA1) cells, astrocytes (except for BD), and microglia (exce

Published
2021
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10. The genetic architecture of human brainstem structures and their involvement in common brain disorders

Author

Elvsåshagen, T., Bahrami, S., Meer, D. van der, Agartz, I., Alnæs, D., Barch, D.M., Baur-Streubel, R., Bertolino, A., Beyer, M.K., Blasi, G., Borgwardt, S., Boye, B., Buitelaar, J.K., Bøen, E., Celius, E.G., Cervenka, S., Conzelmann, A., Coynel, D., Carlo, P. di, Djurovic, S., Eisenacher, S., Espeseth, T., Fatouros-Bergman, H., Flyckt, L., Franke, B., Frei, O., Gelao, B., Harbo, H.F., Hartman, Catharina A., Håberg, A., Heslenfeld, D., Hoekstra, P.J., Høgestøl, E.A., Jonassen, R., Jönsson, E.G., Kirsch, P., Kłoszewska, I., Lagerberg, T.V., Landrø, N.I., Hellard, S. Le, Lesch, K.P., Maglanoc, L.A., Malt, U.F., Mecocci, P., Melle, I., Meyer-Lindenberg, A., Moberget, T., Nordvik, J.E., Nyberg, L., Connell, K.S.O., Oosterlaan, J., Papalino, M., Papassotiropoulos, A., Pauli, P., Pergola, G., Persson, K., Quervain, D. de, Reif, A., Rokicki, J., Rooij, D. van, Shadrin, A.A., Schmidt, A., Schwarz, E., Selbæk, G., Soininen, H., Sowa, P., Steen, V.M., Tsolaki, M., Vellas, B., Wang, L, Westman, E., Ziegler, G.C., Zink, M., Andreassen, O.A., Westlye, L.T., Kaufmann, T., Elvsåshagen, T., Bahrami, S., Meer, D. van der, Agartz, I., Alnæs, D., Barch, D.M., Baur-Streubel, R., Bertolino, A., Beyer, M.K., Blasi, G., Borgwardt, S., Boye, B., Buitelaar, J.K., Bøen, E., Celius, E.G., Cervenka, S., Conzelmann, A., Coynel, D., Carlo, P. di, Djurovic, S., Eisenacher, S., Espeseth, T., Fatouros-Bergman, H., Flyckt, L., Franke, B., Frei, O., Gelao, B., Harbo, H.F., Hartman, Catharina A., Håberg, A., Heslenfeld, D., Hoekstra, P.J., Høgestøl, E.A., Jonassen, R., Jönsson, E.G., Kirsch, P., Kłoszewska, I., Lagerberg, T.V., Landrø, N.I., Hellard, S. Le, Lesch, K.P., Maglanoc, L.A., Malt, U.F., Mecocci, P., Melle, I., Meyer-Lindenberg, A., Moberget, T., Nordvik, J.E., Nyberg, L., Connell, K.S.O., Oosterlaan, J., Papalino, M., Papassotiropoulos, A., Pauli, P., Pergola, G., Persson, K., Quervain, D. de, Reif, A., Rokicki, J., Rooij, D. van, Shadrin, A.A., Schmidt, A., Schwarz, E., Selbæk, G., Soininen, H., Sowa, P., Steen, V.M., Tsolaki, M., Vellas, B., Wang, L, Westman, E., Ziegler, G.C., Zink, M., Andreassen, O.A., Westlye, L.T., and Kaufmann, T.

Abstract

Contains fulltext : 225402.pdf (publisher's version ) (Open Access), Brainstem regions support vital bodily functions, yet their genetic architectures and involvement in common brain disorders remain understudied. Here, using imaging-genetics data from a discovery sample of 27,034 individuals, we identify 45 brainstem-associated genetic loci, including the first linked to midbrain, pons, and medulla oblongata volumes, and map them to 305 genes. In a replication sample of 7432 participants most of the loci show the same effect direction and are significant at a nominal threshold. We detect genetic overlap between brainstem volumes and eight psychiatric and neurological disorders. In additional clinical data from 5062 individuals with common brain disorders and 11,257 healthy controls, we observe differential volume alterations in schizophrenia, bipolar disorder, multiple sclerosis, mild cognitive impairment, dementia, and Parkinson's disease, supporting the relevance of brainstem regions and their genetic architectures in common brain disorders.

Published
2020

11. ENIGMA MDD: seven years of global neuroimaging studies of major depression through worldwide data sharing

Author

Schmaal, L, Pozzi, E, Ho, TC, van Velzen, LS, Veer, IM, Opel, N, Van Someren, EJW, Han, LKM, Aftanas, L, Aleman, A, Baune, BT, Berger, K, Blanken, TF, Capitao, L, Couvy-Duchesne, B, Cullen, KR, Dannlowski, U, Davey, C, Erwin-Grabner, T, Evans, J, Frodl, T, Fu, CHY, Godlewska, B, Gotlib, IH, Goya-Maldonado, R, Grabe, HJ, Groenewold, NA, Grotegerd, D, Gruber, O, Gutman, BA, Hall, GB, Harrison, BJ, Hatton, SN, Hermesdorf, M, Hickie, IB, Hilland, E, Irungu, B, Jonassen, R, Kelly, S, Kircher, T, Klimes-Dougan, B, Krug, A, Landro, NI, Lagopoulos, J, Leerssen, J, Li, M, Linden, DEJ, MacMaster, FP, McIntosh, AM, Mehler, DMA, Nenadic, I, Penninx, BWJH, Portella, MJ, Reneman, L, Renteria, ME, Sacchet, MD, Saemann, PG, Schrantee, A, Sim, K, Soares, JC, Stein, DJ, Tozzi, L, van Der Wee, NJA, van Tol, M-J, Vermeiren, R, Vives-Gilabert, Y, Walter, H, Walter, M, Whalley, HC, Wittfeld, K, Whittle, S, Wright, MJ, Yang, TT, Zarate, C, Thomopoulos, SI, Jahanshad, N, Thompson, PM, Veltman, DJ, Schmaal, L, Pozzi, E, Ho, TC, van Velzen, LS, Veer, IM, Opel, N, Van Someren, EJW, Han, LKM, Aftanas, L, Aleman, A, Baune, BT, Berger, K, Blanken, TF, Capitao, L, Couvy-Duchesne, B, Cullen, KR, Dannlowski, U, Davey, C, Erwin-Grabner, T, Evans, J, Frodl, T, Fu, CHY, Godlewska, B, Gotlib, IH, Goya-Maldonado, R, Grabe, HJ, Groenewold, NA, Grotegerd, D, Gruber, O, Gutman, BA, Hall, GB, Harrison, BJ, Hatton, SN, Hermesdorf, M, Hickie, IB, Hilland, E, Irungu, B, Jonassen, R, Kelly, S, Kircher, T, Klimes-Dougan, B, Krug, A, Landro, NI, Lagopoulos, J, Leerssen, J, Li, M, Linden, DEJ, MacMaster, FP, McIntosh, AM, Mehler, DMA, Nenadic, I, Penninx, BWJH, Portella, MJ, Reneman, L, Renteria, ME, Sacchet, MD, Saemann, PG, Schrantee, A, Sim, K, Soares, JC, Stein, DJ, Tozzi, L, van Der Wee, NJA, van Tol, M-J, Vermeiren, R, Vives-Gilabert, Y, Walter, H, Walter, M, Whalley, HC, Wittfeld, K, Whittle, S, Wright, MJ, Yang, TT, Zarate, C, Thomopoulos, SI, Jahanshad, N, Thompson, PM, and Veltman, DJ

Abstract

A key objective in the field of translational psychiatry over the past few decades has been to identify the brain correlates of major depressive disorder (MDD). Identifying measurable indicators of brain processes associated with MDD could facilitate the detection of individuals at risk, and the development of novel treatments, the monitoring of treatment effects, and predicting who might benefit most from treatments that target specific brain mechanisms. However, despite intensive neuroimaging research towards this effort, underpowered studies and a lack of reproducible findings have hindered progress. Here, we discuss the work of the ENIGMA Major Depressive Disorder (MDD) Consortium, which was established to address issues of poor replication, unreliable results, and overestimation of effect sizes in previous studies. The ENIGMA MDD Consortium currently includes data from 45 MDD study cohorts from 14 countries across six continents. The primary aim of ENIGMA MDD is to identify structural and functional brain alterations associated with MDD that can be reliably detected and replicated across cohorts worldwide. A secondary goal is to investigate how demographic, genetic, clinical, psychological, and environmental factors affect these associations. In this review, we summarize findings of the ENIGMA MDD disease working group to date and discuss future directions. We also highlight the challenges and benefits of large-scale data sharing for mental health research.

Published
2020

13. Common brain disorders are associated with heritable patterns of apparent aging of the brain

Author

Kaufmann, T., van der Meer, D., Doan, N. T., Schwarz, E., Lund, M. J., Agartz, I., Alnaes, D., Barch, D. M., Baur-Streubel, R., Bertolino, A., Bettella, F., Beyer, M. K., Boen, E., Borgwardt, S., Brandt, C. L., Buitelaar, J., Celius, E. G., Cervenka, S., Conzelmann, A., Cordova-Palomera, A., Dale, A. M., de Quervain, D. J. F., Carlo, P. D., Djurovic, S., Dorum, E. S., Eisenacher, S., Elvsashagen, T., Espeseth, T., Fatouros-Bergman, H., Flyckt, L., Franke, B., Frei, O., Haatveit, B., Haberg, A. K., Harbo, H. F., Hartman, C. A., Heslenfeld, D., Hoekstra, P. J., Hogestol, E. A., Jernigan, T. L., Jonassen, R., Jonsson, E. G., Farde, L., Engberg, G., Erhardt, S., Schwieler, L., Piehl, F., Collste, K., Victorsson, P., Malmqvist, A., Hedberg, M., Orhan, F., Kirsch, P., Kloszewska, I., Kolskar, K. K., Landro, N. I., Hellard, S. L., Lesch, K. -P., Lovestone, S., Lundervold, A., Lundervold, A. J., Maglanoc, L. A., Malt, U. F., Mecocci, P., Melle, I., Meyer-Lindenberg, A., Moberget, T., Norbom, L. B., Nordvik, J. E., Nyberg, L., Oosterlaan, J., Papalino, M., Papassotiropoulos, A., Pauli, P., Pergola, G., Persson, K., Richard, G., Rokicki, J., Sanders, A. -M., Selbaek, G., Shadrin, A. A., Smeland, O. B., Soininen, H., Sowa, P., Steen, V. M., Tsolaki, M., Ulrichsen, K. M., Vellas, B., Wang, L., Westman, E., Ziegler, G. C., Zink, M., Andreassen, O. A., Westlye, L. T., Le Hellard, S., Di Carlo, P., Interdisciplinary Centre Psychopathology and Emotion regulation (ICPE), Clinical Cognitive Neuropsychiatry Research Program (CCNP), General Paediatrics, ARD - Amsterdam Reproduction and Development, Pediatric surgery, Psychiatrie & Neuropsychologie, RS: MHeNs - R3 - Neuroscience, and RS: MHeNs - R2 - Mental Health

Subjects
0301 basic medicine, Brain age gap, brain disorders, genetic architecture, pleiotropy, Male, Aging, Schizophrenia/genetics, LOCI, Genome-wide association study, Neuropsychological Tests, 0302 clinical medicine, 80 and over, Brain age gap, Aging/genetics, ALZHEIMERS, Child, Aged, 80 and over, Brain Diseases, Sex Characteristics, General Neuroscience, Mental Disorders, Brain, MULTIPLE-SCLEROSIS, brain disorders, Middle Aged, Magnetic Resonance Imaging, 3. Good health, Schizophrenia, Child, Preschool, Female, Alzheimer's disease, Neurovetenskaper, Algorithms, MRI, Adult, Adolescent, Brain Diseases/diagnostic imaging, Brain Structure and Function, Mental Disorders/diagnostic imaging, Biology, Article, 03 medical and health sciences, Young Adult, AGE, pleiotropy, Genetic architecture, Genetic Pleiotropy, medicine, Humans, Preschool, Brain disorders, Aged, Pleiotropy, Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7], Brain age gaps, Multiple sclerosis, Neurosciences, Infant, medicine.disease, Brain/diagnostic imaging, genetic architecture, 030104 developmental biology, Pleiotropy (drugs), Neuroscience, 030217 neurology & neurosurgery, Genome-Wide Association Study
Abstract

Common risk factors for psychiatric and other brain disorders are likely to converge on biological pathways influencing the development and maintenance of brain structure and function across life. Using structural MRI data from 45,615 individuals aged 3–96 years, we demonstrate distinct patterns of apparent brain aging in several brain disorders and reveal genetic pleiotropy between apparent brain aging in healthy individuals and common brain disorders. The author list between I.A. and M.Z. is in alphabetic order. The authors were funded by the Research Council of Norway (276082 LifespanHealth (T.K.), 213837 (O.A.A), 223273 NORMENT (O.A.A.), 204966 (L.T.W.), 229129 (O.A.A.), 249795 (L.T.W.), 273345 (L.T.W.) and 283798 SYNSCHIZ (O.A.A.)), the South-Eastern Norway Regional Health Authority (2013-123 (O.A.A.), 2014-097 (L.T.W.), 2015-073 (L.T.W.) and 2016083 (L.T.W.)), Stiftelsen Kristian Gerhard Jebsen (SKGJ-MED-008), the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (ERC Starting Grant, Grant agreement No. 802998 BRAINMINT (L.T.W.)), NVIDIA Corporation GPU Grant (T.K.), and the European Commission 7th Framework Programme (602450, IMAGEMEND (A.M.-L.)).

Published
2019

27. The C4 system.

Author

Olaisen, B., Teisberg, P., Jonassen, R., and Gedde-Dahl, T.

Abstract

The present study shows that the C4 system as investigated by high voltage agarose gel electrophoresis is highly polymorphic. In a series of unrelated Norwegian adults, where C4 types have been ascertained through segregation in families, six different haplotypes have been found to occur with a frequency exceeding 1%. The genotype frequencies in the population fit expected Hardy-Weinberg distribution. In family material comprising 89 matings with 327 children the distribution of offspring is as expected according to autosomal codominant inheritance of haplotypes. [ABSTRACT FROM AUTHOR]

Published
1979
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29. The genetic polymorphism of the fourth component of human complement: methodological aspects and a presentation of linkage and association data relevant to its localization in the HLA region.

Author

Teisberg, P, Olaisen, B, Jonassen, R, Gedde-Dahl, T, and Thorsby, E

Abstract

The C4 polymorphism in man has been studied by immunofixation electrophoresis, crossed immunoelectrophoresis, and functional detection after agarose gel electrophoresis. It has so far not been possible to reveal this polymorphism by isoelectric focusing and functional detection of C4 bands. Three common alleles and one less frequently occuring allele have been identified. In a small population sample studied by all the different techniques and verified by family segregation, the following gene frequencies have been found: C4F: 0.46, C4S: 0.32, C4F1: 0.20, and C4M: 0.02. By linkage and association studies in a family material it has been shown that a structural C4 locus is situated in the HLA region of chromosome 6 very close to the HLA-B and Bf loci.

Published
1977
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35. Virtual Histology of Cortical Thickness and Shared Neurobiology in 6 Psychiatric Disorders

Author

Committee, Writing, Disorder, Autism Spectrum, French, Leon, Grevet, Eugenio H, Groenewold, Nynke A, Grotegerd, Dominik, Gruber, Oliver, Gruner, Patricia, Guerrero-Pedraza, Amalia, Gur, Raquel E, Gur, Ruben C, Haar, Shlomi, Haarman, Bartholomeus C M, Thomopoulos, Sophia I, Haavik, Jan, Hahn, Tim, Hajek, Tomas, Harrison, Benjamin J, Harrison, Neil A, Hartman, Catharina A, Whalley, Heather C, Heslenfeld, Dirk J, Hibar, Derrek P, Hilland, Eva, Pozzi, Elena, Hirano, Yoshiyuki, Ho, Tiffany C, Hoekstra, Pieter J, Hoekstra, Liesbeth, Hohmann, Sarah, Hong, L. E., Höschl, Cyril, Høvik, Marie F, Howells, Fleur M, Nenadic, Igor, Abe, Yoshinari, Jalbrzikowski, Maria, James, Anthony C, Janssen, Joost, Jaspers-Fayer, Fern, Xu, Jian, Jonassen, Rune, Karkashadze, Georgii, King, Joseph A, Kircher, Tilo, Kirschner, Matthias, Abé, Christoph, Koch, Kathrin, Kochunov, Peter, Kohls, Gregor, Konrad, Kerstin, Krämer, Bernd, Krug, Axel, Kuntsi, Jonna, Kwon, Jun Soo, Landén, Mikael, Landrø, Nils I, Anticevic, Alan, Lazaro, Luisa, Lebedeva, Irina S, Leehr, Elisabeth J, Lera-Miguel, Sara, Lesch, Klaus-Peter, Lochner, Christine, Louza, Mario R, Luna, Beatriz, Lundervold, Astri J, MacMaster, Frank P, Alda, Martin, Maglanoc, Luigi A, Malpas, Charles B, Portella, Maria J, Marsh, Rachel, Martyn, Fiona M, Mataix-Cols, David, Mathalon, Daniel H, McCarthy, Hazel, McDonald, Colm, McPhilemy, Genevieve, Aleman, Andre, Meinert, Susanne, Menchón, José M, Minuzzi, Luciano, Mitchell, Philip B, Moreno, Carmen, Morgado, Pedro, Muratori, Filippo, Murphy, Clodagh M, Murphy, Declan, Mwangi, Benson, Alloza, Clara, Nabulsi, Leila, Nakagawa, Akiko, Nakamae, Takashi, Namazova, Leyla, Narayanaswamy, Janardhanan, Jahanshad, Neda, Nguyen, Danai D, Nicolau, Rosa, O'Gorman Tuura, Ruth L, O'Hearn, Kirsten, Alonso-Lana, Silvia, Oosterlaan, Jaap, Opel, Nils, Ophoff, Roel A, Oranje, Bob, García de la Foz, Victor Ortiz, Overs, Bronwyn J, Paloyelis, Yannis, Pantelis, Christos, Parellada, Mara, Pauli, Paul, Disorder, Bipolar, Ameis, Stephanie H, Picó-Pérez, Maria, Picon, Felipe A, Piras, Fabrizio, Piras, Federica, Plessen, Kerstin J, Pomarol-Clotet, Edith, Preda, Adrian, Puig, Olga, Quidé, Yann, Radua, Joaquim, Anagnostou, Evdokia, Ramos-Quiroga, J Antoni, Rasser, Paul E, Rauer, Lisa, Reddy, Janardhan, Redlich, Ronny, Reif, Andreas, Reneman, Liesbeth, Repple, Jonathan, Retico, Alessandra, Richarte, Vanesa, McIntosh, Andrew A, Richter, Anja, Rosa, Pedro G P, Rubia, Katya K, Hashimoto, Ryota, Sacchet, Matthew D, Salvador, Raymond, Santonja, Javier, Sarink, Kelvin, Sarró, Salvador, Satterthwaite, Theodore D, Arango, Celso, Sawa, Akira, Schall, Ulrich, Schofield, Peter R, Schrantee, Anouk, Seitz, Jochen, Serpa, Mauricio H, Setién-Suero, Esther, Shaw, Philip, Shook, Devon, Silk, Tim J, Arnold, Paul D, Sim, Kang, Simon, Schmitt, Simpson, Helen Blair, Singh, Aditya, Skoch, Antonin, Skokauskas, Norbert, Soares, Jair C, Soreni, Noam, Soriano-Mas, Carles, Spalletta, Gianfranco, Asherson, Philip, Spaniel, Filip, Lawrie, Stephen M, Stern, Emily R, Stewart, S Evelyn, Takayanagi, Yoichiro, Temmingh, Henk S, Tolin, David F, Tomecek, David, Tordesillas-Gutiérrez, Diana, Tosetti, Michela, Assogna, Francesca, Uhlmann, Anne, van Amelsvoort, Therese, van der Wee, Nic J A, van der Werff, Steven J A, van Haren, Neeltje E M, van Wingen, Guido A, Vance, Alasdair, Vázquez-Bourgon, Javier, Vecchio, Daniela, Venkatasubramanian, Ganesan, Auzias, Guillaume, Vieta, Eduard, Vilarroya, Oscar, Vives-Gilabert, Yolanda, Voineskos, Aristotle N, Völzke, Henry, von Polier, Georg G, Walton, Esther, Weickert, Thomas W, Weickert, Cynthia Shannon, Weideman, Andrea S, Ayesa-Arriola, Rosa, Wittfeld, Katharina, Wolf, Daniel H, Wu, Mon-Ju, Yang, T. T., Yang, Sikun, Yoncheva, Yuliya, Yun, Je-Yeon, Cheng, Yuqi, Zanetti, Marcus V, Ziegler, Georg C, Bakker, Geor, Franke, Barbara, Hoogman, Martine, Buitelaar, Jan K, van Rooij, Daan, Andreassen, Ole A, Ching, Christopher R K, Veltman, Dick J, Schmaal, Lianne, Stein, Dan J, van den Heuvel, Odile A, Disorder, Major Depressive, Banaj, Nerisa, Turner, Jessica A, van Erp, Theo G M, Pausova, Zdenka, Thompson, Paul M, Paus, Tomáš, Attention-Deficit/Hyperactivity Disorder, Banaschewski, Tobias, Bandeira, Cibele E, Baranov, Alexandr, Bargalló, Núria, Bau, Claiton H D, Baumeister, Sarah, Baune, Bernhard T, Bellgrove, Mark A, Benedetti, Francesco, Disorder, Obsessive-Compulsive, Bertolino, Alessandro, Boedhoe, Premika S W, Boks, Marco, Bollettini, Irene, Del Mar Bonnin, Caterina, Borgers, Tiana, Borgwardt, Stefan, Brandeis, Daniel, Brennan, Brian P, Bruggemann, Jason M, Groups, Schizophrenia ENIGMA Working, Bülow, Robin, Busatto, Geraldo F, Calderoni, Sara, Calhoun, Vince D, Calvo, Rosa, Canales-Rodríguez, Erick J, Cannon, Dara M, Carr, Vaughan J, Cascella, Nicola, Cercignani, Mara, Patel, Yash, Chaim-Avancini, Tiffany M, Christakou, Anastasia, Coghill, David, Conzelmann, Annette, Crespo-Facorro, Benedicto, Cubillo, Ana I, Cullen, Kathryn R, Cupertino, Renata B, Daly, Eileen, Dannlowski, Udo, Parker, Nadine, Davey, Christopher G, Denys, Damiaan, Deruelle, Christine, Di Giorgio, Annabella, Dickie, Erin W, Dima, Danai, Dohm, Katharina, Ehrlich, Stefan, Ely, Benjamin A, Erwin-Grabner, Tracy, Shin, Jean, Ethofer, Thomas, Fair, Damien A, Fallgatter, Andreas, Faraone, Stephen V, Fatjó-Vilas, Mar, Fedor, Jennifer M, Fitzgerald, Kate D, Ford, Judith M, Frodl, Thomas, Fu, Cynthia H Y, Howard, Derek, Fullerton, Janice M, Gabel, Matt C, Glahn, David C, Roberts, Gloria, Gogberashvili, Tinatin, Goikolea, Jose M, Gotlib, Ian H, Goya-Maldonado, Roberto, Grabe, Hans, Green, Melissa J, Patel, Y., Parker, N., Shin, J., Howard, D., French, L., Thomopoulos, S. I., Pozzi, E., Abe, Y., Abe, C., Anticevic, A., Alda, M., Aleman, A., Alloza, C., Alonso-Lana, S., Ameis, S. H., Anagnostou, E., Mcintosh, A. A., Arango, C., Arnold, P. D., Asherson, P., Assogna, F., Auzias, G., Ayesa-Arriola, R., Bakker, G., Banaj, N., Banaschewski, T., Bandeira, C. E., Baranov, A., Bargallo, N., Bau, C. H. D., Baumeister, S., Baune, B. T., Bellgrove, M. A., Benedetti, F., Bertolino, A., Boedhoe, P. S. W., Boks, M., Bollettini, I., Del Mar Bonnin, C., Borgers, T., Borgwardt, S., Brandeis, D., Brennan, B. P., Bruggemann, J. M., Bulow, R., Busatto, G. F., Calderoni, S., Calhoun, V. D., Calvo, R., Canales-Rodriguez, E. J., Cannon, D. M., Carr, V. J., Cascella, N., Cercignani, M., Chaim-Avancini, T. M., Christakou, A., Coghill, D., Conzelmann, A., Crespo-Facorro, B., Cubillo, A. I., Cullen, K. R., Cupertino, R. B., Daly, E., Dannlowski, U., Davey, C. G., Denys, D., Deruelle, C., Di Giorgio, A., Dickie, E. W., Dima, D., Dohm, K., Ehrlich, S., Ely, B. A., Erwin-Grabner, T., Ethofer, T., Fair, D. A., Fallgatter, A. J., Faraone, S. V., Fatjo-Vilas, M., Fedor, J. M., Fitzgerald, K. D., Ford, J. M., Frodl, T., Fu, C. H. Y., Fullerton, J. M., Gabel, M. C., Glahn, D. C., Roberts, G., Gogberashvili, T., Goikolea, J. M., Gotlib, I. H., Goya-Maldonado, R., Grabe, H. J., Green, M. J., Grevet, E. H., Groenewold, N. A., Grotegerd, D., Gruber, O., Gruner, P., Guerrero-Pedraza, A., Gur, R. E., Gur, R. C., Haar, S., Haarman, B. C. M., Haavik, J., Hahn, T., Hajek, T., Harrison, B. J., Harrison, N. A., Hartman, C. A., Whalley, H. C., Heslenfeld, D. J., Hibar, D. P., Hilland, E., Hirano, Y., Ho, T. C., Hoekstra, P. J., Hoekstra, L., Hohmann, S., Hong, L. E., Hoschl, C., Hovik, M. F., Howells, F. M., Nenadic, I., Jalbrzikowski, M., James, A. C., Janssen, J., Jaspers-Fayer, F., Xu, J., Jonassen, R., Karkashadze, G., King, J. A., Kircher, T., Kirschner, M., Koch, K., Kochunov, P., Kohls, G., Konrad, K., Kramer, B., Krug, A., Kuntsi, J., Kwon, J. S., Landen, M., Landro, N. I., Lazaro, L., Lebedeva, I. S., Leehr, E. J., Lera-Miguel, S., Lesch, K. -P., Lochner, C., Louza, M. R., Luna, B., Lundervold, A. J., Macmaster, F. P., Maglanoc, L. A., Malpas, C. B., Portella, M. J., Marsh, R., Martyn, F. M., Mataix-Cols, D., Mathalon, D. H., Mccarthy, H., Mcdonald, C., Mcphilemy, G., Meinert, S., Menchon, J. M., Minuzzi, L., Mitchell, P. B., Moreno, C., Morgado, P., Muratori, F., Murphy, C. M., Murphy, D., Mwangi, B., Nabulsi, L., Nakagawa, A., Nakamae, T., Namazova, L., Narayanaswamy, J., Jahanshad, N., Nguyen, D. D., Nicolau, R., O'Gorman Tuura, R. L., O'Hearn, K., Oosterlaan, J., Opel, N., Ophoff, R. A., Oranje, B., Garcia De La Foz, V. O., Overs, B. J., Paloyelis, Y., Pantelis, C., Parellada, M., Pauli, P., Pico-Perez, M., Picon, F. A., Piras, F., Plessen, K. J., Pomarol-Clotet, E., Preda, A., Puig, O., Quide, Y., Radua, J., Ramos-Quiroga, J. A., Rasser, P. E., Rauer, L., Reddy, J., Redlich, R., Reif, A., Reneman, L., Repple, J., Retico, A., Richarte, V., Richter, A., Rosa, P. G. P., Rubia, K. K., Hashimoto, R., Sacchet, M. D., Salvador, R., Santonja, J., Sarink, K., Sarro, S., Satterthwaite, T. D., Sawa, A., Schall, U., Schofield, P. R., Schrantee, A., Seitz, J., Serpa, M. H., Setien-Suero, E., Shaw, P., Shook, D., Silk, T. J., Sim, K., Simon, S., Simpson, H. B., Singh, A., Skoch, A., Skokauskas, N., Soares, J. C., Soreni, N., Soriano-Mas, C., Spalletta, G., Spaniel, F., Lawrie, S. M., Stern, E. R., Stewart, S. E., Takayanagi, Y., Temmingh, H. S., Tolin, D. F., Tomecek, D., Tordesillas-Gutierrez, D., Tosetti, M., Uhlmann, A., Van Amelsvoort, T., Van Der Wee, N. J. A., Van Der Werff, S. J. A., Van Haren, N. E. M., Van Wingen, G. A., Vance, A., Vazquez-Bourgon, J., Vecchio, D., Venkatasubramanian, G., Vieta, E., Vilarroya, O., Vives-Gilabert, Y., Voineskos, A. N., Volzke, H., Von Polier, G. G., Walton, E., Weickert, T. W., Weickert, C. S., Weideman, A. S., Wittfeld, K., Wolf, D. H., Wu, M. -J., Yang, T. T., Yang, K., Yoncheva, Y., Yun, J. -Y., Cheng, Y., Zanetti, M. V., Ziegler, G. C., Franke, B., Hoogman, M., Buitelaar, J. K., Van Rooij, D., Andreassen, O. A., Ching, C. R. K., Veltman, D. J., Schmaal, L., Stein, D. J., Van Den Heuvel, O. A., Turner, J. A., Van Erp, T. G. M., Pausova, Z., Thompson, P. M., Paus, T., Institut de Neurosciences de la Timone (INT), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS), Pediatric surgery, Radiology and nuclear medicine, Anatomy and neurosciences, Psychiatry, Amsterdam Neuroscience - Brain Imaging, Amsterdam Neuroscience - Compulsivity, Impulsivity & Attention, Amsterdam Neuroscience - Mood, Anxiety, Psychosis, Stress & Sleep, Amsterdam Neuroscience - Neurodegeneration, Psychiatrie & Neuropsychologie, RS: MHeNs - R2 - Mental Health, MUMC+: MA Med Staf Spec Psychiatrie (9), Adult Psychiatry, ANS - Compulsivity, Impulsivity & Attention, General Paediatrics, ARD - Amsterdam Reproduction and Development, Radiology and Nuclear Medicine, APH - Personalized Medicine, ANS - Brain Imaging, ANS - Mood, Anxiety, Psychosis, Stress & Sleep, APH - Mental Health, University of Zurich, Clinical Cognitive Neuropsychiatry Research Program (CCNP), Clinical Neuropsychology, Interdisciplinary Centre Psychopathology and Emotion regulation (ICPE), Child and Adolescent Psychiatry / Psychology, IBBA, and Cognitive Psychology

Subjects
Male, Obsessive-Compulsive Disorder, Bipolar Disorder, Autism Spectrum Disorder, Autism, [SDV]Life Sciences [q-bio], Gene Expression, cytology [Cerebral Cortex], Cohort Studies, Fetal Development, physiology [Gene Expression], 2738 Psychiatry and Mental Health, 0302 clinical medicine, diagnostic imaging [Cerebral Cortex], SCHIZOPHRENIA, BRAIN, Child, Obsessive-compulsive disorder (OCD), Original Investigation, Aged, 80 and over, Cerebral Cortex, 0303 health sciences, pathology [Depressive Disorder, Major], Principal Component Analysis, Adolescent psychiatry, 10058 Department of Child and Adolescent Psychiatry, Middle Aged, diagnostic imaging [Obsessive-Compulsive Disorder], REGIONS, Magnetic Resonance Imaging, 3. Good health, FALSE DISCOVERY RATE, Psychiatry and Mental health, Autism spectrum disorder, Schizophrenia, growth & development [Cerebral Cortex], Child, Preschool, Major depressive disorder, diagnostic imaging [Schizophrenia], Esquizofrènia, Female, Psiquiatria infantil, Psiquiatria de l'adolescència, diagnostic imaging [Autism Spectrum Disorder], Adult, medicine.medical_specialty, Adolescent, Human Development, 610 Medicine & health, diagnostic imaging [Bipolar Disorder], pathology [Autism Spectrum Disorder], diagnostic imaging [Depressive Disorder, Major], 03 medical and health sciences, Young Adult, All institutes and research themes of the Radboud University Medical Center, Neuroimaging, SDG 3 - Good Health and Well-being, CEREBRAL-CORTEX, Child psychiatry, medicine, Attention deficit hyperactivity disorder, Humans, Bipolar disorder, ddc:610, Psychiatry, pathology [Schizophrenia], 030304 developmental biology, Aged, Depressive Disorder, Major, Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7], business.industry, DENDRITE, Computational Biology, Correction, pathology [Attention Deficit Disorder with Hyperactivity], physiology [Fetal Development], medicine.disease, PATHOLOGY, pathology [Bipolar Disorder], pathology [Obsessive-Compulsive Disorder], 10036 Medical Clinic, Attention Deficit Disorder with Hyperactivity, 10054 Clinic for Psychiatry, Psychotherapy, and Psychosomatics, Case-Control Studies, DENSITY, ORIGINS, HIPPOCAMPUS, diagnostic imaging [Attention Deficit Disorder with Hyperactivity], pathology [Cerebral Cortex], Autisme, business, Neuroscience, 030217 neurology & neurosurgery, physiology [Human Development]
Abstract

[Importance] Large-scale neuroimaging studies have revealed group differences in cortical thickness across many psychiatric disorders. The underlying neurobiology behind these differences is not well understood., [Objective] To determine neurobiologic correlates of group differences in cortical thickness between cases and controls in 6 disorders: attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), bipolar disorder (BD), major depressive disorder (MDD), obsessive-compulsive disorder (OCD), and schizophrenia., [Design, Setting, and Participants] Profiles of group differences in cortical thickness between cases and controls were generated using T1-weighted magnetic resonance images. Similarity between interregional profiles of cell-specific gene expression and those in the group differences in cortical thickness were investigated in each disorder. Next, principal component analysis was used to reveal a shared profile of group difference in thickness across the disorders. Analysis for gene coexpression, clustering, and enrichment for genes associated with these disorders were conducted. Data analysis was conducted between June and December 2019. The analysis included 145 cohorts across 6 psychiatric disorders drawn from the ENIGMA consortium. The numbers of cases and controls in each of the 6 disorders were as follows: ADHD: 1814 and 1602; ASD: 1748 and 1770; BD: 1547 and 3405; MDD: 2658 and 3572; OCD: 2266 and 2007; and schizophrenia: 2688 and 3244., [Main Outcomes and Measures] Interregional profiles of group difference in cortical thickness between cases and controls., [Results] A total of 12 721 cases and 15 600 controls, ranging from ages 2 to 89 years, were included in this study. Interregional profiles of group differences in cortical thickness for each of the 6 psychiatric disorders were associated with profiles of gene expression specific to pyramidal (CA1) cells, astrocytes (except for BD), and microglia (except for OCD); collectively, gene-expression profiles of the 3 cell types explain between 25% and 54% of variance in interregional profiles of group differences in cortical thickness. Principal component analysis revealed a shared profile of difference in cortical thickness across the 6 disorders (48% variance explained); interregional profile of this principal component 1 was associated with that of the pyramidal-cell gene expression (explaining 56% of interregional variation). Coexpression analyses of these genes revealed 2 clusters: (1) a prenatal cluster enriched with genes involved in neurodevelopmental (axon guidance) processes and (2) a postnatal cluster enriched with genes involved in synaptic activity and plasticity-related processes. These clusters were enriched with genes associated with all 6 psychiatric disorders., [Conclusions and Relevance] In this study, shared neurobiologic processes were associated with differences in cortical thickness across multiple psychiatric disorders. These processes implicate a common role of prenatal development and postnatal functioning of the cerebral cortex in these disorders.

Published
2021

36. Over-the-counter analgesic usage: associations with attentional biases in young women.

Author

Roalsø ES, Klonteig S, Kraft B, Skarstein S, Hilland E, Mirtaheri P, Aalberg M, and Jonassen R

Subjects
Humans, Female, Young Adult, Adult, Anxiety drug therapy, Fear drug effects, Emotions drug effects, Attention drug effects, Depression drug therapy, Attentional Bias drug effects, Attentional Bias physiology, Nonprescription Drugs pharmacology, Analgesics pharmacology
Abstract

The use of over-the-counter analgesics (OTCA) has been found to alter various aspects of emotional processing and has been linked to increased anxiety and depression symptoms. Attentional bias is an aspect of emotional processing that is closely related to anxiety and depression. Although OTCA and attentional bias have both been linked to anxiety and depression, the potential links between OTCA usage and attentional bias are not yet investigated. The present study aimed to determine whether the frequency of OTCA usage is associated with differences in attentional bias by comparing response-based measures of attentional bias in 62 women aged 19-30 years. The findings showed that the small group reporting high OTCA usage demonstrated more orientation avoidance to fearful stimuli than those reporting no or low usage. Based on these preliminary findings, further research on attentional bias and its relationship to high OTCA usage is recommended., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Published
2024
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37. Inhibition moderates the effect of attentional bias modification for reducing residual depressive symptoms: A randomized sham-controlled clinical trial.

Author

Bø R, Kraft B, Skilbrei A, Jonassen R, Harmer CJ, and Landrø NI

Subjects
Humans, Male, Female, Adult, Double-Blind Method, Middle Aged, Young Adult, Cognitive Behavioral Therapy methods, Stroop Test, Outcome Assessment, Health Care, Attentional Bias physiology, Inhibition, Psychological, Depression therapy, Executive Function physiology
Abstract

Objectives: Residual symptoms represent risk factor for relapse. Attention bias modification (ABM) may reduce clinical and sub-clinical depressive symptoms, indicating that is may be of relevance when preventing relapse. Current evidence suggests that executive functions may moderate the outcome of interventions targeting depressive symptoms., Methods: We assessed inhibition and shifting as indicators of executive functioning by means of the Color-Word Interference Test (i.e., "Stroop task"). These baseline characteristics were investigated as moderator of the effect of ABM on depression symptoms in a double-blinded randomized sham-controlled trial of ABM including patients with a history of recurrent depression (N = 301). Inclusion and follow-ups took place from January 2015 to October 2016. The trial was retrospectively registered #NCT02658682 January 2016., Results: The moderation analysis was based on the interaction term ABM x Stroop. Scaled inhibition scores ≤10.8, but not shifting ability, moderated the effect of ABM compared to sham on clinician-rated depression (HDRS). The difference from the 15th to the 85th percentile of the inhibition score was about 1 HDRS-point, indicating a small effect size. No moderation was found when self-reported depression and AB were the outcome. Post-hoc power calculation indicates risk of Type-II error., Conclusion: When targeting depressive symptoms, ABM seems to be somewhat more effective in patients with weak inhibitory control. This suggests that evaluating the level of inhibition in individual patients could provide some information when making decisions about prescribing ABM to reduce residual symptoms, but the clinical implications of this is uncertain due to an overall small effect size attributable to ABM. Future studies should examine whether inhibitory control still is a relevant moderator when comparing ABM to treatment options other than the sham control condition., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Nils Inge Landro reports financial support was provided by Research Council of Norway. Nils Inge Landro reports financial support was provided by South-Eastern Norway Regional Health Authority. Ragnhild Boe reports financial support was provided by Foundation Dam. Catherine J. Harmer reports a relationship with P1 Vital that includes: consulting or advisory. Catherine J. Harmer reports a relationship with Lundbeck that includes: consulting or advisory. Catherine J. Harmer reports a relationship with SAGE Therapeutics Inc that includes: consulting or advisory. Catherine J. Harmer reports a relationship with Compass Pathways Plc that includes: consulting or advisory. Catherine J. Harmer reports a relationship with Zogenix Inc that includes: consulting or advisory. Nils Inge Landro reports a relationship with Lundbeck that includes: consulting or advisory and travel reimbursement. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Published
2024
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38. Investigating Whether a Combination of Electro-Encephalography and Gene Expression Profiling Can Predict the Risk of Chronic Pain: A Protocol for an Observational Prospective Cohort Study.

Author

Sannes AC, Ghani U, Niazi IK, Moberget T, Jonassen R, Haavik H, and Gjerstad J

Abstract

Despite most episodes of low back pain (LBP) being short-lasting, some transition into persistent long-lasting problems. Hence, the need for a deeper understanding of the physiological mechanisms of this is pertinent. Therefore, the aims of the present study are (1) to map pain-induced changes in brain activity and blood gene expression associated with persistent LBP, and (2) to explore whether these brain and gene expression signatures show promise as predictive biomarkers for the development of persistent LBP. The participants will be allocated into three different pain groups (no pain, mild short-lasting, or moderate long-term). One in-person visit, where two blood samples will be collected and sent for RNA sequencing, along with resting 64-channel electro-encephalography measurements before, during, and after a cold pressor test, will be conducted. Thereafter, follow-up questionnaires will be distributed at 2 weeks, 3 months, and 6 months. Recruitment will start during the second quarter of 2024, with expected completion by the last quarter of 2024. The results are expected to provide insight into the relationship between central nervous system activity, gene expression profiles, and LBP. If successful, this study has the potential to provide physiological indicators that are sensitive to the transition from mild, short-term LBP to more problematic, long-term LBP.

Published
2024
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39. Associations between over-the-counter analgesics usage and symptoms of anxiety and depression in adolescents: a network analysis.

Author

Roalsø ES, Klonteig S, Kraft B, Skarstein S, Aalberg M, and Jonassen R

Subjects
Humans, Male, Female, Adolescent, Norway epidemiology, Sex Factors, Surveys and Questionnaires, Nonprescription Drugs therapeutic use, Analgesics therapeutic use, Depression epidemiology, Anxiety epidemiology
Abstract

Background: The use of over-the-counter analgesics (OTCA) is common among adolescents and has been linked with increased symptoms of anxiety and depression. However, little is known about which specific symptoms are most strongly connected to OTCA usage. The current study assessed which anxiety and depression symptoms were most closely associated with OTCA usage in a large sample of adolescents and examined whether this differed across genders., Method: The present study was based on data from 626,581 participants from the Ungdata survey in Norway. Associations between OTCA and anxiety and depression symptoms were examined using network analysis. Non-regularized partial-correlation networks were constructed to estimate the conditional dependent relations between the use of OTCA and symptoms while controlling for pain. Gender-specific networks were created for comparison., Results: OTCA usage was associated with most symptoms, even after controlling for pain, with the strongest associations with "sleep problems", "stiff or tense", "everything is a struggle" and "suddenly scared". There were some gender differences, showing that "sleep problems" and "hopeless" were more strongly related to OTCA usage in females, whereas "stiff or tense" was more strongly related to OTCA usage in males., Conclusion: Overall, the somatic symptoms of anxiety and depression displayed the strongest associations with OTCA usage. When examining the gender-specific networks, both showed similar trends, although males exhibited slightly stronger associations between OTCA usage and somatic symptoms., (© 2024. The Author(s).)

Published
2024
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40. Cognitive predictors of stress-induced mood malleability in depression.

Author

Bø R, Kraft B, Joormann J, Jonassen R, Harmer CJ, and Landrø NI

Subjects
Humans, Affect physiology, Anxiety, Cognition, Depression psychology, Depressive Disorder, Major psychology
Abstract

Background & Objectives: Basic attentional control, negative biases in attention and interpretation, and rumination are all cognitive processes associated with depression; however, less is known about their predictive role in depressive mood reactivity and -recovery in response to stress, and their relation to severity of depression., Design & Methods: We experimentally induced stress based on an autobiographical imagery script in a sample of 92 participants with Major Depressive Disorder with or without comorbid anxiety disorders. We used simple regression analysis for investigating the roles of state- and trait rumination, attentional networks, and attentional and interpretation biases for predicting stress-induced depressive mood reactivity and -recovery, respectively, and whether they in parallel mediated the association between cognitive processes and depression severity., Results: Stress-induced depressive mood reactivity was predicted by better orienting ability and more state rumination. Better recovery was predicted by better orienting efficiency and lower negative interpretation bias. Furthermore, the relation between state rumination and depression severity was partially mediated by depressive mood reactivity, however limited by the lack of temporal precedence in the analysis., Conclusions: We characterized the relation between cognitive processes and mood malleability in response to stress. Findings could refine theoretical models of depression if causality is established., Trial Registration: ClinicalTrials.gov identifier: NCT04137367.

Published
2024
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41. The long-term effects of ABM on symptom severity in patients with recurrent depression: A randomized sham-controlled trial.

Author

Bø R, Kraft B, Jonassen R, Pedersen ML, Harmer CJ, and Landrø NI

Subjects
Humans, Depression therapy, Treatment Outcome, Chronic Disease, Recurrence, Attentional Bias, Cognitive Behavioral Therapy, Depressive Disorder, Major diagnosis, Depressive Disorder, Major therapy
Abstract

Background: The present study reports on long-term outcomes of ABM over one year in self-reported and clinician-rated depression symptoms, anxiety symptoms, and relapse rates., Methods: We conducted a double-blind randomized sham-controlled trial in 301 participants with recurrent major depression disorder between January 2015 and October 2016 (#NCT02658682). Participants were allocated to ABM or sham condition twice daily for 14 consecutive days. Long-term effects of ABM were assessed by BDI-II, HDRS and BAI at one-, six-, and 12-months follow-up. Relapse rates at 12-months follow-up were also assessed., Results: There was no long-term effect of ABM (as compared to sham) on clinician-rated depression symptoms, on anxiety symptoms, nor in relapse rates. By 12 months follow-up, there was a small effect on self-reported depression favoring ABM over sham., Limitations: The lack of an assessment-only condition hinders comparison to natural trajectories of depression symptoms., Conclusions: The overall long-term effect of ABM was limited, and currently there is no convincing evidence for implementing this as a viable treatment option in clinical populations. We speculate if the sham condition should be replaced by another control condition when investigating the clinical utility of ABM., Competing Interests: Declaration of competing interest NIL has received consultancy fees and travel expenses from Lundbeck outside this work. CJH has received consultancy fees from P1vital, Lundbeck, Sage Therapeutics, Compass Pathways, Zogenix outside of this work. Other authors report no financial relationships with commercial interests., (Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.)

Published
2023
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42. The effect of attention bias modification on depressive symptoms in a comorbid sample: a randomized controlled trial.

Author

Bø R, Kraft B, Pedersen ML, Joormann J, Jonassen R, Osnes K, Harmer CJ, and Landrø NI

Subjects
Humans, Depression, Treatment Outcome, Depressive Disorder, Major epidemiology, Depressive Disorder, Major therapy, Cognitive Behavioral Therapy, Attentional Bias
Abstract

Background: Studies investigating the long-term effect of attention bias modification (ABM) in clinical samples are lacking. This study investigates the 6-months follow-up effect of ABM on depressive symptoms in participant with major depressive disorder with and without comorbid disorders., Methods: We conducted a double-blind randomized sham-controlled trial in 101 participants between 19 November 2019, and 17 August 2021. Follow-up ended 3 April 2022. Participants were allocated to ABM or sham condition twice daily for 14 consecutive days. Primary outcomes were the total score on the Beck Depression Inventory-II (BDI-II) at 6 months, mean Brief State Rumination Inventory (BSRI) score post-treatment and reduction in BSRI post-treatment. Secondary outcome was change in attentional bias (AB). The trial was preregistered in ClinicalTrials.gov (#NCT04137367)., Results: A total of 118 patients aged 18-65 years were assessed for eligibility, and 101 were randomized and subjected to intention-to-treat analyses. At 6 months, ABM had no effect on depression and anxiety compared to a sham condition. While rumination decreased during the intervention, there was no effect of condition on rumination and AB. Predictor analysis did not reveal differences between participants with ongoing major depressive episode or comorbid anxiety., Conclusion: Compared to sham training, there was no effect of ABM on depressive symptoms at 6-months follow-up. Since the intervention failed at modifying AB, it is unclear whether changes in AB are related to long-term outcomes.

Published
2023
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44. Virtual Ontogeny of Cortical Growth Preceding Mental Illness.

Author

Patel Y, Shin J, Abé C, Agartz I, Alloza C, Alnæs D, Ambrogi S, Antonucci LA, Arango C, Arolt V, Auzias G, Ayesa-Arriola R, Banaj N, Banaschewski T, Bandeira C, Başgöze Z, Cupertino RB, Bau CHD, Bauer J, Baumeister S, Bernardoni F, Bertolino A, Bonnin CDM, Brandeis D, Brem S, Bruggemann J, Bülow R, Bustillo JR, Calderoni S, Calvo R, Canales-Rodríguez EJ, Cannon DM, Carmona S, Carr VJ, Catts SV, Chenji S, Chew QH, Coghill D, Connolly CG, Conzelmann A, Craven AR, Crespo-Facorro B, Cullen K, Dahl A, Dannlowski U, Davey CG, Deruelle C, Díaz-Caneja CM, Dohm K, Ehrlich S, Epstein J, Erwin-Grabner T, Eyler LT, Fedor J, Fitzgerald J, Foran W, Ford JM, Fortea L, Fuentes-Claramonte P, Fullerton J, Furlong L, Gallagher L, Gao B, Gao S, Goikolea JM, Gotlib I, Goya-Maldonado R, Grabe HJ, Green M, Grevet EH, Groenewold NA, Grotegerd D, Gruber O, Haavik J, Hahn T, Harrison BJ, Heindel W, Henskens F, Heslenfeld DJ, Hilland E, Hoekstra PJ, Hohmann S, Holz N, Howells FM, Ipser JC, Jahanshad N, Jakobi B, Jansen A, Janssen J, Jonassen R, Kaiser A, Kaleda V, Karantonis J, King JA, Kircher T, Kochunov P, Koopowitz SM, Landén M, Landrø NI, Lawrie S, Lebedeva I, Luna B, Lundervold AJ, MacMaster FP, Maglanoc LA, Mathalon DH, McDonald C, McIntosh A, Meinert S, Michie PT, Mitchell P, Moreno-Alcázar A, Mowry B, Muratori F, Nabulsi L, Nenadić I, O'Gorman Tuura R, Oosterlaan J, Overs B, Pantelis C, Parellada M, Pariente JC, Pauli P, Pergola G, Piarulli FM, Picon F, Piras F, Pomarol-Clotet E, Pretus C, Quidé Y, Radua J, Ramos-Quiroga JA, Rasser PE, Reif A, Retico A, Roberts G, Rossell S, Rovaris DL, Rubia K, Sacchet M, Salavert J, Salvador R, Sarró S, Sawa A, Schall U, Scott R, Selvaggi P, Silk T, Sim K, Skoch A, Spalletta G, Spaniel F, Stein DJ, Steinsträter O, Stolicyn A, Takayanagi Y, Tamm L, Tavares M, Teumer A, Thiel K, Thomopoulos SI, Tomecek D, Tomyshev AS, Tordesillas-Gutiérrez D, Tosetti M, Uhlmann A, Van Rheenen T, Vazquez-Bourgón J, Vernooij MW, Vieta E, Vilarroya O, Weickert C, Weickert T, Westlye LT, Whalley H, Willinger D, Winter A, Wittfeld K, Yang TT, Yoncheva Y, Zijlmans JL, Hoogman M, Franke B, van Rooij D, Buitelaar J, Ching CRK, Andreassen OA, Pozzi E, Veltman D, Schmaal L, van Erp TGM, Turner J, Castellanos FX, Pausova Z, Thompson P, and Paus T

Subjects
Cerebral Cortex, Child, Female, Humans, Infant, Newborn, Magnetic Resonance Imaging methods, Pregnancy, Attention Deficit Disorder with Hyperactivity, Autism Spectrum Disorder genetics, Autism Spectrum Disorder pathology, Bipolar Disorder, Depressive Disorder, Major pathology, Premature Birth pathology
Abstract

Background: Morphology of the human cerebral cortex differs across psychiatric disorders, with neurobiology and developmental origins mostly undetermined. Deviations in the tangential growth of the cerebral cortex during pre/perinatal periods may be reflected in individual variations in cortical surface area later in life., Methods: Interregional profiles of group differences in surface area between cases and controls were generated using T1-weighted magnetic resonance imaging from 27,359 individuals including those with attention-deficit/hyperactivity disorder, autism spectrum disorder, bipolar disorder, major depressive disorder, schizophrenia, and high general psychopathology (through the Child Behavior Checklist). Similarity of interregional profiles of group differences in surface area and prenatal cell-specific gene expression was assessed., Results: Across the 11 cortical regions, group differences in cortical area for attention-deficit/hyperactivity disorder, schizophrenia, and Child Behavior Checklist were dominant in multimodal association cortices. The same interregional profiles were also associated with interregional profiles of (prenatal) gene expression specific to proliferative cells, namely radial glia and intermediate progenitor cells (greater expression, larger difference), as well as differentiated cells, namely excitatory neurons and endothelial and mural cells (greater expression, smaller difference). Finally, these cell types were implicated in known pre/perinatal risk factors for psychosis. Genes coexpressed with radial glia were enriched with genes implicated in congenital abnormalities, birth weight, hypoxia, and starvation. Genes coexpressed with endothelial and mural genes were enriched with genes associated with maternal hypertension and preterm birth., Conclusions: Our findings support a neurodevelopmental model of vulnerability to mental illness whereby prenatal risk factors acting through cell-specific processes lead to deviations from typical brain development during pregnancy., (Copyright © 2022 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

Published
2022
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45. Aberrant default mode connectivity in adolescents with early-onset psychosis: A resting state fMRI study.

Author

Hilland E, Johannessen C, Jonassen R, Alnæs D, Jørgensen KN, Barth C, Andreou D, Nerland S, Wortinger LA, Smelror RE, Wedervang-Resell K, Bohman H, Lundberg M, Westlye LT, Andreassen OA, Jönsson EG, and Agartz I

Subjects
Adolescent, Brain diagnostic imaging, Brain Mapping, Cerebral Cortex, Female, Humans, Magnetic Resonance Imaging, Neural Pathways diagnostic imaging, Parietal Lobe, Psychotic Disorders diagnostic imaging, Schizophrenia
Abstract

Abnormal default mode network (DMN) connectivity has been found in schizophrenia and other psychotic disorders. However, there are limited studies on early onset psychosis (EOP), and their results show lack of agreement. Here, we investigated within-network DMN connectivity in EOP compared to healthy controls (HC), and its relationship to clinical characteristics. A sample of 68 adolescent patients with EOP (mean age 16.53 ± 1.12 [SD] years, females 66%) and 95 HC (mean age 16.24 ± 1.50 [SD], females 60%) from two Scandinavian cohorts underwent resting state functional magnetic resonance imaging (rsfMRI). A group independent component analysis (ICA) was performed to identify the DMN across all participants. Dual regression was used to estimate spatial maps reflecting each participant's DMN network, which were compared between EOP and HC using voxel-wise general linear models and permutation-based analyses. Subgroup analyses were performed within the patient group, to explore associations between diagnostic subcategories and current use of psychotropic medication in relation to connectivity strength. The analysis revealed significantly reduced DMN connectivity in EOP compared to HC in the posterior cingulate cortex, precuneus, fusiform cortex, putamen, pallidum, amygdala, and insula. The subgroup analysis in the EOP group showed strongest deviations for affective psychosis, followed by other psychotic disorders and schizophrenia. There was no association between DMN connectivity strength and the current use of psychotropic medication. In conclusion, the findings demonstrate weaker DMN connectivity in adolescent patients with EOP compared to healthy peers, and differential effects across diagnostic subcategories, which may inform our understanding of underlying disease mechanisms in EOP., (Copyright © 2021. Published by Elsevier Inc.)

Published
2022
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46. Mutual learning: exploring collaboration, knowledge and roles in the development of recovery-oriented services. A hermeneutic-phenomenological study.

Author

Klevan T, Jonassen R, Topor A, and Borg M

Subjects
Hermeneutics, Humans, Mental Health, Mental Disorders therapy, Mental Health Services, Substance-Related Disorders therapy
Abstract

Purpose: The concept of recovery is commonly described as multifaceted and contested in the field of mental health and substance abuse. The aim of this study is to explore how understandings of recovery and recovery orientation of services are developed through daily practices and collaboration between service users and professionals., Methods: Eight pairs of participants were interviewed together, in accordance with the dyadic interview method. The dyads/pairs consisted of service users and professional helpers. A collaborative hermeneutic-phenomenological analysis was used to analyse data., Results: Data were analysed into three overarching and entangled themes, exploring how recovery-oriented collaboration and knowledge encompasses (a) recovery as relational processes. These processes are entangled with (b) recovery as situated in time and place. Furthermore, relational processes and dimensions of time and place are situated in and supported or hindered by (c) recovery orientation as part of the municipal policies, understood as the regulations, frameworks and decisions guiding mental health and substance abuse services in the municipality., Conclusions: The further development of recovery-oriented services should focus on facilitating open-ended and flexible ways of developing practices and relationships. This involves recognizing how relationships contribute to the development of knowledge and practices.

Published
2021
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47. Over-the-counter analgesics use is associated with pain and psychological distress among adolescents: a mixed effects approach in cross-sectional survey data from Norway.

Author

Jonassen R, Hilland E, Harmer CJ, Abebe DS, Bergem AK, and Skarstein S

Subjects
Abdominal Pain, Adolescent, Analgesics adverse effects, Anxiety chemically induced, Anxiety epidemiology, Cross-Sectional Studies, Depression chemically induced, Depression epidemiology, Female, Humans, Male, Psychological Distress, Stress, Psychological epidemiology
Abstract

Background: Over-the-counter analgesics (OTCA) such as Paracetamol and Ibuprofen are frequently used by adolescents, and the route of administration and access at home allows unsupervised use. Psychological distress and pain occur simultaneously and are more common among females than among males. There is a dynamic interplay between on-label pain indications and psychological distress, and frequent OTCA use or misuse can exacerbate symptoms. No studies have to date provided an overview of frequent OTCA use in a larger population-based study. The current study used survey data to explore associations between and the relative predictive value of on-label pain indication and measures of psychological distress, together with sex differences for weekly OTCA use., Methods: This study included 349,528 adolescents aged 13-19. The data was collected annually between January 2014 and December 2018 as part of the Norwegian Young Data survey. Performance analysis was conducted to explore the relative roles and associations between on-label pain indication and psychological distress in weekly OTCA use. A mixed-effects logistic regression model was used to explore the unique contributions from four domains of on-label pain indication and psychological distress as measured by a combined measure of anxiety and depression (HSCL-10) and peer-bullying involvement as victims or bullies., Results: Thirty percent of females and 13 % of males use OTCA weekly. Headache is the strongest on-label pain predictor of weekly OTCA use, followed by abdominal pain. Depression and anxiety are the strongest psychological predictor of weekly OTCA use, and higher symptom levels and being female increase the strength of this association. Anxiety and depression also predict weekly OTCA use after controlling for physiological pain., Conclusions: Sex, pain and anxiety and depression are inter-correlated and strong predictors of frequent OTCA use. Frequent OTCA use in the context of psychological distress may be a form of self-medication that can exacerbate symptoms and decrease psychosocial function. Longitudinal studies that explore causal trajectories between frequent on-label OTCA use and psychological distress are required. OTCA use among adolescents, and particularly among females, with anxiety and depression should be administered with caution and closely monitored., (© 2021. The Author(s).)

Published
2021
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48. Editorial: The Cognitive Neuropsychological Hypothesis in Pediatric Anxiety and the Advantage of Revealing Early Changes in Brain Mechanisms Associated With Therapeutic Effects.

Author

Jonassen R

Subjects
Antidepressive Agents therapeutic use, Brain, Child, Cognition, Humans, Anxiety, Anxiety Disorders drug therapy
Abstract

There is a pressing need to improve treatment, and clinical trials should not only focus on efficacy, but also on identifying the underlying mechanisms through which treatments operate. 1 Treatment with a serotonergic antidepressant is commonly used to treat pediatric anxiety disorders, including generalized anxiety disorder (GAD). Serotonergic antidepressants require considerable time to induce clinically observed responses, and tolerability and efficacy are difficult to predict. Risk and precautions have been widely discussed and are weighed against urgent needs for interventions early in life that may prevent recurrent mental health complaints. Drug-induced molecular, cellular, and chemical effects result in neurocognitive changes, which are believed to occur before behavioral changes. Assessments of early neurocognitive changes may therefore be a powerful tool to reveal key mechanisms through which antidepressants work. When the neurofunctional mechanisms believed to cause the symptoms are restored, the clinical manifestation of symptom improvement is expected. The degree of symptom improvement should also follow the degree of positive changes in neurocognitive function. Many patients do not respond early enough in the course of symptom evolution, 2,3 and thus assessments of early neurocognitive mechanisms may guide treatment individualization during titration of doses and effects., (Copyright © 2021 American Academy of Child and Adolescent Psychiatry. Published by Elsevier Inc. All rights reserved.)

Published
2021
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49. Symptom severity moderates the outcome of attention bias modification for depression: An exploratory study.

Author

Bø R, Kraft B, Jonassen R, Harmer CJ, Hilland E, Stiles TC, Haaland VØ, Aspesletten MEB, Sletvold H, and Landrø NI

Subjects
Anxiety, Depression therapy, Double-Blind Method, Humans, Treatment Outcome, Attentional Bias, Cognitive Behavioral Therapy
Abstract

A recent meta-analysis has questioned the relevance of attention bias modification (ABM) for depression outcomes. However, there might be patient characteristics not yet accounted for, that are relevant to the outcome. In the context of personalized treatment, the lack of moderator studies have limited the potential for matching ABM-treatment to individual patient characteristics. Subjects (N = 301) were randomly assigned 1:1 to receive either active or placebo Attention Bias Modification (ABM) twice daily for 14 days in a double-blind design (placebo n = 148; ABM n = 153). The outcome was change in symptoms based on the Hamilton Depression Rating Scale (HDRS). Moderator variables were self-reported depression (Beck Depression Inventory-II; BDI-II), anxiety (Beck Anxiety Inventory; BAI) and attentional bias (AB) assessed at baseline. This trial was registered with ClinicalTrials.gov, number NCT02658682. Only BAI (p for interaction = .01, Bootstrap 95% CI [0.046, 0.337]) moderated the effects of ABM on change in clinician rated depressive symptoms. Interactions were significant for BAI scores ≥8. The relative effect of the intervention increased with the highest symptom load. ABM was not effective in patients with the lowest symptom load. Future research should validate this finding and continue investigating moderators of the ABM-intervention to further enhance personalization of treatment to individual symptom characteristics., (Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Published
2021
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50. Virtual Histology of Cortical Thickness and Shared Neurobiology in 6 Psychiatric Disorders.

Author

Patel Y, Parker N, Shin J, Howard D, French L, Thomopoulos SI, Pozzi E, Abe Y, Abé C, Anticevic A, Alda M, Aleman A, Alloza C, Alonso-Lana S, Ameis SH, Anagnostou E, McIntosh AA, Arango C, Arnold PD, Asherson P, Assogna F, Auzias G, Ayesa-Arriola R, Bakker G, Banaj N, Banaschewski T, Bandeira CE, Baranov A, Bargalló N, Bau CHD, Baumeister S, Baune BT, Bellgrove MA, Benedetti F, Bertolino A, Boedhoe PSW, Boks M, Bollettini I, Del Mar Bonnin C, Borgers T, Borgwardt S, Brandeis D, Brennan BP, Bruggemann JM, Bülow R, Busatto GF, Calderoni S, Calhoun VD, Calvo R, Canales-Rodríguez EJ, Cannon DM, Carr VJ, Cascella N, Cercignani M, Chaim-Avancini TM, Christakou A, Coghill D, Conzelmann A, Crespo-Facorro B, Cubillo AI, Cullen KR, Cupertino RB, Daly E, Dannlowski U, Davey CG, Denys D, Deruelle C, Di Giorgio A, Dickie EW, Dima D, Dohm K, Ehrlich S, Ely BA, Erwin-Grabner T, Ethofer T, Fair DA, Fallgatter AJ, Faraone SV, Fatjó-Vilas M, Fedor JM, Fitzgerald KD, Ford JM, Frodl T, Fu CHY, Fullerton JM, Gabel MC, Glahn DC, Roberts G, Gogberashvili T, Goikolea JM, Gotlib IH, Goya-Maldonado R, Grabe HJ, Green MJ, Grevet EH, Groenewold NA, Grotegerd D, Gruber O, Gruner P, Guerrero-Pedraza A, Gur RE, Gur RC, Haar S, Haarman BCM, Haavik J, Hahn T, Hajek T, Harrison BJ, Harrison NA, Hartman CA, Whalley HC, Heslenfeld DJ, Hibar DP, Hilland E, Hirano Y, Ho TC, Hoekstra PJ, Hoekstra L, Hohmann S, Hong LE, Höschl C, Høvik MF, Howells FM, Nenadic I, Jalbrzikowski M, James AC, Janssen J, Jaspers-Fayer F, Xu J, Jonassen R, Karkashadze G, King JA, Kircher T, Kirschner M, Koch K, Kochunov P, Kohls G, Konrad K, Krämer B, Krug A, Kuntsi J, Kwon JS, Landén M, Landrø NI, Lazaro L, Lebedeva IS, Leehr EJ, Lera-Miguel S, Lesch KP, Lochner C, Louza MR, Luna B, Lundervold AJ, MacMaster FP, Maglanoc LA, Malpas CB, Portella MJ, Marsh R, Martyn FM, Mataix-Cols D, Mathalon DH, McCarthy H, McDonald C, McPhilemy G, Meinert S, Menchón JM, Minuzzi L, Mitchell PB, Moreno C, Morgado P, Muratori F, Murphy CM, Murphy D, Mwangi B, Nabulsi L, Nakagawa A, Nakamae T, Namazova L, Narayanaswamy J, Jahanshad N, Nguyen DD, Nicolau R, O'Gorman Tuura RL, O'Hearn K, Oosterlaan J, Opel N, Ophoff RA, Oranje B, García de la Foz VO, Overs BJ, Paloyelis Y, Pantelis C, Parellada M, Pauli P, Picó-Pérez M, Picon FA, Piras F, Piras F, Plessen KJ, Pomarol-Clotet E, Preda A, Puig O, Quidé Y, Radua J, Ramos-Quiroga JA, Rasser PE, Rauer L, Reddy J, Redlich R, Reif A, Reneman L, Repple J, Retico A, Richarte V, Richter A, Rosa PGP, Rubia KK, Hashimoto R, Sacchet MD, Salvador R, Santonja J, Sarink K, Sarró S, Satterthwaite TD, Sawa A, Schall U, Schofield PR, Schrantee A, Seitz J, Serpa MH, Setién-Suero E, Shaw P, Shook D, Silk TJ, Sim K, Simon S, Simpson HB, Singh A, Skoch A, Skokauskas N, Soares JC, Soreni N, Soriano-Mas C, Spalletta G, Spaniel F, Lawrie SM, Stern ER, Stewart SE, Takayanagi Y, Temmingh HS, Tolin DF, Tomecek D, Tordesillas-Gutiérrez D, Tosetti M, Uhlmann A, van Amelsvoort T, van der Wee NJA, van der Werff SJA, van Haren NEM, van Wingen GA, Vance A, Vázquez-Bourgon J, Vecchio D, Venkatasubramanian G, Vieta E, Vilarroya O, Vives-Gilabert Y, Voineskos AN, Völzke H, von Polier GG, Walton E, Weickert TW, Weickert CS, Weideman AS, Wittfeld K, Wolf DH, Wu MJ, Yang TT, Yang K, Yoncheva Y, Yun JY, Cheng Y, Zanetti MV, Ziegler GC, Franke B, Hoogman M, Buitelaar JK, van Rooij D, Andreassen OA, Ching CRK, Veltman DJ, Schmaal L, Stein DJ, van den Heuvel OA, Turner JA, van Erp TGM, Pausova Z, Thompson PM, and Paus T

Subjects
Adolescent, Adult, Aged, Aged, 80 and over, Attention Deficit Disorder with Hyperactivity diagnostic imaging, Autism Spectrum Disorder diagnostic imaging, Bipolar Disorder diagnostic imaging, Case-Control Studies, Cerebral Cortex cytology, Cerebral Cortex diagnostic imaging, Cerebral Cortex growth & development, Child, Child, Preschool, Cohort Studies, Computational Biology, Depressive Disorder, Major diagnostic imaging, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Obsessive-Compulsive Disorder diagnostic imaging, Principal Component Analysis, Schizophrenia diagnostic imaging, Young Adult, Attention Deficit Disorder with Hyperactivity pathology, Autism Spectrum Disorder pathology, Bipolar Disorder pathology, Cerebral Cortex pathology, Depressive Disorder, Major pathology, Fetal Development physiology, Gene Expression physiology, Human Development physiology, Obsessive-Compulsive Disorder pathology, Schizophrenia pathology
Abstract

Importance: Large-scale neuroimaging studies have revealed group differences in cortical thickness across many psychiatric disorders. The underlying neurobiology behind these differences is not well understood., Objective: To determine neurobiologic correlates of group differences in cortical thickness between cases and controls in 6 disorders: attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), bipolar disorder (BD), major depressive disorder (MDD), obsessive-compulsive disorder (OCD), and schizophrenia., Design, Setting, and Participants: Profiles of group differences in cortical thickness between cases and controls were generated using T1-weighted magnetic resonance images. Similarity between interregional profiles of cell-specific gene expression and those in the group differences in cortical thickness were investigated in each disorder. Next, principal component analysis was used to reveal a shared profile of group difference in thickness across the disorders. Analysis for gene coexpression, clustering, and enrichment for genes associated with these disorders were conducted. Data analysis was conducted between June and December 2019. The analysis included 145 cohorts across 6 psychiatric disorders drawn from the ENIGMA consortium. The numbers of cases and controls in each of the 6 disorders were as follows: ADHD: 1814 and 1602; ASD: 1748 and 1770; BD: 1547 and 3405; MDD: 2658 and 3572; OCD: 2266 and 2007; and schizophrenia: 2688 and 3244., Main Outcomes and Measures: Interregional profiles of group difference in cortical thickness between cases and controls., Results: A total of 12 721 cases and 15 600 controls, ranging from ages 2 to 89 years, were included in this study. Interregional profiles of group differences in cortical thickness for each of the 6 psychiatric disorders were associated with profiles of gene expression specific to pyramidal (CA1) cells, astrocytes (except for BD), and microglia (except for OCD); collectively, gene-expression profiles of the 3 cell types explain between 25% and 54% of variance in interregional profiles of group differences in cortical thickness. Principal component analysis revealed a shared profile of difference in cortical thickness across the 6 disorders (48% variance explained); interregional profile of this principal component 1 was associated with that of the pyramidal-cell gene expression (explaining 56% of interregional variation). Coexpression analyses of these genes revealed 2 clusters: (1) a prenatal cluster enriched with genes involved in neurodevelopmental (axon guidance) processes and (2) a postnatal cluster enriched with genes involved in synaptic activity and plasticity-related processes. These clusters were enriched with genes associated with all 6 psychiatric disorders., Conclusions and Relevance: In this study, shared neurobiologic processes were associated with differences in cortical thickness across multiple psychiatric disorders. These processes implicate a common role of prenatal development and postnatal functioning of the cerebral cortex in these disorders.

Published
2021
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