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168. Changes in serum lipids, independent of weight, are associated with changes in symptoms during long-term clozapine treatment.

Author

Procyshyn RM, Wsan KM, Thornton AE, Barr AM, Chen EYH, Pomarol-Clotet E, Stip E, Williams R, MacEwan W, Birmingham CL, Honer WG, and Clozapine and Risperidone Enhancement Study Group

Abstract

OBJECTIVE: Investigators have reported that weight gain attributed to clozapine is associated with its clinical response. However, weight gain is a nonspecific physiological variable that, in itself, does not explain the mechanism underlying this relation. Alternatively, other biological variables that are often associated with weight gain, such as serum lipids, may assist in explaining this observation. The primary objective of this study was to determine whether an increase in serum lipids is associated with improvement in schizophrenia symptoms during steady state treatment with clozapine. METHODS: The data for this study represent a subset of data from a randomized, double-blinded trial that evaluated subjects with schizophrenia who demonstrated a poor treatment response to clozapine. While continuing their clozapine therapy, subjects were randomly assigned to receive either risperidone 3 mg daily or placebo for 8 weeks. This course of treatment was followed by an optional (open-label) 18 weeks of augmentation with risperidone. In the present study, we included all subjects from the previously reported trial who had fasting lipid analyses and Positive and Negative Syndrome Scale (PANSS) scores from days 7 and 63 (n = 55). For the primary analyses, we used multiple regression to examine the association between serum lipid concentrations and PANSS scores, after controlling for weight. RESULTS: The analyses showed that the change in serum lipid concentration predicted change in symptoms over that of change in weight. Specifically, an increase in serum triglyceride concentration was associated with a decrease in the total PANSS score (p = 0.037). In addition, an increase in either serum total cholesterol concentration (p = 0.007), serum triglyceride concentration (p = 0.017) or their combined effect (p = 0.010) was associated with a decrease in PANSS negative subscale scores. CONCLUSION: Elevation of serum lipids is associated with an improvement in schizophrenia symptoms in subjects treated with clozapine. Although the mechanism is unclear, serum lipids may play a role in influencing clozapine's therapeutic activity. [ABSTRACT FROM AUTHOR]

Published
2007

169. Non redundant functional brain connectivity in schizophrenia

Author

Salvador R, Landin-Romero R, Anguera M, Erick Jorge Canales-Rodríguez, Radua J, Guerrero-Pedraza A, Sarró S, Maristany T, Pj, Mckenna, and Pomarol-Clotet E

Subjects
ALFF, GBC, fMRI, Schizophrenia, NRC, Supervised principal component regression
Abstract

Schizophrenia is considered a disorder of abnormal brain connectivity. Although whole brain maps of averaged bivariate voxel correlations have been successfully applied to study connectivity abnormalities in schizophrenia these maps do not adequately explore the multivariate nature of brain connectivity. Here we adapt a novel method for high-dimensional regression (supervised principal component regression) to estimate brain maps of multivariate non redundant connectivity (NRC) from resting functional Magnetic Resonance Imaging (fMRI) data of 116 patients with schizophrenia and 122 matched controls. Disorder related differences in NRC involved caudate hyper-connectivity and hypo-connectivity of several cortical areas such as the dorsal cingulate, the cuneus and the right postcentral cortex. These abnormalities were coupled with abnormalities in the amplitude of signal fluctuations and, to a minor extent, with differences in the dimensionality of connectivity patterns as quantified by the number of supervised principal components. Second level seed correlation analyses linked the observed abnormalities to an additional set of brain regions relevant to schizophrenia such as the thalamus and the temporal cortex. The non redundant connectivity maps proposed here are a new tool that will complement the information provided by other already available voxel based whole brain connectivity measures.

175. Longitudinal brain functional changes between mania and euthymia in bipolar disorder

Author

Alonso-Lana S, Moro N, Pj, Mckenna, Sarró S, Romaguera A, Gc, Monté, Maristany T, Jm, Goikolea, Eduard Vieta, Salvador R, and Pomarol-Clotet E

Subjects
fMRI, bipolar disorder, working memory, mental disorders, follow-up, default-mode network, behavioral disciplines and activities, psychological phenomena and processes
Abstract

OBJECTIVES: While widespread cortical and subcortical brain functional abnormalities have been found in bipolar disorder, the changes that take place between illness phases and recovery are less clearly documented. Only a small number of longitudinal studies of manic patients, in particular, have been carried out. METHODS: Twenty-six bipolar patients underwent fMRI during performance of the n-back working memory task when manic and again after recovery. Twenty-six matched healthy controls were also scanned on two occasions. Task-related activations and de-activations were examined. RESULTS: When manic, the patients showed clusters of significantly reduced activation in the left dorsolateral prefrontal cortex (DLPFC)/precentral cortex and the parietal cortex/superior precuneus bilaterally. They also showed failure of de-activation in the ventromedial frontal cortex (vmPFC). After recovery, activation in the left DLPFC/precentral cortex and in the bilateral parietal cortex/superior precuneus clusters increased significantly. However, failure of de-activation remained present in the vmPFC. CONCLUSIONS: Recovery from mania is associated with normalization of DLPFC and parietal hypoactivation, but not with vmPFC failure of de-activation, which accordingly appears to represent a trait abnormality in the disorder.

178. Subcortical Volume Trajectories across the Lifespan: Data from 18,605 healthy individuals aged 3-90 years

Author

Dima, D., Papachristou, E., Modabbernia, A., Doucet, G. E., Agartz, I., Aghajani, M., Akudjedu, T. N., Albajes-Eizagirre, A., Alnæs, D., Alpert, K. I., Andersson, M., Andreasen, N., Andreassen, O. A., Asherson, P., Banaschewski, T., Bargallo, N., Baumeister, S., Baur-Streubel, R., Bertolino, A., Bonvino, A., Boomsma, D. I., Borgwardt, S., Bourque, J., Brandeis, D., Breier, A., Brodaty, H., Brouwer, R. M., Buitelaar, J. K., Busatto, G. F., Buckner, R. L., Calhoun, V., Canales-Rodríguez, E. J., Cannon, D. M., Caseras, X., Castellanos, F. X., Cervenka, S., Chaim-Avancini, T. M., Ching, C. R. K., Clark, V. P., Conrod, P., Conzelmann, A., Crespo-Facorro, B., Crivello, F., Crone, E. A. M., Dale, A. M., Davey, C., de Geus, E. J. C., de Haan, L., de Zubicaray, G. I., den Braber, A., Dickie, E. W., Di Giorgio, A., Doan, N. T., Dørum, E. S., Ehrlich, S., Erk, S., Espeseth, T., Fatouros-Bergman, H., Fisher, S. E., Fouche, J-P., Franke, B., Frodl, T., Fuentes-Claramonte, P., Glahn, D. C., Gotlib, I. H., Grabe, H-J., Grimm, O., Groenewold, N. A., Grotegerd, D., Gruber, O., Gruner, P., Gur, R. E., Gur, R. C., Harrison, B. J., Hartman, C. A., Hatton, S. N., Heinz, A., Heslenfeld, D. J., Hibar, D. P., Hickie, I. B., Ho, B-C., Hoekstra, P. J., Hohmann, S., Holmes, A. J., Hoogman, M., Hosten, N., Howells, F. M., Hulshoff Pol, H. E., Huyser, C., Jahanshad, N., James, A., Jiang, J., Jönsson, E. G., Joska, J. A., Kahn, R., Kalnin, A., Kanai, R., Kang, S., Klein, M., Klushnik, T. P., Koenders, L., Koops, S., Krämer, B., Kuntsi, J., Lagopoulos, J., Lázaro, L., Lebedeva, I., Lee, W. H., Lesch, K-P., Lochner, C., Machielsen, M. W. J., Maingault, S., Martin, N. G., Martínez-Zalacaín, I., Mataix-Cols, D., Mazoyer, B., McDonald, C., McDonald, B. C., McIntosh, A. M., McMahon, K. L., McPhilemy, G., Menchón, J. M., Medland, S. E., Meyer-Lindenberg, A., Naaijen, J., Najt, P., Nakao, T., Nordvik, J. E., Nyberg, L., Oosterlaan, J., de la Foz, V. O-G., Paloyelis, Y., Pauli, P., Pergola, G., Pomarol-Clotet, E., Portella, M. J., Potkin, S. G., Radua, J., Reif, A., Roffman, J. L., Rosa, P. G. P., Sacchet, M. D., Sachdev, P. S., Salvador, R., Sánchez-Juan, P., Sarró, S., Satterthwaite, T. D., Saykin, A. J., Serpa, M. H., Schmaal, L., Schnell, K., Schumann, G., Smoller, J. W., Sommer, I., Soriano-Mas, C., Stein, D. J., Strike, L. T., Swagerman, S. C., Tamnes, C. K., Temmingh, H. S., Thomopoulos, S. I., Tomyshev, A. S., Tordesillas-Gutiérrez, D., Trollor, J. N., Turner, J. A., Uhlmann, A., van den Heuvel, O. A., van den Meer, D., van der Wee, N. J. A., van Haren, N. E. M., van ’t Ent, D., van Erp, T. G. M., Veer, I. M., Veltman, D. J., Völzke, H., Walter, H., Walton, E., Wang, L., Wang, Y., Wassink, T. H., Weber, B., Wen, W., West, J. D., Westlye, L. T., Whalley, H., Wierenga, L. M., Williams, S. C. R., Wittfeld, K., Wolf, D. H., Worker, A., Wright, M. J., Yang, K., Yoncheva, Y., Zanetti, M. V., Ziegler, G. C., Thompson, P. M., and Frangou, S.

Subjects
nervous system, BF
Abstract

Age has a major effect on brain volume. However, the normative studies available are constrained by small sample sizes, restricted age coverage and significant methodological variability. These limitations introduce inconsistencies and may obscure or distort the lifespan trajectories of brain morphometry. In response, we capitalised on the resources of the Enhancing Neuroimaging Genetics through Meta-Analysis (ENIGMA) Consortium to examine the age-related morphometric trajectories of the ventricles, the basal ganglia (caudate, putamen, pallidum, and nucleus accumbens), the thalamus, hippocampus and amygdala using magnetic resonance imaging data obtained from 18,605 individuals aged 3-90 years. All subcortical structure volumes were at their maximum early in life; the volume of the basal ganglia showed a gradual monotonic decline thereafter while the volumes of the thalamus, amygdala and the hippocampus remained largely stable (with some degree of decline in thalamus) until the sixth decade of life followed by a steep decline thereafter. The lateral ventricles showed a trajectory of continuous enlargement throughout the lifespan. Significant age-related increase in inter-individual variability was found for the hippocampus and amygdala and the lateral ventricles. These results were robust to potential confounders and could be used to derive risk predictions for the early identification of diverse clinical phenotypes.

179. Longitudinal Structural Brain Changes in Bipolar Disorder: A Multicenter Neuroimaging Study of 1232 Individuals by the ENIGMA Bipolar Disorder Working Group

Author

Abe, C., Ching, C.R.K., Liberg, B., Lebedev, A.V., Agartz, I., Akudjedu, Theophilus. N., Alda, M., Alnæs, D., Alonso-Lana, S., Benedetti, F., Berk, M., Bøen, E., Bonnin, C.D.M., Breuer, F., Brosch, K., Brouwer, R.M., Canales-Rodríguez, E.J., Cannon, D.M., Chye, Y., Dahl, A., Dandash, O., Dannlowski, U., Dohm, K., Elvsåshagen, T., Fisch, L., Fullerton, J.M., Goikolea, J.M., Grotegerd, D., Haatveit, B., Hahn, T., Hajek, T., Heindel, W., Ingvar, M., Sim, K., Kircher, T.T.J., Lenroot, R.K., Malt, U.F., McDonald, C., McWhinney, S.R., Melle, I., Meller, T., Melloni, E.M.T., Mitchell, P.B., Nabulsi, L., Nenadić, I., Opel, N., Overs, B.J., Panicalli, F., Pfarr, J.K., Poletti, S., Pomarol-Clotet, E., Radua, J., Repple, J., Ringwald, K.G., Roberts, G., Rodriguez-Cano, E., Salvador, R., Sarink, K., Sarró, S., Schmitt, S., Stein, F., Suo, C., Thomopoulos, S.I., Tronchin, G., Vieta, E., Westlye, L.T., White, A.G., Yatham, L.N., Zak, N., Thompson, P.M., Andreassen, O.A., Landen, M., Abe, C., Ching, C.R.K., Liberg, B., Lebedev, A.V., Agartz, I., Akudjedu, Theophilus. N., Alda, M., Alnæs, D., Alonso-Lana, S., Benedetti, F., Berk, M., Bøen, E., Bonnin, C.D.M., Breuer, F., Brosch, K., Brouwer, R.M., Canales-Rodríguez, E.J., Cannon, D.M., Chye, Y., Dahl, A., Dandash, O., Dannlowski, U., Dohm, K., Elvsåshagen, T., Fisch, L., Fullerton, J.M., Goikolea, J.M., Grotegerd, D., Haatveit, B., Hahn, T., Hajek, T., Heindel, W., Ingvar, M., Sim, K., Kircher, T.T.J., Lenroot, R.K., Malt, U.F., McDonald, C., McWhinney, S.R., Melle, I., Meller, T., Melloni, E.M.T., Mitchell, P.B., Nabulsi, L., Nenadić, I., Opel, N., Overs, B.J., Panicalli, F., Pfarr, J.K., Poletti, S., Pomarol-Clotet, E., Radua, J., Repple, J., Ringwald, K.G., Roberts, G., Rodriguez-Cano, E., Salvador, R., Sarink, K., Sarró, S., Schmitt, S., Stein, F., Suo, C., Thomopoulos, S.I., Tronchin, G., Vieta, E., Westlye, L.T., White, A.G., Yatham, L.N., Zak, N., Thompson, P.M., Andreassen, O.A., and Landen, M.

Abstract

Background: Bipolar disorder (BD) is associated with cortical and subcortical structural brain abnormalities. It is unclear whether such alterations progressively change over time, and how this is related to the number of mood episodes. To address this question, we analyzed a large and diverse international sample with longitudinal magnetic resonance imaging (MRI) and clinical data to examine structural brain changes over time in BD. Methods: Longitudinal structural MRI and clinical data from the ENIGMA (Enhancing Neuro Imaging Genetics through Meta Analysis) BD Working Group, including 307 patients with BD and 925 healthy control subjects, were collected from 14 sites worldwide. Male and female participants, aged 40 ± 17 years, underwent MRI at 2 time points. Cortical thickness, surface area, and subcortical volumes were estimated using FreeSurfer. Annualized change rates for each imaging phenotype were compared between patients with BD and healthy control subjects. Within patients, we related brain change rates to the number of mood episodes between time points and tested for effects of demographic and clinical variables. Results: Compared with healthy control subjects, patients with BD showed faster enlargement of ventricular volumes and slower thinning of the fusiform and parahippocampal cortex (0.18 < d < 0.22). More (hypo)manic episodes were associated with faster cortical thinning, primarily in the prefrontal cortex. Conclusions: In the hitherto largest longitudinal MRI study on BD, we did not detect accelerated cortical thinning but noted faster ventricular enlargements in BD. However, abnormal frontocortical thinning was observed in association with frequent manic episodes. Our study yields insights into disease progression in BD and highlights the importance of mania prevention in BD treatment.

180. Greater male than female variability in regional brain structure across the lifespan

Author

Wierenga, L.M., Doucet, G.E., Dima, D., Agartz, I., Aghajani, M., Akudjedu, T.N., Albajes-Eizagirr, A., Alnæs, D., Alpert, K.I., Andreassen, O.A., Anticevic, A., Asherson, P., Banaschewski, T., Bargallo, N., Baumeister, S., Baur-Streubel, R., Bertolino, A., Bonvino, A., Boomsma, D.I., Borgwardt, S., Bourque, J., den Braber, A., Brandeis, D., Breier, A., Brodaty, H., Brouwer, R.M., Buitelaar, J.K., Busatt, G.F., Calhoun, V.D., Canales-Rodríguez, E.J., Cannon, D.M., Caseras, X., Castellanos, F.X., Chaim-Avancin, T.M., Ching, C.R.K., Clark, V.P., Conrod, P.J., Conzelmann, A., Crivello, F., Davey, C.G., Dickie, E.W., Ehrlich, S., van't Ent, D., Fisher, S.E., Fouche, J.P., Franke, B., Fuentes-Claramonte, P., de Geus, E.J.C, Di Giorgio, A., Glahn, D.C., Gotlib, I.H., Grabe, H.J., Gruber, O., Gruner, P., Gur, R.E., Gur, R.C., Gurholt, T.P., de Haan, L., Haatveit, B., Harrison, B.J., Hartman, C.A., Hatton, S.N., Heslenfeld, D.J., van den Heuvel, O.A., Hickie, I.B., Hoekstra, P.J., Hohmann, S., Holmes, A.J., Hoogman, M., Hosten, N., Howells, F.M., Hulshoff Pol, H.E., Huyser, C., Jahanshad, N., James, A.C., Jiang, J., Jönsson, E.G., Joska, J.A., Kalnin, A.J., Consortium, Karolinska Schizophrenia Project (KaSP), Klein, M., Koenders, L., Kolskår, K.K., Krämer, B., Kuntsi, J., Lagopoulos, J., Lazaro, L., Lebedeva, I.S., Lee, P.H., Lochner, C., Machielsen, M.W.J., Maingault, S., Martin, N.G., Martínez-Zalacaín, I., Mataix-Cols, D., Mazoyer, B., McDonald, B.C., McDonald, C., McIntosh, A.M., McMahon, K.L., McPhilemy, G., van der Meer, D., Menchón, J.M., Naaijen, J., Nyberg, L., Oosterlaan, J., Paloyelis, Y., Pauli, P., Pergola, G., Pomarol-Clotet, E., Portella, M.J., Radua, J., Reif, A., Richards, G., Roffman, J.L., Rosa, P.G.P., Sacchet, M.D., Sachdev, P.S., Salvador, R., Sarró, S., Satterthwaite, T.D., Saykin, A.J., Serpa, M.H., Sim, K., Simmons, A., Smoller, J.W., Sommer, I.E., Soriano-Mas, C., Stein, D.J., Strike, L.T., Szeszko, P.R., Temmingh, H.S., Thomopoulos, S., Tomyshev, A.S., Trollor, J.N., Uhlmann, A., Veer, I.M., Veltman, D.J., Voineskos, A., Völzke, H., Walter, H., Wang, L., Wang, Y., Weber, B., Wen, W., West, J.D., Westlye, L.T., Whalley, H.C., Williams, S.C.R., Wittfeld, K., Wolf, D.H., Wright, M.J., Yoncheva, Y.N., Zanetti, M.V., Ziegler, G.C., de Zubicaray, G.I., Thompson, P.M., Crone, E.A., Frangou, S., Tamnes, C.K., Wierenga, L.M., Doucet, G.E., Dima, D., Agartz, I., Aghajani, M., Akudjedu, T.N., Albajes-Eizagirr, A., Alnæs, D., Alpert, K.I., Andreassen, O.A., Anticevic, A., Asherson, P., Banaschewski, T., Bargallo, N., Baumeister, S., Baur-Streubel, R., Bertolino, A., Bonvino, A., Boomsma, D.I., Borgwardt, S., Bourque, J., den Braber, A., Brandeis, D., Breier, A., Brodaty, H., Brouwer, R.M., Buitelaar, J.K., Busatt, G.F., Calhoun, V.D., Canales-Rodríguez, E.J., Cannon, D.M., Caseras, X., Castellanos, F.X., Chaim-Avancin, T.M., Ching, C.R.K., Clark, V.P., Conrod, P.J., Conzelmann, A., Crivello, F., Davey, C.G., Dickie, E.W., Ehrlich, S., van't Ent, D., Fisher, S.E., Fouche, J.P., Franke, B., Fuentes-Claramonte, P., de Geus, E.J.C, Di Giorgio, A., Glahn, D.C., Gotlib, I.H., Grabe, H.J., Gruber, O., Gruner, P., Gur, R.E., Gur, R.C., Gurholt, T.P., de Haan, L., Haatveit, B., Harrison, B.J., Hartman, C.A., Hatton, S.N., Heslenfeld, D.J., van den Heuvel, O.A., Hickie, I.B., Hoekstra, P.J., Hohmann, S., Holmes, A.J., Hoogman, M., Hosten, N., Howells, F.M., Hulshoff Pol, H.E., Huyser, C., Jahanshad, N., James, A.C., Jiang, J., Jönsson, E.G., Joska, J.A., Kalnin, A.J., Consortium, Karolinska Schizophrenia Project (KaSP), Klein, M., Koenders, L., Kolskår, K.K., Krämer, B., Kuntsi, J., Lagopoulos, J., Lazaro, L., Lebedeva, I.S., Lee, P.H., Lochner, C., Machielsen, M.W.J., Maingault, S., Martin, N.G., Martínez-Zalacaín, I., Mataix-Cols, D., Mazoyer, B., McDonald, B.C., McDonald, C., McIntosh, A.M., McMahon, K.L., McPhilemy, G., van der Meer, D., Menchón, J.M., Naaijen, J., Nyberg, L., Oosterlaan, J., Paloyelis, Y., Pauli, P., Pergola, G., Pomarol-Clotet, E., Portella, M.J., Radua, J., Reif, A., Richards, G., Roffman, J.L., Rosa, P.G.P., Sacchet, M.D., Sachdev, P.S., Salvador, R., Sarró, S., Satterthwaite, T.D., Saykin, A.J., Serpa, M.H., Sim, K., Simmons, A., Smoller, J.W., Sommer, I.E., Soriano-Mas, C., Stein, D.J., Strike, L.T., Szeszko, P.R., Temmingh, H.S., Thomopoulos, S., Tomyshev, A.S., Trollor, J.N., Uhlmann, A., Veer, I.M., Veltman, D.J., Voineskos, A., Völzke, H., Walter, H., Wang, L., Wang, Y., Weber, B., Wen, W., West, J.D., Westlye, L.T., Whalley, H.C., Williams, S.C.R., Wittfeld, K., Wolf, D.H., Wright, M.J., Yoncheva, Y.N., Zanetti, M.V., Ziegler, G.C., de Zubicaray, G.I., Thompson, P.M., Crone, E.A., Frangou, S., and Tamnes, C.K.

Abstract

For many traits, males show greater variability than females, with possible implications for understanding sex differences in health and disease. Here, the ENIGMA (Enhancing Neuro Imaging Genetics through Meta‐Analysis) Consortium presents the largest‐ever mega‐analysis of sex differences in variability of brain structure, based on international data spanning nine decades of life. Subcortical volumes, cortical surface area and cortical thickness were assessed in MRI data of 16,683 healthy individuals 1‐90 years old (47% females). We observed significant patterns of greater male than female between‐subject variance for all subcortical volumetric measures, all cortical surface area measures, and 60% of cortical thickness measures. This pattern was stable across the lifespan for 50% of the subcortical structures, 70% of the regional area measures, and nearly all regions for thickness. Our findings that these sex differences are present in childhood implicate early life genetic or gene‐environment interaction mechanisms. The findings highlight the importance of individual differences within the sexes, that may underpin sex‐specific vulnerability to disorders.

181. Subcortical volumes across the lifespan: Data from 18,605 healthy individuals aged 3–90 years

Author

Dima, D., Modabbernia, A., Papachristou4, E., Doucet, G. E., Agartz, I., Aghajani, M., Akudjedu, Theophilus. N., Albajes-Eizagirre, A., Alnaes, D, Alpert, K. I., Andersson, M., Andreasen, N. C., Andreassen, O. A., Asherson, P., Banaschewski, T., Bargallo, N., Baumeister, S., Baur-Streubel, R., Bertolino, A., Bonvino, A., Boomsma, D. I., Borgwardt, S., Bourque, J., Brandeis, D., Breier, A., Brodaty, H., Brouwer, R. M., Buitelaar, J. K., Busatto, G. F., Buckner, R. L., Calhoun, V., Canales-Rodríguez, E. J., Cannon, D. M., Caseras, X., Castellanos, F. X., Cervenka, S, Chaim-Avancini, T. M., Ching, C. R. K., Chubar, V., Clark, V. P., Conrod, P., Conzelmann, A., Crespo-Facorro, B, Crivello, F., Crone, E. A., Dale, A. M., Davey, C., de Geus, E. J. C, de Haan, L., de Zubicaray, G. I., den Braber, A., Dickie, E. W., Di Giorgio, A., Doan, N. T., Dørum, E. S., Ehrlich, S., Erk, S., Espeseth, T., Fatouros- Bergman, H., Fisher, S. E., Fouche, J. P., Franke, B., Frodl, T., Fuentes-Claramonte, P., Glahn, D. C., Gotlib, I. H., Grabe, H. J., Grimm, O., Groenewold, N. A., Grotegerd, D., Gruber, O., Gruner, P., Gur, R. E., Gur, R. C., Harrison, B. J., Hartman, C. A., Hatton, S. N., Heinz, A., Heslenfeld, D. J., Hibar, D. P., Hickie, I. B., Ho, B. C., Hoekstra, P. J., Hohmann, S., Holmes, A. J., Hoogman, M., Hosten, N., Howells, F. M., Hulshoff Pol, H. E., Huyser, C., Jahanshad, N., James, A., Jernigan, T. L., Jiang, J., Jönsson, E. G., Joska, J. A., Kahn, R., Kalnin, A., Kanai, R., Klein, M., Klyushnik, T. P., Koenders, L., Koops, S., Krämer, B., Kuntsi, J., Lagopoulos, J., Lázaro, L., Lebedeva, I., Lee, W. H., Lesch, K. P., Lochner, C., Machielsen, M. W. J., Maingault, S., Martin, N. G., Martínez-Zalacaín, I., Mataix-Cols, D., Mazoyer, B., McDonald, C., McDonald, B. C., McIntosh, A. M., McMahon, K. L., McPhilemy, G., Menchón, J. M., Medland, S. E., Meyer-Lindenberg, A., Naaijen, J., Najt, P., Nakao, T., Nordvik, J. E., Nyberg, L., Oosterlaan, J., Ortiz-García de la Foz, V., Paloyelis, Y., Pauli, P., Pergola, G., Pomarol-Clotet, E., Portella, M. J., Potkin, S. G., Radua, J., Reif, A., Rinker, D. A., Roffman, J. L., Rosa, P. G. P., Sacchet, M. D., Sachdev, P. S., Salvador, R., Sánchez-Juan, P., Sarró, S., Satterthwaite, T. D., Saykin, A. J., Serpa, M. H., Schmaal, L., Schnell, K., Schumann, G., Sim, K., Smoller, J. W., Sommer, I., Soriano-Mas, C., Stein, D. J., Strike, L. T., Swagerman, S. C., Tamnes, C. K., Temmingh, H. S., Thomopoulos, S. I., Tomyshev, A. S., Tordesillas-Gutiérrez, D., Trollor, J. N., Turner, J. A., Uhimann, A., van den Heuvel, O. A., van den Meer, D., van der Wee, N. J. A., van Haren, N. E. M., van't Ent, D., van Erp, T. G. M., Veer, I. M., Veltman, D. J., Voineskos, A., Völzke, H., Walter, H., Walton, E., Wang, L., Wang, Y., Wassink, T. H., Weber, B., Wen, W., West, J. D., Westlye, L. T., Whalley, H., Wierenga, L. M., Williams, S. C. R., Wittfeld, K., Wolf, D. H., Worker, A., Wright, M. J., Yang, K., Yoncheva, Y., Zanetti, M. V., Ziegler, G. C., Thompson, P. M., Frangou, S., Karolinska Schizophrenia Project (KaSP), Dima, D., Modabbernia, A., Papachristou4, E., Doucet, G. E., Agartz, I., Aghajani, M., Akudjedu, Theophilus. N., Albajes-Eizagirre, A., Alnaes, D, Alpert, K. I., Andersson, M., Andreasen, N. C., Andreassen, O. A., Asherson, P., Banaschewski, T., Bargallo, N., Baumeister, S., Baur-Streubel, R., Bertolino, A., Bonvino, A., Boomsma, D. I., Borgwardt, S., Bourque, J., Brandeis, D., Breier, A., Brodaty, H., Brouwer, R. M., Buitelaar, J. K., Busatto, G. F., Buckner, R. L., Calhoun, V., Canales-Rodríguez, E. J., Cannon, D. M., Caseras, X., Castellanos, F. X., Cervenka, S, Chaim-Avancini, T. M., Ching, C. R. K., Chubar, V., Clark, V. P., Conrod, P., Conzelmann, A., Crespo-Facorro, B, Crivello, F., Crone, E. A., Dale, A. M., Davey, C., de Geus, E. J. C, de Haan, L., de Zubicaray, G. I., den Braber, A., Dickie, E. W., Di Giorgio, A., Doan, N. T., Dørum, E. S., Ehrlich, S., Erk, S., Espeseth, T., Fatouros- Bergman, H., Fisher, S. E., Fouche, J. P., Franke, B., Frodl, T., Fuentes-Claramonte, P., Glahn, D. C., Gotlib, I. H., Grabe, H. J., Grimm, O., Groenewold, N. A., Grotegerd, D., Gruber, O., Gruner, P., Gur, R. E., Gur, R. C., Harrison, B. J., Hartman, C. A., Hatton, S. N., Heinz, A., Heslenfeld, D. J., Hibar, D. P., Hickie, I. B., Ho, B. C., Hoekstra, P. J., Hohmann, S., Holmes, A. J., Hoogman, M., Hosten, N., Howells, F. M., Hulshoff Pol, H. E., Huyser, C., Jahanshad, N., James, A., Jernigan, T. L., Jiang, J., Jönsson, E. G., Joska, J. A., Kahn, R., Kalnin, A., Kanai, R., Klein, M., Klyushnik, T. P., Koenders, L., Koops, S., Krämer, B., Kuntsi, J., Lagopoulos, J., Lázaro, L., Lebedeva, I., Lee, W. H., Lesch, K. P., Lochner, C., Machielsen, M. W. J., Maingault, S., Martin, N. G., Martínez-Zalacaín, I., Mataix-Cols, D., Mazoyer, B., McDonald, C., McDonald, B. C., McIntosh, A. M., McMahon, K. L., McPhilemy, G., Menchón, J. M., Medland, S. E., Meyer-Lindenberg, A., Naaijen, J., Najt, P., Nakao, T., Nordvik, J. E., Nyberg, L., Oosterlaan, J., Ortiz-García de la Foz, V., Paloyelis, Y., Pauli, P., Pergola, G., Pomarol-Clotet, E., Portella, M. J., Potkin, S. G., Radua, J., Reif, A., Rinker, D. A., Roffman, J. L., Rosa, P. G. P., Sacchet, M. D., Sachdev, P. S., Salvador, R., Sánchez-Juan, P., Sarró, S., Satterthwaite, T. D., Saykin, A. J., Serpa, M. H., Schmaal, L., Schnell, K., Schumann, G., Sim, K., Smoller, J. W., Sommer, I., Soriano-Mas, C., Stein, D. J., Strike, L. T., Swagerman, S. C., Tamnes, C. K., Temmingh, H. S., Thomopoulos, S. I., Tomyshev, A. S., Tordesillas-Gutiérrez, D., Trollor, J. N., Turner, J. A., Uhimann, A., van den Heuvel, O. A., van den Meer, D., van der Wee, N. J. A., van Haren, N. E. M., van't Ent, D., van Erp, T. G. M., Veer, I. M., Veltman, D. J., Voineskos, A., Völzke, H., Walter, H., Walton, E., Wang, L., Wang, Y., Wassink, T. H., Weber, B., Wen, W., West, J. D., Westlye, L. T., Whalley, H., Wierenga, L. M., Williams, S. C. R., Wittfeld, K., Wolf, D. H., Worker, A., Wright, M. J., Yang, K., Yoncheva, Y., Zanetti, M. V., Ziegler, G. C., Thompson, P. M., Frangou, S., and Karolinska Schizophrenia Project (KaSP)

Abstract

Age has a major effect on brain volume. However, the normative studies available are constrained by small sample sizes, restricted age coverage and significant methodological variability. These limitations introduce inconsistencies and may obscure or distort the lifespan trajectories of brain morphometry. In response, we capitalized on the resources of the Enhancing Neuroimaging Genetics through Meta‐Analysis (ENIGMA) Consortium to examine age‐related trajectories inferred from cross‐sectional measures of the ventricles, the basal ganglia (caudate, putamen, pallidum, and nucleus accumbens), the thalamus, hippocampus and amygdala using magnetic resonance imaging data obtained from 18,605 individuals aged 3–90 years. All subcortical structure volumes were at their maximum value early in life. The volume of the basal ganglia showed a monotonic negative association with age thereafter; there was no significant association between age and the volumes of the thalamus, amygdala and the hippocampus (with some degree of decline in thalamus) until the sixth decade of life after which they also showed a steep negative association with age. The lateral ventricles showed continuous enlargement throughout the lifespan. Age was positively associated with inter‐individual variability in the hippocampus and amygdala and the lateral ventricles. These results were robust to potential confounders and could be used to examine the functional significance of deviations from typical age‐related morphometric patterns.

182. Cortical Thickness across the Lifespan: Data from 17,075 healthy individuals aged 3-90 years

Author

Frangou, S., Modabbernia, A., Williams, S.C.R., Papachristou, E., Doucet, G. E., Agartz, I., Aghajani, M., Akudjedu, T.N., Albajes-Eizagirre, A., Alnæs, D., Alpert, K. I., Andersson, M., Andreasen, N. C., Andreassen, O.A., Asherson, P., Banaschewski, T., Bargallo, N., Baumeister, S., Baur-Streubel, R., Bertolino, A., Bonvino, A., Boomsma, D.I., Borgwardt, S., Bourque, J., Brandeis, D., Breier, A., Brodaty, H., Brouwer, R. M., Buitelaar, J. K., Busatto, G. F., Buckner, R. L., Calhoun, V., Canales-Rodríguez, E. J., Cannon, D.M., Caseras, X., Castellanos, F. X., Cervenka, S, Chaim-Avancini, T. M., Ching, C. R. K., Chubar, V., Clark, V.P., Conrod, P., Conzelmann, A., Crespo-Facorro, B, Crivello, F., Crone, E. A., Dale, A. M., Davey, C., de Geus, E. J. C, de Haan, L., de Zubicaray, G. I., den Braber, A., Dickie, E. W., Di Giorgio, A., Doan, N.T., Dørum, E. S., Ehrlich, S., Erk, S., Espeseth, T., Fatouros-Bergman, H., Fisher, S. E., Fouche, J. P., Franke, B., Frodl, T., Fuentes-Claramonte, P., Glahn, D. C., Gotlib, I. H., Grabe, H.J., Grimm, O., Groenewold, N. A., Grotegerd, D., Gruber, O., Gruner, P., Gur, R. E., Gur, R. C., Harrison, B. J., Hartman, C. A., Hatton, S. N., Heinz, A., Heslenfeld, D. J., Hibar, D. P., Hickie, I.B., Ho, B.C., Hoekstra, P. J., Hohmann, S., Holmes, A. J., Hoogman, M., Hosten, N., Howells, F. M., Hulshoff Pol, H. E., Huyser, C., Jahanshad, N., James, A., Jernigan, T. L., Jiang, J., Jönsson, E. G., Joska, J. A., Kahn, R., Kalnin, A., Kanai, R., Klein, M., Klyushnik, T. P., Koenders, L., Koops, S., Krämer, B., Kuntsi, J., Lagopoulos, J., Lazaro, L., Lebedeva, I., Lee, W. H., Lesch, K. P., Lochner, C., Machielsen, M. W. J., Maingault, S., Martin, N.G., Martínez-Zalacaín, I., Mataix-Cols, D., Mazoyer, B., McDonald, C., McDonald, B. C., McIntosh, A.M., McMahon, K. L., McPhilemy, G., Menchón, J.M., Medland, S. E., Meyer-Lindenberg, A., Naaijen, J., Najt, P., Nakao, T., Nordvik, J. E., Nyberg, L., Oosterlaan, J., Ortiz-García de la Foz, V., Paloyelis, Y., Pauli, P., Pergola, G., Pomarol-Clotet, E., Portella, M. J., Potkin, S. G., Radua, J., Reif, A., Rinker, D. A., Roffman, J. L., Rosa, P. G. P., Sacchet, M. D., Sachdev, P. S., Salvador, R., Sánchez-Juan, P., Sarró, S., Satterthwaite, T. D., Saykin, A. J., Serpa, M. H., Schmaal, L., Schnell, K., Schumann, G., Sim, K., Smoller, J.W., Sommer, I., Soriano-Mas, C., Stein, D.J., Strike, L.T., Swagerman, S. C., Tamnes, C. K., Temmingh, H. S., Thomopoulos, S.I., Tomyshev, A. S., Tordesillas-Gutiérrez, D., Trollor, J.N., Turner, J.A., Uhlmann, A., van den Heuvel, O. A., van den Meer, D., van der Wee, N. J. A., van Haren, N. E. M., van 't Ent, D., van Erp, T. G. M., Veer, I. M., Veltman, D. J., Voineskos, A., Völzke, H., Walter, H., Walton, E., Wang, L., Wang, Y., Wassink, T. H., Weber, B., Wen, W., West, J.D., Westlye, L. T., Whalley, H., Wierenga, L. M., Wittfeld, K., Wolf, D. H., Worker, A., Wright, M. J., Yang, K., Yoncheva, Y., Zanetti, M. V., Ziegler, G. C., Karolinska Schizophrenia Project, K.a.S.P., Thompson, P.M., Dima, D., Frangou, S., Modabbernia, A., Williams, S.C.R., Papachristou, E., Doucet, G. E., Agartz, I., Aghajani, M., Akudjedu, T.N., Albajes-Eizagirre, A., Alnæs, D., Alpert, K. I., Andersson, M., Andreasen, N. C., Andreassen, O.A., Asherson, P., Banaschewski, T., Bargallo, N., Baumeister, S., Baur-Streubel, R., Bertolino, A., Bonvino, A., Boomsma, D.I., Borgwardt, S., Bourque, J., Brandeis, D., Breier, A., Brodaty, H., Brouwer, R. M., Buitelaar, J. K., Busatto, G. F., Buckner, R. L., Calhoun, V., Canales-Rodríguez, E. J., Cannon, D.M., Caseras, X., Castellanos, F. X., Cervenka, S, Chaim-Avancini, T. M., Ching, C. R. K., Chubar, V., Clark, V.P., Conrod, P., Conzelmann, A., Crespo-Facorro, B, Crivello, F., Crone, E. A., Dale, A. M., Davey, C., de Geus, E. J. C, de Haan, L., de Zubicaray, G. I., den Braber, A., Dickie, E. W., Di Giorgio, A., Doan, N.T., Dørum, E. S., Ehrlich, S., Erk, S., Espeseth, T., Fatouros-Bergman, H., Fisher, S. E., Fouche, J. P., Franke, B., Frodl, T., Fuentes-Claramonte, P., Glahn, D. C., Gotlib, I. H., Grabe, H.J., Grimm, O., Groenewold, N. A., Grotegerd, D., Gruber, O., Gruner, P., Gur, R. E., Gur, R. C., Harrison, B. J., Hartman, C. A., Hatton, S. N., Heinz, A., Heslenfeld, D. J., Hibar, D. P., Hickie, I.B., Ho, B.C., Hoekstra, P. J., Hohmann, S., Holmes, A. J., Hoogman, M., Hosten, N., Howells, F. M., Hulshoff Pol, H. E., Huyser, C., Jahanshad, N., James, A., Jernigan, T. L., Jiang, J., Jönsson, E. G., Joska, J. A., Kahn, R., Kalnin, A., Kanai, R., Klein, M., Klyushnik, T. P., Koenders, L., Koops, S., Krämer, B., Kuntsi, J., Lagopoulos, J., Lazaro, L., Lebedeva, I., Lee, W. H., Lesch, K. P., Lochner, C., Machielsen, M. W. J., Maingault, S., Martin, N.G., Martínez-Zalacaín, I., Mataix-Cols, D., Mazoyer, B., McDonald, C., McDonald, B. C., McIntosh, A.M., McMahon, K. L., McPhilemy, G., Menchón, J.M., Medland, S. E., Meyer-Lindenberg, A., Naaijen, J., Najt, P., Nakao, T., Nordvik, J. E., Nyberg, L., Oosterlaan, J., Ortiz-García de la Foz, V., Paloyelis, Y., Pauli, P., Pergola, G., Pomarol-Clotet, E., Portella, M. J., Potkin, S. G., Radua, J., Reif, A., Rinker, D. A., Roffman, J. L., Rosa, P. G. P., Sacchet, M. D., Sachdev, P. S., Salvador, R., Sánchez-Juan, P., Sarró, S., Satterthwaite, T. D., Saykin, A. J., Serpa, M. H., Schmaal, L., Schnell, K., Schumann, G., Sim, K., Smoller, J.W., Sommer, I., Soriano-Mas, C., Stein, D.J., Strike, L.T., Swagerman, S. C., Tamnes, C. K., Temmingh, H. S., Thomopoulos, S.I., Tomyshev, A. S., Tordesillas-Gutiérrez, D., Trollor, J.N., Turner, J.A., Uhlmann, A., van den Heuvel, O. A., van den Meer, D., van der Wee, N. J. A., van Haren, N. E. M., van 't Ent, D., van Erp, T. G. M., Veer, I. M., Veltman, D. J., Voineskos, A., Völzke, H., Walter, H., Walton, E., Wang, L., Wang, Y., Wassink, T. H., Weber, B., Wen, W., West, J.D., Westlye, L. T., Whalley, H., Wierenga, L. M., Wittfeld, K., Wolf, D. H., Worker, A., Wright, M. J., Yang, K., Yoncheva, Y., Zanetti, M. V., Ziegler, G. C., Karolinska Schizophrenia Project, K.a.S.P., Thompson, P.M., and Dima, D.

Abstract

Delineating the association of age and cortical thickness in healthy individuals is critical given the association of cortical thickness with cognition and behavior. Previous research has shown that robust estimates of the association between age and brain morphometry require large‐scale studies. In response, we used cross‐sectional data from 17,075 individuals aged 3–90 years from the Enhancing Neuroimaging Genetics through Meta‐Analysis (ENIGMA) Consortium to infer age‐related changes in cortical thickness. We used fractional polynomial (FP) regression to quantify the association between age and cortical thickness, and we computed normalized growth centiles using the parametric Lambda, Mu, and Sigma method. Interindividual variability was estimated using meta‐analysis and one‐way analysis of variance. For most regions, their highest cortical thickness value was observed in childhood. Age and cortical thickness showed a negative association; the slope was steeper up to the third decade of life and more gradual thereafter; notable exceptions to this general pattern were entorhinal, temporopolar, and anterior cingulate cortices. Interindividual variability was largest in temporal and frontal regions across the lifespan. Age and its FP combinations explained up to 59% variance in cortical thickness. These results may form the basis of further investigation on normative deviation in cortical thickness and its significance for behavioral and cognitive outcomes.

183. Using structural MRI to identify bipolar disorders - 13 site machine learning study in 3020 individuals from the ENIGMA Bipolar Disorders Working Group.

Author

Nunes, A., Schnack, H.G., Ching, C.R.K., Agartz, I., Akudjedu, T.N., Alda, M., Alnæs, D., Alonso-Lana, S., Bauer, J., Baune, B.T., Bøen, E., Bonnin, C.D.M., Busatto, G.F., Canales-Rodríguez, E.J., Cannon, D.M., Caseras, X., Chaim-Avancini, T.M., Dannlowski, U., Díaz-Zuluaga, A.M., Dietsche, B., Doan, N.T., Duchesnay, E., Elvsåshagen, T., Emden, D., Eyler, L.T., Fatjó-Vilas, M., Favre, P., Foley, S.F., Fullerton, J.M., Glahn, D.C., Goikolea, J.M., Grotegerd, D., Hahn, T., Henry, C., Hibar, D.P., Houenou, J., Howells, F.M., Jahanshad, N., Kaufmann, T., Kenney, J., Kircher, T.T.J., Krug, A., Lagerberg, T.V., Lenroot, R.K., López-Jaramillo, C., Machado-Vieira, R., Malt, U.F., McDonald, C., Mitchell, P.B., Mwangi, B., Nabulsi, L., Opel, N., Overs, B.J., Pineda-Zapata, J.A., Pomarol-Clotet, E., Redlich, R., Roberts, G., Rosa, P.G., Salvador, R., Satterthwaite, T.D., Soares, J.C., Stein, D.J., Temmingh, H.S., Trappenberg, T., Uhlmann, A., van Haren, N.E.M., Vieta, E., Westlye, L.T., Wolf, D.H., Yüksel, D., Zanetti, M.V., Andreassen, O.A., Thompson, P.M., Hajek, T., ENIGMA Bipolar Disorders Working Group, Nunes, A., Schnack, H.G., Ching, C.R.K., Agartz, I., Akudjedu, T.N., Alda, M., Alnæs, D., Alonso-Lana, S., Bauer, J., Baune, B.T., Bøen, E., Bonnin, C.D.M., Busatto, G.F., Canales-Rodríguez, E.J., Cannon, D.M., Caseras, X., Chaim-Avancini, T.M., Dannlowski, U., Díaz-Zuluaga, A.M., Dietsche, B., Doan, N.T., Duchesnay, E., Elvsåshagen, T., Emden, D., Eyler, L.T., Fatjó-Vilas, M., Favre, P., Foley, S.F., Fullerton, J.M., Glahn, D.C., Goikolea, J.M., Grotegerd, D., Hahn, T., Henry, C., Hibar, D.P., Houenou, J., Howells, F.M., Jahanshad, N., Kaufmann, T., Kenney, J., Kircher, T.T.J., Krug, A., Lagerberg, T.V., Lenroot, R.K., López-Jaramillo, C., Machado-Vieira, R., Malt, U.F., McDonald, C., Mitchell, P.B., Mwangi, B., Nabulsi, L., Opel, N., Overs, B.J., Pineda-Zapata, J.A., Pomarol-Clotet, E., Redlich, R., Roberts, G., Rosa, P.G., Salvador, R., Satterthwaite, T.D., Soares, J.C., Stein, D.J., Temmingh, H.S., Trappenberg, T., Uhlmann, A., van Haren, N.E.M., Vieta, E., Westlye, L.T., Wolf, D.H., Yüksel, D., Zanetti, M.V., Andreassen, O.A., Thompson, P.M., Hajek, T., and ENIGMA Bipolar Disorders Working Group

Abstract

Bipolar disorders (BDs) are among the leading causes of morbidity and disability. Objective biological markers, such as those based on brain imaging, could aid in clinical management of BD. Machine learning (ML) brings neuroimaging analyses to individual subject level and may potentially allow for their diagnostic use. However, fair and optimal application of ML requires large, multi-site datasets. We applied ML (support vector machines) to MRI data (regional cortical thickness, surface area, subcortical volumes) from 853 BD and 2167 control participants from 13 cohorts in the ENIGMA consortium. We attempted to differentiate BD from control participants, investigated different data handling strategies and studied the neuroimaging/clinical features most important for classification. Individual site accuracies ranged from 45.23% to 81.07%. Aggregate subject-level analyses yielded the highest accuracy (65.23%, 95% CI = 63.47-67.00, ROC-AUC = 71.49%, 95% CI = 69.39-73.59), followed by leave-one-site-out cross-validation (accuracy = 58.67%, 95% CI = 56.70-60.63). Meta-analysis of individual site accuracies did not provide above chance results. There was substantial agreement between the regions that contributed to identification of BD participants in the best performing site and in the aggregate dataset (Cohen's Kappa = 0.83, 95% CI = 0.829-0.831). Treatment with anticonvulsants and age were associated with greater odds of correct classification. Although short of the 80% clinically relevant accuracy threshold, the results are promising and provide a fair and realistic estimate of classification performance, which can be achieved in a large, ecologically valid, multi-site sample of BD participants based on regional neurostructural measures. Furthermore, the significant classification in different samples was based on plausible and similar neuroanatomical features. Future multi-site studies should move towards sharing of raw/voxelwise neuroimaging data.

184. Detection of illicit phrasal movement in Huntington's disease.

Author

Tovar, A., Perry, S. J., Muñoz, E., Painous, C., Santacruz, P., Ruiz-Idiago, J., Mareca, C., Pomarol-Clotet, E., and Hinzen, W.

Subjects
*COMPARATIVE grammar, *CROSS-sectional method, *RESEARCH funding, *EXECUTIVE function, *LOGISTIC regression analysis, *BASAL ganglia, *MOVEMENT disorders, *DESCRIPTIVE statistics, *NATURAL language processing, *RESEARCH, *NEUROPSYCHOLOGICAL tests, *COGNITION disorders, *SEMANTICS, *JUDGMENT (Psychology), *DATA analysis software, *HUNTINGTON disease, *DISEASE progression, *DISEASE complications, SPEECH disorder diagnosis
Abstract

The role of the basal ganglia has been a longstanding issue in neural language models. Huntington's disease (HD) shows primary impairment in the striatum and has previously been shown to affect the processing of phrase-structural hierarchies that are built by phrasal movement (e.g. in passives). Here we asked patients with HD to judge the acceptability of sentences containing different types of illicit phrasal movement, which were contrasted with semantic violations involving no movement. A logistic mixed-effects regression showed that patients had a profound impairment in judging incorrect but not correct sentences across all types of illicit movement, while the semantic condition was also affected, but significantly less so. Adding neuropsychological variables to the model did not improve predictions. These results demonstrate a loss of cognitive control, worsening with disease progression, over phrase-structural hierarchies, which extends to forms of meaning built at sentential levels. [ABSTRACT FROM AUTHOR]

Published
2024
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186. Reward and fictive prediction error signals in ventral striatum: asymmetry between factual and counterfactual processing.

Author

Santo-Angles, A., Fuentes-Claramonte, P., Argila-Plaza, I., Guardiola-Ripoll, M., Almodóvar-Payá, C., Munuera, J., McKenna, P. J., Pomarol-Clotet, E., and Radua, J.

Subjects
*REWARD (Psychology), *REINFORCEMENT learning
Abstract

Reward prediction error, the difference between the expected and obtained reward, is known to act as a reinforcement learning neural signal. In the current study, we propose a model fitting approach that combines behavioral and neural data to fit computational models of reinforcement learning. Briefly, we penalized subject-specific fitted parameters that moved away too far from the group median, except when that deviation led to an improvement in the model's fit to neural responses. By means of a probabilistic monetary learning task and fMRI, we compared our approach with standard model fitting methods. Q-learning outperformed actor-critic at both behavioral and neural level, although the inclusion of neuroimaging data into model fitting improved the fit of actor-critic models. We observed both action-value and state-value prediction error signals in the striatum, while standard model fitting approaches failed to capture state-value signals. Finally, left ventral striatum correlated with reward prediction error while right ventral striatum with fictive prediction error, suggesting a functional hemispheric asymmetry regarding prediction-error driven learning. [ABSTRACT FROM AUTHOR]

Published
2021
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187. What we learn about bipolar disorder from large-scale neuroimaging

Author

Christian K. Tamnes, Bartholomeus C M Haarman, Jair C. Soares, Ole A. Andreassen, Viola Oertel, Theodore D. Satterthwaite, G. Tronchin, Michael Stäblein, Bradley J. MacIntosh, Melissa Pauling, Christopher R.K. Ching, Daniel H. Wolf, Dick J. Veltman, Ingrid Agartz, Bernhard T. Baune, Salvador Sarró, Mon-Ju Wu, Scott C Fears, Eduard Vieta, Melissa J. Green, Neeltje E.M. van Haren, Yann Quidé, Erlend Bøen, Yash Patel, Igor Nenadic, Martin Alda, Lisa T. Eyler, Arnaud Pouchon, Danai Dima, Tomáš Paus, Irene Bollettini, Torbjørn Elvsåshagen, Rachel M. Brouwer, Lakshmi N. Yatham, Michael Bauer, Caterina del Mar Bonnín, C. McDonald, Udo Dannlowski, Bronwyn Overs, Edith Pomarol-Clotet, Cristian Vargas Upegui, Oliver Gruber, Henricus G. Ruhé, Márcio Gerhardt Soeiro-de-Souza, Edouard Duchesnay, Hilary P. Blumberg, Tilo Kircher, Miho Ota, Michael Berk, Christoph Abé, Andreas Jansen, Kang Sim, Heather C. Whalley, Derrek P. Hibar, Roel A. Ophoff, Georgios V Thomaidis, Henrik Walter, Sophia Frangou, Michèle Wessa, Dara M. Cannon, Cara M. Altimus, Allison C. Nugent, Rodrigo Machado-Vieira, Orwa Dandash, Marcella Bellani, Unn K. Haukvik, Philip B. Mitchell, Ling-Li Zeng, Christian Knöchel, Jose Manuel Goikolea, Sonja M C de Zwarte, Francesco Benedetti, Sara Poletti, Janice M. Fullerton, Carlos A. Zarate, Aart H. Schene, Dan J. Stein, Chantal Henry, Tristram A. Lett, Mikael Landén, Daniel L Pham, Paolo Brambilla, Silvia Alonso-Lana, Sophia I. Thomopoulos, Carlos López-Jaramillo, Tomas Hajek, Bernd Kramer, G. Delvecchio, Maria M. Rive, Lars T. Westlye, Erick J. Canales-Rodríguez, Victoria L. Ives-Deliperi, Dominik Grotegerd, Beny Lafer, Abraham Nunes, Carrie E. Bearden, Raymond Salvador, Joaquim Radua, Amy C Bilderbeck, Xavier Caseras, Paul M. Thompson, Jorge R. C. Almeida, Pauline Favre, Gloria Roberts, David C. Glahn, Dag Alnæs, Julian A Pineda-Zapata, Tiril P. Gurholt, Mircea Polosan, Josselin Houenou, Fabiano G. Nery, Leila Nabulsi, Mary L. Phillips, Fleur M. Howells, Ana M. Díaz-Zuluaga, Elisa M T Melloni, Ching, C. R. K., Hibar, D. P., Gurholt, T. P., Nunes, A., Thomopoulos, S. I., Abe, C., Agartz, I., Brouwer, R. M., Cannon, D. M., de Zwarte, S. M. C., Eyler, L. T., Favre, P., Hajek, T., Haukvik, U. K., Houenou, J., Landen, M., Lett, T. A., Mcdonald, C., Nabulsi, L., Patel, Y., Pauling, M. E., Paus, T., Radua, J., Soeiro-de-Souza, M. G., Tronchin, G., van Haren, N. E. M., Vieta, E., Walter, H., Zeng, L. -L., Alda, M., Almeida, J., Alnaes, D., Alonso-Lana, S., Altimus, C., Bauer, M., Baune, B. T., Bearden, C. E., Bellani, M., Benedetti, F., Berk, M., Bilderbeck, A. C., Blumberg, H. P., Boen, E., Bollettini, I., del Mar Bonnin, C., Brambilla, P., Canales-Rodriguez, E. J., Caseras, X., Dandash, O., Dannlowski, U., Delvecchio, G., Diaz-Zuluaga, A. M., Dima, D., Duchesnay, E., Elvsashagen, T., Fears, S. C., Frangou, S., Fullerton, J. M., Glahn, D. C., Goikolea, J. M., Green, M. J., Grotegerd, D., Gruber, O., Haarman, B. C. M., Henry, C., Howells, F. M., Ives-Deliperi, V., Jansen, A., Kircher, T. T. J., Knochel, C., Kramer, B., Lafer, B., Lopez-Jaramillo, C., Machado-Vieira, R., Macintosh, B. J., Melloni, E. M. T., Mitchell, P. B., Nenadic, I., Nery, F., Nugent, A. C., Oertel, V., Ophoff, R. A., Ota, M., Overs, B. J., Pham, D. L., Phillips, M. L., Pineda-Zapata, J. A., Poletti, S., Polosan, M., Pomarol-Clotet, E., Pouchon, A., Quide, Y., Rive, M. M., Roberts, G., Ruhe, H. G., Salvador, R., Sarro, S., Satterthwaite, T. D., Schene, A. H., Sim, K., Soares, J. C., Stablein, M., Stein, D. J., Tamnes, C. K., Thomaidis, G. V., Upegui, C. V., Veltman, D. J., Wessa, M., Westlye, L. T., Whalley, H. C., Wolf, D. H., Wu, M. -J., Yatham, L. N., Zarate, C. A., Thompson, P. M., and Andreassen, O. A.

Subjects
mega-analysis, Stress-related disorders Donders Center for Medical Neuroscience [Radboudumc 13], cortical surface area, Review Article, 0302 clinical medicine, Manic-depressive illness, Multicenter Studies as Topic, Spectrum disorder, Review Articles, bipolar disorder, Cerebral Cortex, Trastorn bipolar, neuroimaging, Radiological and Ultrasound Technology, 05 social sciences, ENIGMA, HUMAN BRAIN, Magnetic Resonance Imaging, psychiatry, 3. Good health, Neurology, Meta-analysis, Scale (social sciences), Anatomy, Psychology, Clinical risk factor, Clinical psychology, MRI, MAJOR PSYCHIATRIC-DISORDERS, Schizoaffective disorder, 050105 experimental psychology, 03 medical and health sciences, Magnetic resonance imaging, Neuroimaging, Meta-Analysis as Topic, SDG 3 - Good Health and Well-being, Imatges per ressonància magnètica, medicine, Humans, 0501 psychology and cognitive sciences, Radiology, Nuclear Medicine and imaging, Bipolar disorder, HIPPOCAMPAL VOLUMES, mega‐analysis, GRAY-MATTER VOLUME, SPECTRUM DISORDER, volume, DIABETES-MELLITUS, cortical thickness, COGNITIVE IMPAIRMENT, medicine.disease, Mental illness, meta-analysis, meta‐analysis, RC0321, Neurology (clinical), SCHIZOAFFECTIVE DISORDER, PSYCHOTIC FEATURES, 030217 neurology & neurosurgery
Abstract

MRI‐derived brain measures offer a link between genes, the environment and behavior and have been widely studied in bipolar disorder (BD). However, many neuroimaging studies of BD have been underpowered, leading to varied results and uncertainty regarding effects. The Enhancing Neuro Imaging Genetics through Meta‐Analysis (ENIGMA) Bipolar Disorder Working Group was formed in 2012 to empower discoveries, generate consensus findings and inform future hypothesis‐driven studies of BD. Through this effort, over 150 researchers from 20 countries and 55 institutions pool data and resources to produce the largest neuroimaging studies of BD ever conducted. The ENIGMA Bipolar Disorder Working Group applies standardized processing and analysis techniques to empower large‐scale meta‐ and mega‐analyses of multimodal brain MRI and improve the replicability of studies relating brain variation to clinical and genetic data. Initial BD Working Group studies reveal widespread patterns of lower cortical thickness, subcortical volume and disrupted white matter integrity associated with BD. Findings also include mapping brain alterations of common medications like lithium, symptom patterns and clinical risk profiles and have provided further insights into the pathophysiological mechanisms of BD. Here we discuss key findings from the BD working group, its ongoing projects and future directions for large‐scale, collaborative studies of mental illness., This review discusses the major challenges facing neuroimaging research of bipolar disorder and highlights the major accomplishments, ongoing challenges and future goals of the ENIGMA Bipolar Disorder Working Group.

Published
2022

188. Association between body mass index and subcortical brain volumes in bipolar disorders–ENIGMA study in 2735 individuals

Author

Eduard Vieta, Jose Manuel Goikolea, Joaquim Raduà, Janice M. Fullerton, Lakshmi N. Yatham, Peter R. Schofield, Carlos López-Jaramillo, Tomas Hajek, Edith Pomarol-Clotet, Henk Temmingh, Francesco Benedetti, Ulrik Fredrik Malt, Erlend Bøen, Roel A. Ophoff, Bartholomeus C M Haarman, Cristian Vargas, Kang Sim, Katharina Thiel, Ole A. Andreassen, Tim Hahn, Lisa T. Eyler, Philip B. Mitchell, Christopher R.K. Ching, Axel Krug, Jonathan Repple, Annabel Vreeker, Dara M. Cannon, Sandra Meier, Colm McDonald, Holly Van Gestel, Hannah Lemke, Maike Richter, Caterina del Mar Bonnín, Udo Dannlowski, Tilo Kircher, Martin Alda, Mikael Landén, Janik Goltermann, Torbjørn Elvsåshagen, Genevieve McPhilemy, Jonathan Savitz, Susanne Meinert, Igor Nenadic, Simon Schmitt, Bronwyn Overs, Katharina Brosch, Dan J. Stein, Raymond Salvador, Dominik Grotegerd, Nils Opel, Martin Ingvar, Sean R. McWhinney, Erick J. Canales-Rodríguez, Elena Mazza, Gloria Roberts, Paul M. Thompson, Neeltje E.M. van Haren, Tiana Borgers, Fiona M. Martyn, Frederike Stein, Julia-Katharina Pfarr, Benny Liberg, Julian A Pineda-Zapata, Christoph Abé, Lena Waltemate, Tina Meller, Kai Ringwald, Ana M. Díaz-Zuluaga, Elisa M T Melloni, Rayus Kuplicki, Leila Nabulsi, Fleur M. Howells, Psychiatry, Child and Adolescent Psychiatry / Psychology, Mcwhinney, S. R., Abe, C., Alda, M., Benedetti, F., Boen, E., del Mar Bonnin, C., Borgers, T., Brosch, K., Canales-Rodriguez, E. J., Cannon, D. M., Dannlowski, U., Diaz-Zuluaga, A. M., Elvsashagen, T., Eyler, L. T., Fullerton, J. M., Goikolea, J. M., Goltermann, J., Grotegerd, D., Haarman, B. C. M., Hahn, T., Howells, F. M., Ingvar, M., Kircher, T. T. J., Krug, A., Kuplicki, R. T., Landen, M., Lemke, H., Liberg, B., Lopez-Jaramillo, C., Malt, U. F., Martyn, F. M., Mazza, E., Mcdonald, C., Mcphilemy, G., Meier, S., Meinert, S., Meller, T., Melloni, E. M. T., Mitchell, P. B., Nabulsi, L., Nenadic, I., Opel, N., Ophoff, R. A., Overs, B. J., Pfarr, J. -K., Pineda-Zapata, J. A., Pomarol-Clotet, E., Radua, J., Repple, J., Richter, M., Ringwald, K. G., Roberts, G., Salvador, R., Savitz, J., Schmitt, S., Schofield, P. R., Sim, K., Stein, D. J., Stein, F., Temmingh, H. S., Thiel, K., van Haren, N. E. M., Gestel, H. V., Vargas, C., Vieta, E., Vreeker, A., Waltemate, L., Yatham, L. N., Ching, C. R. K., Andreassen, O., Thompson, P. M., Hajek, T., and Clinical Cognitive Neuropsychiatry Research Program (CCNP)

Subjects
medicine.medical_specialty, Bipolar Disorder, Hippocampus, Amygdala, Article, Body Mass Index, Cellular and Molecular Neuroscience, Lateral ventricles, SDG 3 - Good Health and Well-being, Neuroimaging, Internal medicine, medicine, Humans, Risk factor, Molecular Biology, business.industry, Brain, medicine.disease, Magnetic Resonance Imaging, Obesity, Comorbidity, Psychiatry and Mental health, medicine.anatomical_structure, Cardiology, business, Body mass index, Neuroscience
Abstract

Individuals with bipolar disorders (BD) frequently suffer from obesity, which is often associated with neurostructural alterations. Yet, the effects of obesity on brain structure in BD are under-researched. We obtained MRI-derived brain subcortical volumes and body mass index (BMI) from 1134 BD and 1601 control individuals from 17 independent research sites within the ENIGMA-BD Working Group. We jointly modeled the effects of BD and BMI on subcortical volumes using mixed-effects modeling and tested for mediation of group differences by obesity using nonparametric bootstrapping. All models controlled for age, sex, hemisphere, total intracranial volume, and data collection site. Relative to controls, individuals with BD had significantly higher BMI, larger lateral ventricular volume, and smaller volumes of amygdala, hippocampus, pallidum, caudate, and thalamus. BMI was positively associated with ventricular and amygdala and negatively with pallidal volumes. When analyzed jointly, both BD and BMI remained associated with volumes of lateral ventricles and amygdala. Adjusting for BMI decreased the BD vs control differences in ventricular volume. Specifically, 18.41% of the association between BD and ventricular volume was mediated by BMI (Z = 2.73, p = 0.006). BMI was associated with similar regional brain volumes as BD, including lateral ventricles, amygdala, and pallidum. Higher BMI may in part account for larger ventricles, one of the most replicated findings in BD. Comorbidity with obesity could explain why neurostructural alterations are more pronounced in some individuals with BD. Future prospective brain imaging studies should investigate whether obesity could be a modifiable risk factor for neuroprogression.

Published
2021

189. Longitudinal structural brain changes in bipolar disorder: A multicenter neuroimaging study of 1232 individuals by the ENIGMA Bipolar Disorder Working Group

Author

Theophilus N. Akudjedu, Frederike Stein, Edith Pomarol-Clotet, Lars T. Westlye, Ulrik Fredrik Malt, Erlend Bøen, Fabian Breuer, Chao Suo, Tina Meller, Tim Hahn, Francesco Benedetti, Jose Manuel Goikolea, Silvia Alonso-Lana, Adam George White, Dag Alnæs, Julia-Katharina Pfarr, Beathe Haatveit, Sara Poletti, Kai Ringwald, Nathalia Zak, Benny Liberg, Kelvin Sarink, Giulia Tronchin, Yann Chye, Janice M. Fullerton, Orwa Dandash, Igor Nenadic, Caterina del Mar Bonnín, Elisa M T Melloni, Udo Dannlowski, Michael Berk, Dominik Grotegerd, Christopher R.K. Ching, Lukas Fisch, Torbjørn Elvsåshagen, Andreas Dahl, Martin Alda, Francesco Panicalli, Ingrid Agartz, Martin Ingvar, Bronwyn Overs, Joaquim Radua, Katharina Brosch, Alexander V. Lebedev, Kang Sim, Tilo Kircher, Leila Nabulsi, Dara M. Cannon, Erick J. Canales-Rodríguez, Paul M. Thompson, Nils Opel, Jonathan Repple, R. Salvador, Katharina Dohm, Philip B. Mitchell, Colm McDonald, Salvador Sarró, Rachel M. Brouwer, Ole A. Andreassen, Tomas Hajek, Mikael Landén, Simon Schmitt, Sophia I. Thomopoulos, Elena Rodriguez-Cano, Eduard Vieta, Ingrid Melle, Rhoshel K. Lenroot, Lakshmi N. Yatham, Sean R. McWhinney, Gloria Roberts, Christoph Abé, Walter Heindel, Abe, C., Ching, C. R. K., Liberg, B., Lebedev, A. V., Agartz, I., Akudjedu, T. N., Alda, M., Alnaes, D., Alonso-Lana, S., Benedetti, F., Berk, M., Boen, E., Bonnin, C. D. M., Breuer, F., Brosch, K., Brouwer, R. M., Canales-Rodriguez, E. J., Cannon, D. M., Chye, Y., Dahl, A., Dandash, O., Dannlowski, U., Dohm, K., Elvsashagen, T., Fisch, L., Fullerton, J. M., Goikolea, J. M., Grotegerd, D., Haatveit, B., Hahn, T., Hajek, T., Heindel, W., Ingvar, M., Sim, K., Kircher, T. T. J., Lenroot, R. K., Malt, U. F., Mcdonald, C., Mcwhinney, S. R., Melle, I., Meller, T., Melloni, E. M. T., Mitchell, P. B., Nabulsi, L., Nenadic, I., Opel, N., Overs, B. J., Panicalli, F., Pfarr, J. -K., Poletti, S., Pomarol-Clotet, E., Radua, J., Repple, J., Ringwald, K. G., Roberts, G., Rodriguez-Cano, E., Salvador, R., Sarink, K., Sarro, S., Schmitt, S., Stein, F., Suo, C., Thomopoulos, S. I., Tronchin, G., Vieta, E., Westlye, L. T., White, A. G., Yatham, L. N., Zak, N., Thompson, P. M., Andreassen, O. A., Landen, M., Complex Trait Genetics, and Amsterdam Neuroscience - Complex Trait Genetics

Subjects
Adult, Male, Longitudinal study, medicine.medical_specialty, Bipolar disorder, Neuroimaging, volume changes, surface-based analysis, Young Adult, gray-matter, Cortex (anatomy), Internal medicine, medicine, Humans, Multicenter Studies as Topic, Biological Psychiatry, mri, human cerebral-cortex, Psychiatry, medicine.diagnostic_test, business.industry, ENIGMA, Brain, Magnetic resonance imaging, Cerebral Cortical Thinning, Middle Aged, cortical thickness, medicine.disease, Magnetic Resonance Imaging, Neuroprogression, Mania, genetic influences, medicine.anatomical_structure, Mood, Meta-analysis, Cardiology, lithium treatment, Female, medicine.symptom, i disorder, business, metaanalysis
Abstract

Background: Bipolar disorder (BD) is associated with cortical and subcortical structural brain abnormalities. It is unclear whether such alterations progressively change over time, and how this is related to the number of mood episodes. To address this question, we analyzed a large and diverse international sample with longitudinal magnetic resonance imaging (MRI) and clinical data to examine structural brain changes over time in BD. Methods: Longitudinal structural MRI and clinical data from the ENIGMA (Enhancing Neuro Imaging Genetics through Meta Analysis) BD Working Group, including 307 patients with BD and 925 healthy control subjects, were collected from 14 sites worldwide. Male and female participants, aged 40 ± 17 years, underwent MRI at 2 time points. Cortical thickness, surface area, and subcortical volumes were estimated using FreeSurfer. Annualized change rates for each imaging phenotype were compared between patients with BD and healthy control subjects. Within patients, we related brain change rates to the number of mood episodes between time points and tested for effects of demographic and clinical variables. Results: Compared with healthy control subjects, patients with BD showed faster enlargement of ventricular volumes and slower thinning of the fusiform and parahippocampal cortex (0.18 < d < 0.22). More (hypo)manic episodes were associated with faster cortical thinning, primarily in the prefrontal cortex. Conclusions: In the hitherto largest longitudinal MRI study on BD, we did not detect accelerated cortical thinning but noted faster ventricular enlargements in BD. However, abnormal frontocortical thinning was observed in association with frequent manic episodes. Our study yields insights into disease progression in BD and highlights the importance of mania prevention in BD treatment.

Published
2022

190. Neurotrophins role in depressive symptoms and executive function performance: Association analysis of NRN1 gene and its interaction with BDNF gene in a non-clinical sample.

Author

Prats, C., Arias, B., Ortet, G., Ibáñez, M.I., Moya, J., Pomarol-Clotet, E., Fañanás, L., and Fatjó-Vilas, M.

Subjects
*NEUROTROPHINS, *EXECUTIVE function, *NEUROPLASTICITY, *PATHOLOGICAL psychology, *MENTAL depression, *DISEASE susceptibility, *GENETIC polymorphisms, *NEUROPSYCHOLOGICAL tests, *NERVE tissue proteins, *PSYCHOLOGICAL tests, *SCHIZOPHRENIA, *GENETIC carriers, *GENOTYPES, *BRIEF Symptom Inventory
Abstract

Background: Neuritin-1 is a neurotrophic factor involved in synaptic plasticity that has been associated with depressive disorders, schizophrenia and cognitive performance. The study of genotype-phenotype relationships in healthy individuals is a useful framework to investigate the etiology of brain dysfunctions. We therefore aimed to investigate in a non-clinical sample whether NRN1 gene contributes to the psychopathological profile, with a particular focus on the clinical dimensions previously related to the NRN1 gene (i.e. depressive and psychotic). Furthermore, we aimed to analyze: i) the role of NRN1 on executive functions, ii) whether the association between either NRN1-psychopathological profile or NRN1-cognitive performance is moderated by the BDNF gene.Methods: The sample comprised 410 non-clinical subjects who filled in the self-reported Brief Symptom Inventory (BSI) and were assessed for executive performance (Verbal Fluency, Wisconsin Card Sorting Test (WCST) and Letter-Number subscale (WAIS-III)). Genotyping included nine SNPs in NRN1 and one in BDNF.Results: i) GG homozygotes (rs1475157-NRN1) showed higher scores on BSI depressive dimension and on total scores compared to A carriers (corrected p-values: 0.0004 and 0.0003, respectively). ii) a linear trend was detected between GG genotype of rs1475157 and a worse cognitive performance in WCST total correct responses (uncorrected p-value: 0.029). iii) Interaction between rs1475157-NRN1 and Val66Met-BDNF was found to modulate depressive symptoms (p=0.001, significant after correction).Limitations: Moderate sample size; replication in a larger sample is needed.Conclusions: NRN1 is associated with depressive symptoms and executive function in a non-clinical sample. Our results also suggest that the role of NRN1 seems to be modulated by BDNF. [ABSTRACT FROM AUTHOR]

Published
2017
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191. Evidence of an epistatic effect between Dysbindin-1 and Neuritin-1 genes on the risk for schizophrenia spectrum disorders.

Author

Prats, C., Arias, B., Moya-Higueras, J., Pomarol-Clotet, E., Parellada, M., González-Pinto, A., Peralta, V., Ibáñez, M.I., Martín, M., Fañanás, L., and Fatjó-Vilas, M.

Subjects
*MENTAL illness, *SCHIZOPHRENIA, *DYSBINDIN, *NEUROPLASTICITY, *ETIOLOGY of diseases
Abstract

Background The interest in studying gene–gene interactions is increasing for psychiatric diseases such as schizophrenia-spectrum disorders (SSD), where multiple genes are involved. Dysbindin-1 ( DTNBP1 ) and Neuritin-1 ( NRN1 ) genes have been previously associated with SSD and both are involved in synaptic plasticity. We aimed to study whether these genes show an epistatic effect on the risk for SSD. Methods The sample comprised 388 SSD patients and 397 healthy subjects. Interaction was tested between: (i) three DTNBP1 SNPs (rs2619537, rs2743864, rs1047631) related to changes in gene expression; and (ii) an haplotype in NRN1 previously associated with the risk for SSD (rs645649-rs582262: HAP-risk C-C). Results An interaction between DTNBP1 rs2743864 and NRN1 HAP-risk was detected by using the model based multifactor dimensionality reduction (MB-MDR) approach ( P = 0.0049, after permutation procedure), meaning that the risk for SSD is significantly higher in those subjects carrying both the A allele of rs2743864 and the HAP-risk C-C. This interaction was confirmed by using a logistic regression model ( P = 0.033, OR (95%CI) = 2.699 (1.08–6.71), R 2 = 0.162). Discussion Our results suggest that DTNBP1 and NRN1 genes show a joint effect on the risk for SSD. Although the precise mechanism underlying this effect is unclear, the fact that these genes have been involved in synaptic maturation, connectivity and glutamate signalling suggests that our findings could be of value as a link to the schizophrenia aetiology. [ABSTRACT FROM AUTHOR]

Published
2017
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192. Examining the continuum of psychosis: Frequency and characteristics of psychotic-like symptoms in relatives and non-relatives of patients with schizophrenia.

Author

Landin-Romero, R., McKenna, P.J., Romaguera, A., Álvarez-Moya, E., Sarró, S., Aguirre, C., Sarri, C., Compte, A., Bosque, C., Salvador, R., and Pomarol-Clotet, E.

Subjects
*PSYCHOSES, *CONTINUITY, *SCHIZOPHRENIA, *MENTAL illness, *MEDICAL care, *FAMILIES & psychology, *DISEASE susceptibility, *LONGITUDINAL method, *MENTAL status examination, *PSYCHOLOGY, *QUESTIONNAIRES, *SCHIZOTYPAL personality disorder, *PHENOTYPES, *PSYCHOLOGICAL factors
Abstract

Background: A key finding underlying the continuum of psychosis concept is the presence of psychotic-like experiences (PLEs) in healthy subjects. However, it remains uncertain to what extent these experiences are related to the genetic risk for schizophrenia and how far they actually resemble attenuated forms of psychotic symptoms.Methods: Forty-nine adults with no history of mental illness in first-degree relatives and 59 siblings of patients with schizophrenia were rated on the psychosis section of the Computerized Diagnostic Interview Schedule IV (C DIS-IV) and the Rust Inventory of Schizotypal Cognitions (RISC). Those who rated positive on the CDIS-IV were re-interviewed using the lifetime version of the Present State Examination 9th edition (PSE-9) and the Structured interview for Schizotypy (SIS).Results: Seventeen (34.69%) of the non-relatives and 22 (37.29%) of the relatives responded positively to one or more of the psychosis questions on the DIS. This difference was not significant. RISC scores were also similar between the groups. At follow-up interview with the PSE-9, 13/40 PLEs (32.50%) in the non-relatives were classified as possible or probable psychotic symptoms compared to 11/46 (23.91%) in the relatives. Using liberal symptom thresholds, 5 of those who attended the follow-up interview (2 non-relatives and 3 relatives) met SIS criteria for schizotypal personality disorder.Conclusions: Rates of PLEs, however considered, do not differ substantially between relatives and non-relatives of patients with schizophrenia. Only a minority of PLEs picked up by screening interviews resemble attenuated forms of psychotic symptoms. [ABSTRACT FROM AUTHOR]

Published
2016
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193. In vivo hippocampal subfield volumes in bipolar disorder-A mega-analysis from The Enhancing Neuro Imaging Genetics throughMeta-AnalysisBipolar Disorder Working Group

Author

Sophia I. Thomopoulos, Julian A Pineda-Zapata, Ronny Redlich, Bartholomeus C M Haarman, Mathew A. Harris, Orwa Dandash, Ulrik Fredrik Malt, Lauren E. Salminen, Michael Stäblein, Theo G.M. van Erp, Gloria Roberts, Michael Berk, Jochen Bauer, Edith Pomarol-Clotet, Carlos López-Jaramillo, Dominik Grotegerd, Tomas Hajek, Paul M. Thompson, Philipp G. Sämann, Francesco Benedetti, Tilo Kircher, Brian Hallahan, Jonathan Repple, Lena Waltemate, Maria M. Rive, Heather C. Whalley, Caterina del Mar Bonnín, Oliver Gruber, Igor Nenadic, Udo Dannlowski, Henricus G. Ruhé, Raymond Salvador, Bronwyn Overs, Torbjørn Elvsåshagen, Márcio Gerhardt Soeiro-de-Souza, Ana M. Díaz-Zuluaga, Katharina Förster, Jose Manuel Goikolea, Emma L. Hawkins, Vera Lonning, Silvia Alonso-Lana, Dan J. Stein, Theophilus N. Akudjedu, Elisa M T Melloni, Dag Alnæs, Nils Opel, Martin Alda, Rayus Kuplicki, Erlend Bøen, Salvador Sarró, Unn K. Haukvik, Philip B. Mitchell, Kang Sim, Lisa Rauer, Ole A. Andreassen, Colm McDonald, Eduard Vieta, Erick J. Canales-Rodríguez, Axel Krug, Viola Oertel, Frederike Stein, Xavier Caseras, Christopher R.K. Ching, Lucio Oldani, Dara M. Cannon, Andrew M. McIntosh, Kjetil Nordbø Jørgensen, Ingrid Melle, Rhoshel K. Lenroot, Lars T. Westlye, Giuseppe Delvecchio, Dick J. Veltman, Mar Fatjó-Vilas, Trine Vik Lagerberg, Leila Nabulsi, Henk Temmingh, Carina Hülsmann, Francesco Bettella, Paolo Brambilla, Dennis van der Meer, Sonya Foley, Tiril P. Gurholt, Fleur M. Howells, Joaquim Radua, Thomas M. Lancaster, Christian K. Tamnes, Maria Cg Otaduy, Jonathan Savitz, Stener Nerland, Genevieve McPhilemy, Janice M. Fullerton, Aart H. Schene, Neda Jahanshad, Ingrid Agartz, Bernhard T. Baune, Beathe Haatveit, Bernd Krämer, Psychiatrie & Neuropsychologie, RS: MHeNs - R2 - Mental Health, Haukvik, U. K., Gurholt, T. P., Nerland, S., Elvsashagen, T., Akudjedu, T. N., Alda, M., Alnaes, D., Alonso-Lana, S., Bauer, J., Baune, B. T., Benedetti, F., Berk, M., Bettella, F., Boen, E., Bonnin, C. M., Brambilla, P., Canales-Rodriguez, E. J., Cannon, D. M., Caseras, X., Dandash, O., Dannlowski, U., Delvecchio, G., Diaz-Zuluaga, A. M., van Erp, T. G. M., Fatjo-Vilas, M., Foley, S. F., Forster, K., Fullerton, J. M., Goikolea, J. M., Grotegerd, D., Gruber, O., Haarman, B. C. M., Haatveit, B., Hajek, T., Hallahan, B., Harris, M., Hawkins, E. L., Howells, F. M., Hulsmann, C., Jahanshad, N., Jorgensen, K. N., Kircher, T., Kramer, B., Krug, A., Kuplicki, R., Lagerberg, T. V., Lancaster, T. M., Lenroot, R. K., Lonning, V., Lopez-Jaramillo, C., Malt, U. F., Mcdonald, C., Mcintosh, A. M., Mcphilemy, G., van der Meer, D., Melle, I., Melloni, E. M. T., Mitchell, P. B., Nabulsi, L., Nenadic, I., Oertel, V., Oldani, L., Opel, N., Otaduy, M. C. G., Overs, B. J., Pineda-Zapata, J. A., Pomarol-Clotet, E., Radua, J., Rauer, L., Redlich, R., Repple, J., Rive, M. M., Roberts, G., Ruhe, H. G., Salminen, L. E., Salvador, R., Sarro, S., Savitz, J., Schene, A. H., Sim, K., Soeiro-de-Souza, M. G., Stablein, M., Stein, D. J., Stein, F., Tamnes, C. K., Temmingh, H. S., Thomopoulos, S. I., Veltman, D. J., Vieta, E., Waltemate, L., Westlye, L. T., Whalley, H. C., Samann, P. G., Thompson, P. M., Ching, C. R. K., Andreassen, O. A., Agartz, I., Clinical Cognitive Neuropsychiatry Research Program (CCNP), Psychiatry, Anatomy and neurosciences, Amsterdam Neuroscience - Brain Imaging, Amsterdam Neuroscience - Compulsivity, Impulsivity & Attention, Amsterdam Neuroscience - Mood, Anxiety, Psychosis, Stress & Sleep, and Adult Psychiatry

Subjects
structural brain MRI, Bipolar Disorder, HALOPERIDOL, hippocampus, Stress-related disorders Donders Center for Medical Neuroscience [Radboudumc 13], SEGMENTATION, Hippocampus, Hippocampal formation, 0302 clinical medicine, SCHIZOPHRENIA, Manic-depressive illness, psychosis, BRAIN, Research Articles, Trastorn bipolar, Radiological and Ultrasound Technology, 05 social sciences, Subiculum, ATLAS, Magnetic Resonance Imaging, Liti, 3. Good health, medicine.anatomical_structure, Neurology, Schizophrenia, lithium, Anatomy, Hippocampus (Brain), Research Article, MRI, INTERNEURONS, Psychosis, Hipocamp (Cervell), Neuroimaging, Amygdala, 050105 experimental psychology, CELL-PROLIFERATION, 03 medical and health sciences, Genetics, medicine, Humans, 0501 psychology and cognitive sciences, Radiology, Nuclear Medicine and imaging, Bipolar disorder, large‐scale, LITHIUM-TREATED PATIENTS, business.industry, Dentate gyrus, medicine.disease, nervous system, DENTATE GYRUS, large-scale, bipolar disorder subtype, Neurology (clinical), business, Neuroscience, 030217 neurology & neurosurgery
Abstract

The hippocampus consists of anatomically and functionally distinct subfields that may be differentially involved in the pathophysiology of bipolar disorder (BD). Here we, the Enhancing NeuroImaging Genetics through Meta‐Analysis Bipolar Disorder workinggroup, study hippocampal subfield volumetry in BD. T1‐weighted magnetic resonance imaging scans from 4,698 individuals (BD = 1,472, healthy controls [HC] = 3,226) from 23 sites worldwide were processed with FreeSurfer. We used linear mixed‐effects models and mega‐analysis to investigate differences in hippocampal subfield volumes between BD and HC, followed by analyses of clinical characteristics and medication use. BD showed significantly smaller volumes of the whole hippocampus (Cohen's d = −0.20), cornu ammonis (CA)1 (d = −0.18), CA2/3 (d = −0.11), CA4 (d = −0.19), molecular layer (d = −0.21), granule cell layer of dentate gyrus (d = −0.21), hippocampal tail (d = −0.10), subiculum (d = −0.15), presubiculum (d = −0.18), and hippocampal amygdala transition area (d = −0.17) compared to HC. Lithium users did not show volume differences compared to HC, while non‐users did. Antipsychotics or antiepileptic use was associated with smaller volumes. In this largest study of hippocampal subfields in BD to date, we show widespread reductions in nine of 12 subfields studied. The associations were modulated by medication use and specifically the lack of differences between lithium users and HC supports a possible protective role of lithium in BD., The hippocampus consists of anatomically and functionally distinct subfields that may be differentially involved in the pathophysiology of bipolar disorder.In the largest study of hippocampal subfields in bipolar disorder to date, from 23 sites worldwide, we report widespread reductions in nine of 12 subfields.The lack of differences between lithium users and healthy controls supports a possible protective role of lithium in bipolar disorder.

Published
2022

194. Brain structural changes in schizoaffective disorder compared to schizophrenia and bipolar disorder.

Author

Amann, B. L., Canales‐Rodríguez, E. J., Madre, M., Radua, J., Monte, G., Alonso‐Lana, S., Landin‐Romero, R., Moreno‐Alcázar, A., Bonnin, C. M., Sarró, S., Ortiz‐Gil, J., Gomar, J. J., Moro, N., Fernandez‐Corcuera, P., Goikolea, J. M., Blanch, J., Salvador, R., Vieta, E., McKenna, P. J., and Pomarol‐Clotet, E.

Subjects
*SCHIZOAFFECTIVE disorders, *PEOPLE with schizophrenia, *BIPOLAR disorder, *VOXEL-based morphometry, *GRAY matter (Nerve tissue), *CONTROL groups
Abstract

Objective Brain structural changes in schizoaffective disorder, and how far they resemble those seen in schizophrenia and bipolar disorder, have only been studied to a limited extent. Method Forty-five patients meeting DSM- IV and RDC criteria for schizoaffective disorder, groups of patients with 45 matched schizophrenia and bipolar disorder, and 45 matched healthy controls were examined using voxel-based morphometry ( VBM). Results Analyses comparing each patient group with the healthy control subjects found that the patients with schizoaffective disorder and the patients with schizophrenia showed widespread and overlapping areas of significant volume reduction, but the patients with bipolar disorder did not. A subsequent analysis compared the combined group of patients with the controls followed by extraction of clusters. In regions where the patients differed significantly from the controls, no significant differences in mean volume between patients with schizoaffective disorder and patients with schizophrenia in any of five regions of volume reduction were found, but mean volumes in the patients with bipolar disorder were significantly smaller in three of five. Conclusion The findings provide evidence that, in terms of structural gray matter brain abnormality, schizoaffective disorder resembles schizophrenia more than bipolar disorder. [ABSTRACT FROM AUTHOR]

Published
2016
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195. P.0788 Surface-based morphometry abnormality in schizophrenia and its relation to positive, negative and disorganized syndromes.

Author

Garcia-Leon, M.A., Fuentes-Claramonte, P., Canales-Rodriguez, E., Soler, J., Santo, A., Ramiro, N., Torres, M.L., Aquino, A., Bosque, C., Saló, L., Portillo, F., Panicali, F., Argila, I., Salgado-Pineda, P., Sarro, S., Salvador, R., McKenna, P., and Pomarol-Clotet, E.

Subjects
*MORPHOMETRICS, *SCHIZOPHRENIA, *SYNDROMES, *HUMAN abnormalities, *22Q11 deletion syndrome, *VOXEL-based morphometry
Published
2021
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197. P.0670 Shaped before birth: obstetric complications identify a more severe clinical phenotype among patients presenting an affective or non-affective first-episode psychosis.

Author

Sagué-Vilavella, M., Amoretti, S., Garriga, M., Mezquida, G., Williams, E., Fico, G., Anmella, G., Serra, M., Forte, M.F., Varo, C., Montejo, L., Palacios-Garran, R., Madero, S., Sparacino, G., Giménez, A., Salgado-Pineda, P., Salvatierra, I. Montoro, Gustau, V. Sánchez, Pomarol-Clotet, E., and Ramos-Quiroga, J.A.

Subjects
*AFFECT (Psychology), *PSYCHOSES, *PHENOTYPES, *PATIENTS
Published
2021
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200. Failure of deactivation in the default mode network: a trait marker for schizophrenia?

Author

Landin-Romero, R., McKenna, P. J., Salgado-Pineda, P., Sarró, S., Aguirre, C., Sarri, C., Compte, A., Bosque, C., Blanch, J., Salvador, R., and Pomarol-Clotet, E.

Subjects
*BRAIN physiology, *ANALYSIS of variance, *BRAIN, *BRAIN mapping, *CHLORPROMAZINE, *CHRONIC diseases, *INTERVIEWING, *MAGNETIC resonance imaging, *PHYSIOLOGICAL research, *RESEARCH funding, *SCHIZOPHRENIA, *SHORT-term memory, *T-test (Statistics), *REPEATED measures design, *CASE-control method, *DESCRIPTIVE statistics
Abstract

Background.Functional imaging studies in relatives of schizophrenic patients have had inconsistent findings, particularly with respect to altered dorsolateral prefrontal cortex activation. Some recent studies have also suggested that failure of deactivation may be seen.Method.A total of 28 patients with schizophrenia, 28 of their siblings and 56 healthy controls underwent functional magnetic resonance imaging during performance of the n-back working memory task. An analysis of variance was fitted to individual whole-brain maps from each set of patient–relative–matched pair of controls. Clusters of significant difference among the groups were then used as regions of interest to compare mean activations and deactivations among the groups.Results.In all, five clusters of significant differences were found. The schizophrenic patients, but not the relatives, showed reduced activation compared with the controls in the lateral frontal cortex bilaterally, the left basal ganglia and the cerebellum. In contrast, both the patients and the relatives showed significant failure of deactivation compared with the healthy controls in the medial frontal cortex, with the relatives also showing less failure than the patients. Failure of deactivation was not associated with schizotypy scores or presence of psychotic-like experiences in the relatives.Conclusions.Both schizophrenic patients and their relatives show altered task-related deactivation in the medial frontal cortex. This in turn suggests that default mode network dysfunction may function as a trait marker for schizophrenia. [ABSTRACT FROM AUTHOR]

Published
2015
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