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1. Principal component analysis as an efficient method for capturing multivariate brain signatures of complex disorders-ENIGMA study in people with bipolar disorders and obesity.

Author

McWhinney, SR, Hlinka, J, Bakstein, E, Dietze, LMF, Corkum, ELV, Abé, C, Alda, M, Alexander, N, Benedetti, F, Berk, M, Bøen, E, Bonnekoh, LM, Boye, B, Brosch, K, Canales-Rodríguez, EJ, Cannon, DM, Dannlowski, U, Demro, C, Diaz-Zuluaga, A, Elvsåshagen, T, Eyler, LT, Fortea, L, Fullerton, JM, Goltermann, J, Gotlib, IH, Grotegerd, D, Haarman, B, Hahn, T, Howells, FM, Jamalabadi, H, Jansen, A, Kircher, T, Klahn, AL, Kuplicki, R, Lahud, E, Landén, M, Leehr, EJ, Lopez-Jaramillo, C, Mackey, S, Malt, U, Martyn, F, Mazza, E, McDonald, C, McPhilemy, G, Meier, S, Meinert, S, Melloni, E, Mitchell, PB, Nabulsi, L, Nenadić, I, Nitsch, R, Opel, N, Ophoff, RA, Ortuño, M, Overs, BJ, Pineda-Zapata, J, Pomarol-Clotet, E, Radua, J, Repple, J, Roberts, G, Rodriguez-Cano, E, Sacchet, MD, Salvador, R, Savitz, J, Scheffler, F, Schofield, PR, Schürmeyer, N, Shen, C, Sim, K, Sponheim, SR, Stein, DJ, Stein, F, Straube, B, Suo, C, Temmingh, H, Teutenberg, L, Thomas-Odenthal, F, Thomopoulos, SI, Urosevic, S, Usemann, P, van Haren, NEM, Vargas, C, Vieta, E, Vilajosana, E, Vreeker, A, Winter, NR, Yatham, LN, Thompson, PM, Andreassen, OA, Ching, CRK, Hajek, T, McWhinney, SR, Hlinka, J, Bakstein, E, Dietze, LMF, Corkum, ELV, Abé, C, Alda, M, Alexander, N, Benedetti, F, Berk, M, Bøen, E, Bonnekoh, LM, Boye, B, Brosch, K, Canales-Rodríguez, EJ, Cannon, DM, Dannlowski, U, Demro, C, Diaz-Zuluaga, A, Elvsåshagen, T, Eyler, LT, Fortea, L, Fullerton, JM, Goltermann, J, Gotlib, IH, Grotegerd, D, Haarman, B, Hahn, T, Howells, FM, Jamalabadi, H, Jansen, A, Kircher, T, Klahn, AL, Kuplicki, R, Lahud, E, Landén, M, Leehr, EJ, Lopez-Jaramillo, C, Mackey, S, Malt, U, Martyn, F, Mazza, E, McDonald, C, McPhilemy, G, Meier, S, Meinert, S, Melloni, E, Mitchell, PB, Nabulsi, L, Nenadić, I, Nitsch, R, Opel, N, Ophoff, RA, Ortuño, M, Overs, BJ, Pineda-Zapata, J, Pomarol-Clotet, E, Radua, J, Repple, J, Roberts, G, Rodriguez-Cano, E, Sacchet, MD, Salvador, R, Savitz, J, Scheffler, F, Schofield, PR, Schürmeyer, N, Shen, C, Sim, K, Sponheim, SR, Stein, DJ, Stein, F, Straube, B, Suo, C, Temmingh, H, Teutenberg, L, Thomas-Odenthal, F, Thomopoulos, SI, Urosevic, S, Usemann, P, van Haren, NEM, Vargas, C, Vieta, E, Vilajosana, E, Vreeker, A, Winter, NR, Yatham, LN, Thompson, PM, Andreassen, OA, Ching, CRK, and Hajek, T

Abstract

Multivariate techniques better fit the anatomy of complex neuropsychiatric disorders which are characterized not by alterations in a single region, but rather by variations across distributed brain networks. Here, we used principal component analysis (PCA) to identify patterns of covariance across brain regions and relate them to clinical and demographic variables in a large generalizable dataset of individuals with bipolar disorders and controls. We then compared performance of PCA and clustering on identical sample to identify which methodology was better in capturing links between brain and clinical measures. Using data from the ENIGMA-BD working group, we investigated T1-weighted structural MRI data from 2436 participants with BD and healthy controls, and applied PCA to cortical thickness and surface area measures. We then studied the association of principal components with clinical and demographic variables using mixed regression models. We compared the PCA model with our prior clustering analyses of the same data and also tested it in a replication sample of 327 participants with BD or schizophrenia and healthy controls. The first principal component, which indexed a greater cortical thickness across all 68 cortical regions, was negatively associated with BD, BMI, antipsychotic medications, and age and was positively associated with Li treatment. PCA demonstrated superior goodness of fit to clustering when predicting diagnosis and BMI. Moreover, applying the PCA model to the replication sample yielded significant differences in cortical thickness between healthy controls and individuals with BD or schizophrenia. Cortical thickness in the same widespread regional network as determined by PCA was negatively associated with different clinical and demographic variables, including diagnosis, age, BMI, and treatment with antipsychotic medications or lithium. PCA outperformed clustering and provided an easy-to-use and interpret method to study multivariate associati

Published
2024

2. In vivo hippocampal subfield volumes in bipolar disorder—A mega-analysis from The Enhancing Neuro Imaging Genetics through Meta-Analysis Bipolar Disorder Working Group

Author

Haukvik, UK, Gurholt, TP, Nerland, S, Elvsåshagen, T, Akudjedu, TN, Alda, M, Alnæs, D, Alonso-Lana, S, Bauer, J, Baune, BT, Benedetti, F, Berk, Michael, Bettella, F, Bøen, E, Bonnín, CM, Brambilla, P, Canales-Rodríguez, EJ, Cannon, DM, Caseras, X, Dandash, O, Dannlowski, U, Delvecchio, G, Díaz-Zuluaga, AM, van Erp, TGM, Fatjó-Vilas, M, Foley, SF, Förster, K, Fullerton, JM, Goikolea, JM, Grotegerd, D, Gruber, O, Haarman, BCM, Haatveit, B, Hajek, T, Hallahan, B, Harris, M, Hawkins, EL, Howells, FM, Hülsmann, C, Jahanshad, N, Jørgensen, KN, Kircher, T, Krämer, B, Krug, A, Kuplicki, R, Lagerberg, TV, Lancaster, TM, Lenroot, RK, Lonning, V, López-Jaramillo, C, Malt, UF, McDonald, C, McIntosh, AM, McPhilemy, G, van der Meer, D, Melle, I, Melloni, EMT, Mitchell, PB, Nabulsi, L, Nenadić, I, Oertel, V, Oldani, L, Opel, N, Otaduy, MCG, Overs, BJ, Pineda-Zapata, JA, Pomarol-Clotet, E, Radua, J, Rauer, L, Redlich, R, Repple, J, Rive, MM, Roberts, G, Ruhe, HG, Salminen, LE, Salvador, R, Sarró, S, Savitz, J, Schene, AH, Sim, K, Soeiro-de-Souza, MG, Stäblein, M, Stein, DJ, Stein, F, Tamnes, CK, Temmingh, HS, Thomopoulos, SI, Veltman, DJ, Vieta, E, Waltemate, L, Westlye, LT, Whalley, HC, Sämann, PG, Thompson, PM, Ching, CRK, Andreassen, OA, Agartz, I, Haukvik, UK, Gurholt, TP, Nerland, S, Elvsåshagen, T, Akudjedu, TN, Alda, M, Alnæs, D, Alonso-Lana, S, Bauer, J, Baune, BT, Benedetti, F, Berk, Michael, Bettella, F, Bøen, E, Bonnín, CM, Brambilla, P, Canales-Rodríguez, EJ, Cannon, DM, Caseras, X, Dandash, O, Dannlowski, U, Delvecchio, G, Díaz-Zuluaga, AM, van Erp, TGM, Fatjó-Vilas, M, Foley, SF, Förster, K, Fullerton, JM, Goikolea, JM, Grotegerd, D, Gruber, O, Haarman, BCM, Haatveit, B, Hajek, T, Hallahan, B, Harris, M, Hawkins, EL, Howells, FM, Hülsmann, C, Jahanshad, N, Jørgensen, KN, Kircher, T, Krämer, B, Krug, A, Kuplicki, R, Lagerberg, TV, Lancaster, TM, Lenroot, RK, Lonning, V, López-Jaramillo, C, Malt, UF, McDonald, C, McIntosh, AM, McPhilemy, G, van der Meer, D, Melle, I, Melloni, EMT, Mitchell, PB, Nabulsi, L, Nenadić, I, Oertel, V, Oldani, L, Opel, N, Otaduy, MCG, Overs, BJ, Pineda-Zapata, JA, Pomarol-Clotet, E, Radua, J, Rauer, L, Redlich, R, Repple, J, Rive, MM, Roberts, G, Ruhe, HG, Salminen, LE, Salvador, R, Sarró, S, Savitz, J, Schene, AH, Sim, K, Soeiro-de-Souza, MG, Stäblein, M, Stein, DJ, Stein, F, Tamnes, CK, Temmingh, HS, Thomopoulos, SI, Veltman, DJ, Vieta, E, Waltemate, L, Westlye, LT, Whalley, HC, Sämann, PG, Thompson, PM, Ching, CRK, Andreassen, OA, and Agartz, I

Published
2022

3. What we learn about bipolar disorder from large-scale neuroimaging: Findings and future directions from theENIGMABipolar Disorder Working Group

Author

Ching, CRK, Hibar, DP, Gurholt, TP, Nunes, A, Thomopoulos, SI, Abe, C, Agartz, I, Brouwer, RM, Cannon, DM, de Zwarte, SMC, Eyler, LT, Favre, P, Hajek, T, Haukvik, UK, Houenou, J, Landen, M, Lett, TA, McDonald, C, Nabulsi, L, Patel, Y, Pauling, ME, Paus, T, Radua, J, Soeiro-de-Souza, MG, Tronchin, G, van Haren, NEM, Vieta, E, Walter, H, Zeng, L-L, Alda, M, Almeida, J, Alnaes, D, Alonso-Lana, S, Altimus, C, Bauer, M, Baune, BT, Bearden, CE, Bellani, M, Benedetti, F, Berk, M, Bilderbeck, AC, Blumberg, HP, Boen, E, Bollettini, I, del Mar Bonnin, C, Brambilla, P, Canales-Rodriguez, EJ, Caseras, X, Dandash, O, Dannlowski, U, Delvecchio, G, Diaz-Zuluaga, AM, Dima, D, Duchesnay, E, Elvsashagen, T, Fears, SC, Frangou, S, Fullerton, JM, Glahn, DC, Goikolea, JM, Green, MJ, Grotegerd, D, Gruber, O, Haarman, BCM, Henry, C, Howells, FM, Ives-Deliperi, V, Jansen, A, Kircher, TTJ, Knoechel, C, Kramer, B, Lafer, B, Lopez-Jaramillo, C, Machado-Vieira, R, MacIntosh, BJ, Melloni, EMT, Mitchell, PB, Nenadic, I, Nery, F, Nugent, AC, Oertel, V, Ophoff, RA, Ota, M, Overs, BJ, Pham, DL, Phillips, ML, Pineda-Zapata, JA, Poletti, S, Polosan, M, Pomarol-Clotet, E, Pouchon, A, Quide, Y, Rive, MM, Roberts, G, Ruhe, HG, Salvador, R, Sarro, S, Satterthwaite, TD, Schene, AH, Sim, K, Soares, JC, Staeblein, M, Stein, DJ, Tamnes, CK, Thomaidis, GV, Upegui, CV, Veltman, DJ, Wessa, M, Westlye, LT, Whalley, HC, Wolf, DH, Wu, M-J, Yatham, LN, Zarate, CA, Thompson, PM, Andreassen, OA, Ching, CRK, Hibar, DP, Gurholt, TP, Nunes, A, Thomopoulos, SI, Abe, C, Agartz, I, Brouwer, RM, Cannon, DM, de Zwarte, SMC, Eyler, LT, Favre, P, Hajek, T, Haukvik, UK, Houenou, J, Landen, M, Lett, TA, McDonald, C, Nabulsi, L, Patel, Y, Pauling, ME, Paus, T, Radua, J, Soeiro-de-Souza, MG, Tronchin, G, van Haren, NEM, Vieta, E, Walter, H, Zeng, L-L, Alda, M, Almeida, J, Alnaes, D, Alonso-Lana, S, Altimus, C, Bauer, M, Baune, BT, Bearden, CE, Bellani, M, Benedetti, F, Berk, M, Bilderbeck, AC, Blumberg, HP, Boen, E, Bollettini, I, del Mar Bonnin, C, Brambilla, P, Canales-Rodriguez, EJ, Caseras, X, Dandash, O, Dannlowski, U, Delvecchio, G, Diaz-Zuluaga, AM, Dima, D, Duchesnay, E, Elvsashagen, T, Fears, SC, Frangou, S, Fullerton, JM, Glahn, DC, Goikolea, JM, Green, MJ, Grotegerd, D, Gruber, O, Haarman, BCM, Henry, C, Howells, FM, Ives-Deliperi, V, Jansen, A, Kircher, TTJ, Knoechel, C, Kramer, B, Lafer, B, Lopez-Jaramillo, C, Machado-Vieira, R, MacIntosh, BJ, Melloni, EMT, Mitchell, PB, Nenadic, I, Nery, F, Nugent, AC, Oertel, V, Ophoff, RA, Ota, M, Overs, BJ, Pham, DL, Phillips, ML, Pineda-Zapata, JA, Poletti, S, Polosan, M, Pomarol-Clotet, E, Pouchon, A, Quide, Y, Rive, MM, Roberts, G, Ruhe, HG, Salvador, R, Sarro, S, Satterthwaite, TD, Schene, AH, Sim, K, Soares, JC, Staeblein, M, Stein, DJ, Tamnes, CK, Thomaidis, GV, Upegui, CV, Veltman, DJ, Wessa, M, Westlye, LT, Whalley, HC, Wolf, DH, Wu, M-J, Yatham, LN, Zarate, CA, Thompson, PM, and Andreassen, OA

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.

Published
2022

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

Author

Haukvik, UK, Gurholt, TP, Nerland, S, Elvsashagen, T, Akudjedu, TN, Alda, M, Alnaes, D, Alonso-Lana, S, Bauer, J, Baune, BT, Benedetti, F, Berk, M, Bettella, F, Boen, E, Bonnin, CM, Brambilla, P, Canales-Rodriguez, EJ, Cannon, DM, Caseras, X, Dandash, O, Dannlowski, U, Delvecchio, G, Diaz-Zuluaga, AM, Erp, TGM, Fatjo-Vilas, M, Foley, SF, Foerster, K, Fullerton, JM, Goikolea, JM, Grotegerd, D, Gruber, O, Haarman, BCM, Haatveit, B, Hajek, T, Hallahan, B, Harris, M, Hawkins, EL, Howells, FM, Huelsmann, C, Jahanshad, N, Jorgensen, KN, Kircher, T, Kraemer, B, Krug, A, Kuplicki, R, Lagerberg, T, Lancaster, TM, Lenroot, RK, Lonning, V, Lopez-Jaramillo, C, Malt, UF, McDonald, C, McIntosh, AM, McPhilemy, G, Meer, D, Melle, I, Melloni, EMT, Mitchell, PB, Nabulsi, L, Nenadic, I, Oertel, V, Oldani, L, Opel, N, Otaduy, MCG, Overs, BJ, Pineda-Zapata, JA, Pomarol-Clotet, E, Radua, J, Rauer, L, Redlich, R, Repple, J, Rive, MM, Roberts, G, Ruhe, HG, Salminen, LE, Salvador, R, Sarro, S, Savitz, J, Schene, AH, Sim, K, Soeiro-de-Souza, MG, Staeblein, M, Stein, DJ, Stein, F, Tamnes, CK, Temmingh, HS, Thomopoulos, S, Veltman, DJ, Vieta, E, Waltemate, L, Westlye, LT, Whalley, HC, Saemann, PG, Thompson, PM, Ching, CRK, Andreassen, OA, Agartz, I, Haukvik, UK, Gurholt, TP, Nerland, S, Elvsashagen, T, Akudjedu, TN, Alda, M, Alnaes, D, Alonso-Lana, S, Bauer, J, Baune, BT, Benedetti, F, Berk, M, Bettella, F, Boen, E, Bonnin, CM, Brambilla, P, Canales-Rodriguez, EJ, Cannon, DM, Caseras, X, Dandash, O, Dannlowski, U, Delvecchio, G, Diaz-Zuluaga, AM, Erp, TGM, Fatjo-Vilas, M, Foley, SF, Foerster, K, Fullerton, JM, Goikolea, JM, Grotegerd, D, Gruber, O, Haarman, BCM, Haatveit, B, Hajek, T, Hallahan, B, Harris, M, Hawkins, EL, Howells, FM, Huelsmann, C, Jahanshad, N, Jorgensen, KN, Kircher, T, Kraemer, B, Krug, A, Kuplicki, R, Lagerberg, T, Lancaster, TM, Lenroot, RK, Lonning, V, Lopez-Jaramillo, C, Malt, UF, McDonald, C, McIntosh, AM, McPhilemy, G, Meer, D, Melle, I, Melloni, EMT, Mitchell, PB, Nabulsi, L, Nenadic, I, Oertel, V, Oldani, L, Opel, N, Otaduy, MCG, Overs, BJ, Pineda-Zapata, JA, Pomarol-Clotet, E, Radua, J, Rauer, L, Redlich, R, Repple, J, Rive, MM, Roberts, G, Ruhe, HG, Salminen, LE, Salvador, R, Sarro, S, Savitz, J, Schene, AH, Sim, K, Soeiro-de-Souza, MG, Staeblein, M, Stein, DJ, Stein, F, Tamnes, CK, Temmingh, HS, Thomopoulos, S, Veltman, DJ, Vieta, E, Waltemate, L, Westlye, LT, Whalley, HC, Saemann, PG, Thompson, PM, Ching, CRK, Andreassen, OA, and Agartz, I

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.

Published
2022

5. Consensus on nomenclature for clinical staging models in bipolar disorder: A narrative review from the International Society for Bipolar Disorders (ISBD) Staging Task Force

Author

Kupka R, Duffy A, Scott J, Almeida J, Balanza-Martinez V, Birmaher B, Bond D, Brietzke E, Chendo I, Frey B, Grande I, Hafeman D, Hajek T, Hillegers M, Kauer-Sant'Anna M, Mansur R, van der Markt A, Post R, Tohen M, Tremain H, Vazquez G, Vieta E, Yatham L, Berk M, Alda M, and Kapczinski F

Subjects
bipolar disorders, clinical staging, nomenclature
Abstract

Objectives Clinical staging is widely used in medicine to map disease progression, inform prognosis, and guide treatment decisions; in psychiatry, however, staging remains a hypothetical construct. To facilitate future research in bipolar disorders (BD), a well-defined nomenclature is needed, especially since diagnosis is often imprecise with blurred boundaries, and a full understanding of pathophysiology is lacking. Methods Under the auspices of the International Society of Bipolar Disorders, a Task Force of international experts was convened to review, discuss, and integrate findings from the scientific literature relevant to the development of a consensus staging model and standardize a terminology that could be used to advance future research including staging of BD and related disorders. Results Consensus opinion and areas of uncertainty or difference were identified in regard to terms referring to staging as it may apply to BD, to at-risk status and subthreshold stages, and to various clinical stages of BD as it is currently diagnosed. Conclusion The use of a standardized nomenclature about the clinical stages of BD will facilitate communication about research on clinical and pathological components of this heterogeneous group of disorders. The concepts presented are based on current evidence, but the template provided allows for further refinements as etiological advances come to light.

Published
2021

6. Consensus on nomenclature for clinical staging models in bipolar disorder: A narrative review from the International Society for Bipolar Disorders (ISBD) Staging Task Force

Author

Kupka, R, Duffy, A, Scott, J, Almeida, J, Balanzá-Martínez, V, Birmaher, B, Bond, DJ, Brietzke, E, Chendo, I, Frey, BN, Grande, I, Hafeman, D, Hajek, T, Hillegers, M, Kauer-Sant’Anna, M, Mansur, RB, van der Markt, A, Post, R, Tohen, M, Tremain, H, Vazquez, G, Vieta, E, Yatham, LN, Berk, Michael, Alda, M, Kapczinski, F, Kupka, R, Duffy, A, Scott, J, Almeida, J, Balanzá-Martínez, V, Birmaher, B, Bond, DJ, Brietzke, E, Chendo, I, Frey, BN, Grande, I, Hafeman, D, Hajek, T, Hillegers, M, Kauer-Sant’Anna, M, Mansur, RB, van der Markt, A, Post, R, Tohen, M, Tremain, H, Vazquez, G, Vieta, E, Yatham, LN, Berk, Michael, Alda, M, and Kapczinski, F

Published
2021

7. What we learn about bipolar disorder from large-scale neuroimaging: Findings and future directions from the ENIGMA Bipolar Disorder Working Group

Author

Ching, CRK, Hibar, DP, Gurholt, TP, Nunes, A, Thomopoulos, SI, Abé, C, Agartz, I, Brouwer, RM, Cannon, DM, de Zwarte, SMC, Eyler, LT, Favre, P, Hajek, T, Haukvik, UK, Houenou, J, Landén, M, Lett, TA, McDonald, C, Nabulsi, L, Patel, Y, Pauling, ME, Paus, T, Radua, J, Soeiro-de-Souza, MG, Tronchin, G, van Haren, NEM, Vieta, E, Walter, H, Zeng, LL, Alda, M, Almeida, J, Alnæs, D, Alonso-Lana, S, Altimus, C, Bauer, M, Baune, BT, Bearden, CE, Bellani, M, Benedetti, F, Berk, Michael, Bilderbeck, AC, Blumberg, HP, Bøen, E, Bollettini, I, del Mar Bonnin, C, Brambilla, P, Canales-Rodríguez, EJ, Caseras, X, Dandash, O, Dannlowski, U, Delvecchio, G, Díaz-Zuluaga, AM, Dima, D, Duchesnay, É, Elvsåshagen, T, Fears, SC, Frangou, S, Fullerton, JM, Glahn, DC, Goikolea, JM, Green, MJ, Grotegerd, D, Gruber, O, Haarman, BCM, Henry, C, Howells, FM, Ives-Deliperi, V, Jansen, A, Kircher, TTJ, Knöchel, C, Kramer, B, Lafer, B, López-Jaramillo, C, Machado-Vieira, R, MacIntosh, BJ, Melloni, EMT, Mitchell, PB, Nenadic, I, Nery, F, Nugent, AC, Oertel, V, Ophoff, RA, Ota, M, Overs, BJ, Pham, DL, Phillips, ML, Pineda-Zapata, JA, Poletti, S, Polosan, M, Pomarol-Clotet, E, Pouchon, A, Quidé, Y, Rive, MM, Roberts, G, Ruhe, HG, Salvador, R, Sarró, S, Satterthwaite, TD, Schene, AH, Sim, K, Ching, CRK, Hibar, DP, Gurholt, TP, Nunes, A, Thomopoulos, SI, Abé, C, Agartz, I, Brouwer, RM, Cannon, DM, de Zwarte, SMC, Eyler, LT, Favre, P, Hajek, T, Haukvik, UK, Houenou, J, Landén, M, Lett, TA, McDonald, C, Nabulsi, L, Patel, Y, Pauling, ME, Paus, T, Radua, J, Soeiro-de-Souza, MG, Tronchin, G, van Haren, NEM, Vieta, E, Walter, H, Zeng, LL, Alda, M, Almeida, J, Alnæs, D, Alonso-Lana, S, Altimus, C, Bauer, M, Baune, BT, Bearden, CE, Bellani, M, Benedetti, F, Berk, Michael, Bilderbeck, AC, Blumberg, HP, Bøen, E, Bollettini, I, del Mar Bonnin, C, Brambilla, P, Canales-Rodríguez, EJ, Caseras, X, Dandash, O, Dannlowski, U, Delvecchio, G, Díaz-Zuluaga, AM, Dima, D, Duchesnay, É, Elvsåshagen, T, Fears, SC, Frangou, S, Fullerton, JM, Glahn, DC, Goikolea, JM, Green, MJ, Grotegerd, D, Gruber, O, Haarman, BCM, Henry, C, Howells, FM, Ives-Deliperi, V, Jansen, A, Kircher, TTJ, Knöchel, C, Kramer, B, Lafer, B, López-Jaramillo, C, Machado-Vieira, R, MacIntosh, BJ, Melloni, EMT, Mitchell, PB, Nenadic, I, Nery, F, Nugent, AC, Oertel, V, Ophoff, RA, Ota, M, Overs, BJ, Pham, DL, Phillips, ML, Pineda-Zapata, JA, Poletti, S, Polosan, M, Pomarol-Clotet, E, Pouchon, A, Quidé, Y, Rive, MM, Roberts, G, Ruhe, HG, Salvador, R, Sarró, S, Satterthwaite, TD, Schene, AH, and Sim, K

Published
2020

8. Call to action regarding the vascular-bipolar link: A report from the Vascular Task Force of the International Society for Bipolar Disorders

Author

Goldstein, BI, Baune, BT, Bond, DJ, Chen, P-H, Eyler, L, Fagiolini, A, Gomes, F, Hajek, T, Hatch, J, McElroy, SL, McIntyre, RS, Prieto, M, Sylvia, LG, Tsai, S-Y, Kcomt, A, Fiedorowicz, JG, Goldstein, BI, Baune, BT, Bond, DJ, Chen, P-H, Eyler, L, Fagiolini, A, Gomes, F, Hajek, T, Hatch, J, McElroy, SL, McIntyre, RS, Prieto, M, Sylvia, LG, Tsai, S-Y, Kcomt, A, and Fiedorowicz, JG

Abstract

OBJECTIVES: The association of bipolar disorder with early and excessive cardiovascular disease was identified over a century ago. Nonetheless, the vascular-bipolar link remains underrecognized, particularly with regard to how this link can contribute to our understanding of pathogenesis and treatment. METHODS: An international group of experts completed a selective review of the literature, distilling core themes, identifying limitations and gaps in the literature, and highlighting future directions to bridge these gaps. RESULTS: The association between bipolar disorder and vascular disease is large in magnitude, consistent across studies, and independent of confounding variables where assessed. The vascular-bipolar link is multifactorial and is difficult to study given the latency between the onset of bipolar disorder, often in adolescence or early adulthood, and subsequent vascular disease, which usually occurs decades later. As a result, studies have often focused on risk factors for vascular disease or intermediate phenotypes, such as structural and functional vascular imaging measures. There is interest in identifying the most relevant mediators of this relationship, including lifestyle (eg, smoking, diet, exercise), medications, and systemic biological mediators (eg, inflammation). Nonetheless, there is a paucity of treatment studies that deliberately engage these mediators, and thus far no treatment studies have focused on engaging vascular imaging targets. CONCLUSIONS: Further research focused on the vascular-bipolar link holds promise for gleaning insights regarding the underlying causes of bipolar disorder, identifying novel treatment approaches, and mitigating disparities in cardiovascular outcomes for people with bipolar disorder.

Published
2020

9. Refined diagnostic criteria for the bipolar disorders: phase two of the AREDOC project

Author

Parker, G., primary, Tavella, G., additional, Ricciardi, T., additional, Hadzi‐Pavlovic, D., additional, Alda, M., additional, Hajek, T., additional, Dunner, D. L., additional, O'Donovan, C., additional, Rybakowski, J. K., additional, Goldberg, J. F., additional, Bayes, A., additional, Sharma, V., additional, Boyce, P., additional, and Manicavasagar, V., additional

Published
2020
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10. What is the optimal serum level for lithium in the maintenance treatment of bipolar disorder? A systematic review and recommendations from the ISBD/IGSLI Task Force on treatment with lithium

Author

Nolen, WA, Licht, RW, Young, AH, Malhi, GS, Tohen, M, Vieta, E, Kupka, RW, Zarate, C, Nielsen, RE, Baldessarini, RJ, Severus, E, Alda, M, Bauer, M, Berghoefer, A, Berk, M, Bocchetta, A, Calkin, CV, Duffy, A, Fountoulakis, KN, Gonzalez-Pinto, A, Hajek, T, Kessing, LV, Lopez-Jaramillo, C, Machado-Vieira, R, Post, RM, Rybakowski, JK, Simhandl, C, Soares, JC, Tondo, L, Nolen, WA, Licht, RW, Young, AH, Malhi, GS, Tohen, M, Vieta, E, Kupka, RW, Zarate, C, Nielsen, RE, Baldessarini, RJ, Severus, E, Alda, M, Bauer, M, Berghoefer, A, Berk, M, Bocchetta, A, Calkin, CV, Duffy, A, Fountoulakis, KN, Gonzalez-Pinto, A, Hajek, T, Kessing, LV, Lopez-Jaramillo, C, Machado-Vieira, R, Post, RM, Rybakowski, JK, Simhandl, C, Soares, JC, and Tondo, L

Abstract

AIMS: To systematically review the existing trials on optimal serum levels for lithium for maintenance treatment of bipolar disorder and to develop clinical recommendations. METHODS: Systematic literature search. Discussion of major characteristics, limitations, methodological quality, and results of selected trials. Delphi survey consisting of clinical questions and corresponding statements. For statements endorsed by at least 80% of the members, consensus was considered as having been achieved. RESULTS: With strict inclusion criteria no studies could be selected, making it difficult to formulate evidence-based recommendations. After loosening the inclusion criteria 7 trials were selected addressing our aims at least to some extent. Four of these studies suggest better efficacy being associated with lithium serum levels in a range above a lower threshold around 0.45/0.60 and up to 0.80/1.00 mmol/L. These findings support the outcome of the Delphi survey. CONCLUSIONS: For adults with bipolar disorder there was consensus that the standard lithium serum level should be 0.60-0.80 mmol/L with the option to reduce it to 0.40-0.60 mmol/L in case of good response but poor tolerance or to increase it to 0.80-1.00 mmol/L in case of insufficient response and good tolerance. For children and adolescents there was no consensus, but the majority of the members endorsed the same recommendation. For the elderly there was also no consensus, but the majority of the members endorsed a more conservative approach: usually 0.40-0.60 mmol/L, with the option to go to maximally 0.70 or 0.80 mmol/L at ages 65-79 years, and to maximally 0.70 mmol/L over age 80 years.

Published
2019

11. Prediction of lithium response using clinical data

Author

Nunes, A., primary, Ardau, R., additional, Berghöfer, A., additional, Bocchetta, A., additional, Chillotti, C., additional, Deiana, V., additional, Garnham, J., additional, Grof, E., additional, Hajek, T., additional, Manchia, M., additional, Müller‐Oerlinghausen, B., additional, Pinna, M., additional, Pisanu, C., additional, O’Donovan, C., additional, Severino, G., additional, Slaney, C., additional, Suwalska, A., additional, Zvolsky, P., additional, Cervantes, P., additional, Zompo, M., additional, Grof, P., additional, Rybakowski, J., additional, Tondo, L., additional, Trappenberg, T., additional, and Alda, M., additional

Published
2019
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12. Cerebellar parcellation in schizophrenia and bipolar disorder

Author

Laidi, C., primary, Hajek, T., additional, Spaniel, F., additional, Kolenic, M., additional, d'Albis, M.‐A., additional, Sarrazin, S., additional, Mangin, J.‐F., additional, Duchesnay, E., additional, Brambilla, P., additional, Wessa, M., additional, Linke, J., additional, Polosan, M., additional, Favre, P., additional, Versace, A. L., additional, Phillips, M. L., additional, Manjon, J. V., additional, Romero, J. E., additional, Hozer, F., additional, Leboyer, M., additional, Coupe, P., additional, and Houenou, J., additional

Published
2019
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13. Identifying a neuroanatomical signature of schizophrenia, reproducible across sites and stages, using machine learning with structured sparsity

Author

de Pierrefeu, A., primary, Löfstedt, T., additional, Laidi, C., additional, Hadj‐Selem, F., additional, Bourgin, J., additional, Hajek, T., additional, Spaniel, F., additional, Kolenic, M., additional, Ciuciu, P., additional, Hamdani, N., additional, Leboyer, M., additional, Fovet, T., additional, Jardri, R., additional, Houenou, J., additional, and Duchesnay, E., additional

Published
2018
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16. Principal component analysis as an efficient method for capturing multivariate brain signatures of complex disorders-ENIGMA study in people with bipolar disorders and obesity.

Author

McWhinney SR, Hlinka J, Bakstein E, Dietze LMF, Corkum ELV, Abé C, Alda M, Alexander N, Benedetti F, Berk M, Bøen E, Bonnekoh LM, Boye B, Brosch K, Canales-Rodríguez EJ, Cannon DM, Dannlowski U, Demro C, Diaz-Zuluaga A, Elvsåshagen T, Eyler LT, Fortea L, Fullerton JM, Goltermann J, Gotlib IH, Grotegerd D, Haarman B, Hahn T, Howells FM, Jamalabadi H, Jansen A, Kircher T, Klahn AL, Kuplicki R, Lahud E, Landén M, Leehr EJ, Lopez-Jaramillo C, Mackey S, Malt U, Martyn F, Mazza E, McDonald C, McPhilemy G, Meier S, Meinert S, Melloni E, Mitchell PB, Nabulsi L, Nenadić I, Nitsch R, Opel N, Ophoff RA, Ortuño M, Overs BJ, Pineda-Zapata J, Pomarol-Clotet E, Radua J, Repple J, Roberts G, Rodriguez-Cano E, Sacchet MD, Salvador R, Savitz J, Scheffler F, Schofield PR, Schürmeyer N, Shen C, Sim K, Sponheim SR, Stein DJ, Stein F, Straube B, Suo C, Temmingh H, Teutenberg L, Thomas-Odenthal F, Thomopoulos SI, Urosevic S, Usemann P, van Haren NEM, Vargas C, Vieta E, Vilajosana E, Vreeker A, Winter NR, Yatham LN, Thompson PM, Andreassen OA, Ching CRK, and Hajek T

Subjects
Humans, Adult, Female, Male, Middle Aged, Schizophrenia diagnostic imaging, Schizophrenia pathology, Schizophrenia drug therapy, Schizophrenia physiopathology, Cerebral Cortex diagnostic imaging, Cerebral Cortex pathology, Cluster Analysis, Young Adult, Brain diagnostic imaging, Brain pathology, Bipolar Disorder diagnostic imaging, Bipolar Disorder drug therapy, Bipolar Disorder pathology, Principal Component Analysis, Magnetic Resonance Imaging methods, Obesity diagnostic imaging
Abstract

Multivariate techniques better fit the anatomy of complex neuropsychiatric disorders which are characterized not by alterations in a single region, but rather by variations across distributed brain networks. Here, we used principal component analysis (PCA) to identify patterns of covariance across brain regions and relate them to clinical and demographic variables in a large generalizable dataset of individuals with bipolar disorders and controls. We then compared performance of PCA and clustering on identical sample to identify which methodology was better in capturing links between brain and clinical measures. Using data from the ENIGMA-BD working group, we investigated T1-weighted structural MRI data from 2436 participants with BD and healthy controls, and applied PCA to cortical thickness and surface area measures. We then studied the association of principal components with clinical and demographic variables using mixed regression models. We compared the PCA model with our prior clustering analyses of the same data and also tested it in a replication sample of 327 participants with BD or schizophrenia and healthy controls. The first principal component, which indexed a greater cortical thickness across all 68 cortical regions, was negatively associated with BD, BMI, antipsychotic medications, and age and was positively associated with Li treatment. PCA demonstrated superior goodness of fit to clustering when predicting diagnosis and BMI. Moreover, applying the PCA model to the replication sample yielded significant differences in cortical thickness between healthy controls and individuals with BD or schizophrenia. Cortical thickness in the same widespread regional network as determined by PCA was negatively associated with different clinical and demographic variables, including diagnosis, age, BMI, and treatment with antipsychotic medications or lithium. PCA outperformed clustering and provided an easy-to-use and interpret method to study multivariate associations between brain structure and system-level variables. PRACTITIONER POINTS: In this study of 2770 Individuals, we confirmed that cortical thickness in widespread regional networks as determined by principal component analysis (PCA) was negatively associated with relevant clinical and demographic variables, including diagnosis, age, BMI, and treatment with antipsychotic medications or lithium. Significant associations of many different system-level variables with the same brain network suggest a lack of one-to-one mapping of individual clinical and demographic factors to specific patterns of brain changes. PCA outperformed clustering analysis in the same data set when predicting group or BMI, providing a superior method for studying multivariate associations between brain structure and system-level variables., (© 2024 The Authors. Human Brain Mapping published by Wiley Periodicals LLC.)

Published
2024
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17. In vivo hippocampal subfield volumes in bipolar disorder-A mega-analysis from The Enhancing Neuro Imaging Genetics through Meta-Analysis Bipolar Disorder Working Group.

Author

Haukvik UK, Gurholt TP, Nerland S, Elvsåshagen T, Akudjedu TN, Alda M, Alnaes D, Alonso-Lana S, Bauer J, Baune BT, Benedetti F, Berk M, Bettella F, Bøen E, Bonnín CM, Brambilla P, Canales-Rodríguez EJ, Cannon DM, Caseras X, Dandash O, Dannlowski U, Delvecchio G, Díaz-Zuluaga AM, van Erp TGM, Fatjó-Vilas M, Foley SF, Förster K, Fullerton JM, Goikolea JM, Grotegerd D, Gruber O, Haarman BCM, Haatveit B, Hajek T, Hallahan B, Harris M, Hawkins EL, Howells FM, Hülsmann C, Jahanshad N, Jørgensen KN, Kircher T, Krämer B, Krug A, Kuplicki R, Lagerberg TV, Lancaster TM, Lenroot RK, Lonning V, López-Jaramillo C, Malt UF, McDonald C, McIntosh AM, McPhilemy G, van der Meer D, Melle I, Melloni EMT, Mitchell PB, Nabulsi L, Nenadić I, Oertel V, Oldani L, Opel N, Otaduy MCG, Overs BJ, Pineda-Zapata JA, Pomarol-Clotet E, Radua J, Rauer L, Redlich R, Repple J, Rive MM, Roberts G, Ruhe HG, Salminen LE, Salvador R, Sarró S, Savitz J, Schene AH, Sim K, Soeiro-de-Souza MG, Stäblein M, Stein DJ, Stein F, Tamnes CK, Temmingh HS, Thomopoulos SI, Veltman DJ, Vieta E, Waltemate L, Westlye LT, Whalley HC, Sämann PG, Thompson PM, Ching CRK, Andreassen OA, and Agartz I

Subjects
Bipolar Disorder drug therapy, Genetics, Hippocampus drug effects, Humans, Bipolar Disorder diagnostic imaging, Bipolar Disorder pathology, Hippocampus diagnostic imaging, Hippocampus pathology, Magnetic Resonance Imaging, Neuroimaging
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., (© 2020 The Authors. Human Brain Mapping published by Wiley Periodicals LLC.)

Published
2022
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18. Intelligence, educational attainment, and brain structure in those at familial high-risk for schizophrenia or bipolar disorder.

Author

de Zwarte SMC, Brouwer RM, Agartz I, Alda M, Alonso-Lana S, Bearden CE, Bertolino A, Bonvino A, Bramon E, Buimer EEL, Cahn W, Canales-Rodríguez EJ, Cannon DM, Cannon TD, Caseras X, Castro-Fornieles J, Chen Q, Chung Y, De la Serna E, Del Mar Bonnin C, Demro C, Di Giorgio A, Doucet GE, Eker MC, Erk S, Fatjó-Vilas M, Fears SC, Foley SF, Frangou S, Fullerton JM, Glahn DC, Goghari VM, Goikolea JM, Goldman AL, Gonul AS, Gruber O, Hajek T, Hawkins EL, Heinz A, Hidiroglu Ongun C, Hillegers MHJ, Houenou J, Hulshoff Pol HE, Hultman CM, Ingvar M, Johansson V, Jönsson EG, Kane F, Kempton MJ, Koenis MMG, Kopecek M, Krämer B, Lawrie SM, Lenroot RK, Marcelis M, Mattay VS, McDonald C, Meyer-Lindenberg A, Michielse S, Mitchell PB, Moreno D, Murray RM, Mwangi B, Nabulsi L, Newport J, Olman CA, van Os J, Overs BJ, Ozerdem A, Pergola G, Picchioni MM, Piguet C, Pomarol-Clotet E, Radua J, Ramsay IS, Richter A, Roberts G, Salvador R, Saricicek Aydogan A, Sarró S, Schofield PR, Simsek EM, Simsek F, Soares JC, Sponheim SR, Sugranyes G, Toulopoulou T, Tronchin G, Vieta E, Walter H, Weinberger DR, Whalley HC, Wu MJ, Yalin N, Andreassen OA, Ching CRK, Thomopoulos SI, van Erp TGM, Jahanshad N, Thompson PM, Kahn RS, and van Haren NEM

Subjects
Bipolar Disorder complications, Bipolar Disorder diagnostic imaging, Cognitive Dysfunction diagnostic imaging, Family, Humans, Magnetic Resonance Imaging, Schizophrenia complications, Schizophrenia diagnostic imaging, Schizophrenia etiology, Bipolar Disorder pathology, Cognitive Dysfunction pathology, Educational Status, Genetic Predisposition to Disease, Intelligence physiology, Neuroimaging, Schizophrenia pathology
Abstract

First-degree relatives of patients diagnosed with schizophrenia (SZ-FDRs) show similar patterns of brain abnormalities and cognitive alterations to patients, albeit with smaller effect sizes. First-degree relatives of patients diagnosed with bipolar disorder (BD-FDRs) show divergent patterns; on average, intracranial volume is larger compared to controls, and findings on cognitive alterations in BD-FDRs are inconsistent. Here, we performed a meta-analysis of global and regional brain measures (cortical and subcortical), current IQ, and educational attainment in 5,795 individuals (1,103 SZ-FDRs, 867 BD-FDRs, 2,190 controls, 942 schizophrenia patients, 693 bipolar patients) from 36 schizophrenia and/or bipolar disorder family cohorts, with standardized methods. Compared to controls, SZ-FDRs showed a pattern of widespread thinner cortex, while BD-FDRs had widespread larger cortical surface area. IQ was lower in SZ-FDRs (d = -0.42, p = 3 × 10 -5 ), with weak evidence of IQ reductions among BD-FDRs (d = -0.23, p = .045). Both relative groups had similar educational attainment compared to controls. When adjusting for IQ or educational attainment, the group-effects on brain measures changed, albeit modestly. Changes were in the expected direction, with less pronounced brain abnormalities in SZ-FDRs and more pronounced effects in BD-FDRs. To conclude, SZ-FDRs and BD-FDRs show a differential pattern of structural brain abnormalities. In contrast, both had lower IQ scores and similar school achievements compared to controls. Given that brain differences between SZ-FDRs and BD-FDRs remain after adjusting for IQ or educational attainment, we suggest that differential brain developmental processes underlying predisposition for schizophrenia or bipolar disorder are likely independent of general cognitive impairment., (© 2020 The Authors. Human Brain Mapping published by Wiley Periodicals LLC.)

Published
2022
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19. What we learn about bipolar disorder from large-scale neuroimaging: Findings and future directions from the ENIGMA Bipolar Disorder Working Group.

Author

Ching CRK, Hibar DP, Gurholt TP, Nunes A, Thomopoulos SI, Abé C, Agartz I, Brouwer RM, Cannon DM, de Zwarte SMC, Eyler LT, Favre P, Hajek T, Haukvik UK, Houenou J, Landén M, Lett TA, McDonald C, Nabulsi L, Patel Y, Pauling ME, Paus T, Radua J, Soeiro-de-Souza MG, Tronchin G, van Haren NEM, Vieta E, Walter H, Zeng LL, Alda M, Almeida J, Alnaes D, Alonso-Lana S, Altimus C, Bauer M, Baune BT, Bearden CE, Bellani M, Benedetti F, Berk M, Bilderbeck AC, Blumberg HP, Bøen E, Bollettini I, Del Mar Bonnin C, Brambilla P, Canales-Rodríguez EJ, Caseras X, Dandash O, Dannlowski U, Delvecchio G, Díaz-Zuluaga AM, Dima D, Duchesnay É, Elvsåshagen T, Fears SC, Frangou S, Fullerton JM, Glahn DC, Goikolea JM, Green MJ, Grotegerd D, Gruber O, Haarman BCM, Henry C, Howells FM, Ives-Deliperi V, Jansen A, Kircher TTJ, Knöchel C, Kramer B, Lafer B, López-Jaramillo C, Machado-Vieira R, MacIntosh BJ, Melloni EMT, Mitchell PB, Nenadic I, Nery F, Nugent AC, Oertel V, Ophoff RA, Ota M, Overs BJ, Pham DL, Phillips ML, Pineda-Zapata JA, Poletti S, Polosan M, Pomarol-Clotet E, Pouchon A, Quidé Y, Rive MM, Roberts G, Ruhe HG, Salvador R, Sarró S, Satterthwaite TD, Schene AH, Sim K, Soares JC, Stäblein M, Stein DJ, Tamnes CK, Thomaidis GV, Upegui CV, Veltman DJ, Wessa M, Westlye LT, Whalley HC, Wolf DH, Wu MJ, Yatham LN, Zarate CA, Thompson PM, and Andreassen OA

Subjects
Humans, Meta-Analysis as Topic, Multicenter Studies as Topic, Bipolar Disorder diagnostic imaging, Bipolar Disorder pathology, Cerebral Cortex diagnostic imaging, Cerebral Cortex pathology, Magnetic Resonance Imaging, Neuroimaging
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., (© 2020 The Authors. Human Brain Mapping published by Wiley Periodicals LLC.)

Published
2022
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