Search

Your search keyword '"Cannon, D"' showing total 14 results
Start Over Author "Cannon, D" Topic bipolar disorder
14 results on '"Cannon, D"'

1. Lithium prevents grey matter atrophy in patients with bipolar disorder: an international multicenter study.

Author

Hozer F, Sarrazin S, Laidi C, Favre P, Pauling M, Cannon D, McDonald C, Emsell L, Mangin JF, Duchesnay E, Bellani M, Brambilla P, Wessa M, Linke J, Polosan M, Versace A, Phillips ML, Delavest M, Bellivier F, Hamdani N, d'Albis MA, Leboyer M, and Houenou J

Subjects
Adult, Case-Control Studies, Female, Gyrus Cinguli pathology, Hippocampus pathology, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Temporal Lobe pathology, Antimanic Agents therapeutic use, Atrophy prevention & control, Bipolar Disorder drug therapy, Gray Matter pathology, Lithium Compounds therapeutic use
Abstract

Background: Lithium (Li) is the gold standard treatment for bipolar disorder (BD). However, its mechanisms of action remain unknown but include neurotrophic effects. We here investigated the influence of Li on cortical and local grey matter (GM) volumes in a large international sample of patients with BD and healthy controls (HC)., Methods: We analyzed high-resolution T1-weighted structural magnetic resonance imaging scans of 271 patients with BD type I (120 undergoing Li) and 316 HC. Cortical and local GM volumes were compared using voxel-wise approaches with voxel-based morphometry and SIENAX using FSL. We used multiple linear regression models to test the influence of Li on cortical and local GM volumes, taking into account potential confounding factors such as a history of alcohol misuse., Results: Patients taking Li had greater cortical GM volume than patients without. Patients undergoing Li had greater regional GM volumes in the right middle frontal gyrus, the right anterior cingulate gyrus, and the left fusiform gyrus in comparison with patients not taking Li., Conclusions: Our results in a large multicentric sample support the hypothesis that Li could exert neurotrophic and neuroprotective effects limiting pathological GM atrophy in key brain regions associated with BD.

Published
2021
Full Text
View/download PDF

2. Cortical abnormalities in bipolar disorder: an MRI analysis of 6503 individuals from the ENIGMA Bipolar Disorder Working Group.

Author

Hibar DP, Westlye LT, Doan NT, Jahanshad N, Cheung JW, Ching CRK, Versace A, Bilderbeck AC, Uhlmann A, Mwangi B, Krämer B, Overs B, Hartberg CB, Abé C, Dima D, Grotegerd D, Sprooten E, Bøen E, Jimenez E, Howells FM, Delvecchio G, Temmingh H, Starke J, Almeida JRC, Goikolea JM, Houenou J, Beard LM, Rauer L, Abramovic L, Bonnin M, Ponteduro MF, Keil M, Rive MM, Yao N, Yalin N, Najt P, Rosa PG, Redlich R, Trost S, Hagenaars S, Fears SC, Alonso-Lana S, van Erp TGM, Nickson T, Chaim-Avancini TM, Meier TB, Elvsåshagen T, Haukvik UK, Lee WH, Schene AH, Lloyd AJ, Young AH, Nugent A, Dale AM, Pfennig A, McIntosh AM, Lafer B, Baune BT, Ekman CJ, Zarate CA, Bearden CE, Henry C, Simhandl C, McDonald C, Bourne C, Stein DJ, Wolf DH, Cannon DM, Glahn DC, Veltman DJ, Pomarol-Clotet E, Vieta E, Canales-Rodriguez EJ, Nery FG, Duran FLS, Busatto GF, Roberts G, Pearlson GD, Goodwin GM, Kugel H, Whalley HC, Ruhe HG, Soares JC, Fullerton JM, Rybakowski JK, Savitz J, Chaim KT, Fatjó-Vilas M, Soeiro-de-Souza MG, Boks MP, Zanetti MV, Otaduy MCG, Schaufelberger MS, Alda M, Ingvar M, Phillips ML, Kempton MJ, Bauer M, Landén M, Lawrence NS, van Haren NEM, Horn NR, Freimer NB, Gruber O, Schofield PR, Mitchell PB, Kahn RS, Lenroot R, Machado-Vieira R, Ophoff RA, Sarró S, Frangou S, Satterthwaite TD, Hajek T, Dannlowski U, Malt UF, Arolt V, Gattaz WF, Drevets WC, Caseras X, Agartz I, Thompson PM, and Andreassen OA

Subjects
Adolescent, Adult, Age Factors, Bipolar Disorder metabolism, Brain pathology, Case-Control Studies, Cerebral Cortex physiopathology, Female, Frontal Lobe pathology, Humans, Magnetic Resonance Imaging methods, Male, Middle Aged, Neuroimaging, Prefrontal Cortex pathology, Psychotic Disorders pathology, Sex Factors, Temporal Lobe pathology, Young Adult, Bipolar Disorder diagnostic imaging, Bipolar Disorder pathology, Gray Matter pathology
Abstract

Despite decades of research, the pathophysiology of bipolar disorder (BD) is still not well understood. Structural brain differences have been associated with BD, but results from neuroimaging studies have been inconsistent. To address this, we performed the largest study to date of cortical gray matter thickness and surface area measures from brain magnetic resonance imaging scans of 6503 individuals including 1837 unrelated adults with BD and 2582 unrelated healthy controls for group differences while also examining the effects of commonly prescribed medications, age of illness onset, history of psychosis, mood state, age and sex differences on cortical regions. In BD, cortical gray matter was thinner in frontal, temporal and parietal regions of both brain hemispheres. BD had the strongest effects on left pars opercularis (Cohen's d=-0.293; P=1.71 × 10 -21 ), left fusiform gyrus (d=-0.288; P=8.25 × 10 -21 ) and left rostral middle frontal cortex (d=-0.276; P=2.99 × 10 -19 ). Longer duration of illness (after accounting for age at the time of scanning) was associated with reduced cortical thickness in frontal, medial parietal and occipital regions. We found that several commonly prescribed medications, including lithium, antiepileptic and antipsychotic treatment showed significant associations with cortical thickness and surface area, even after accounting for patients who received multiple medications. We found evidence of reduced cortical surface area associated with a history of psychosis but no associations with mood state at the time of scanning. Our analysis revealed previously undetected associations and provides an extensive analysis of potential confounding variables in neuroimaging studies of BD.

Published
2018
Full Text
View/download PDF

3. Anatomical integration and rich-club connectivity in euthymic bipolar disorder.

Author

O'Donoghue S, Kilmartin L, O'Hora D, Emsell L, Langan C, McInerney S, Forde NJ, Leemans A, Jeurissen B, Barker GJ, McCarthy P, Cannon DM, and McDonald C

Subjects
Adult, Diffusion Magnetic Resonance Imaging methods, Female, Humans, Male, Middle Aged, Bipolar Disorder diagnostic imaging, Brain diagnostic imaging, Magnetic Resonance Imaging methods, Nerve Net diagnostic imaging
Abstract

Background: Although repeatedly associated with white matter microstructural alterations, bipolar disorder (BD) has been relatively unexplored using complex network analysis. This method combines structural and diffusion magnetic resonance imaging (MRI) to model the brain as a network and evaluate its topological properties. A group of highly interconnected high-density structures, termed the 'rich-club', represents an important network for integration of brain functioning. This study aimed to assess structural and rich-club connectivity properties in BD through graph theory analyses., Method: We obtained structural and diffusion MRI scans from 42 euthymic patients with BD type I and 43 age- and gender-matched healthy volunteers. Weighted fractional anisotropy connections mapped between cortical and subcortical structures defined the neuroanatomical networks. Next, we examined between-group differences in features of graph properties and sub-networks., Results: Patients exhibited significantly reduced clustering coefficient and global efficiency, compared with controls globally and regionally in frontal and occipital regions. Additionally, patients displayed weaker sub-network connectivity in distributed regions. Rich-club analysis revealed subtly reduced density in patients, which did not withstand multiple comparison correction. However, hub identification in most participants indicated differentially affected rich-club membership in the BD group, with two hubs absent when compared with controls, namely the superior frontal gyrus and thalamus., Conclusions: This graph theory analysis presents a thorough investigation of topological features of connectivity in euthymic BD. Abnormalities of global and local measures and network components provide further neuroanatomically specific evidence for distributed dysconnectivity as a trait feature of BD.

Published
2017
Full Text
View/download PDF

4. Subcortical volumetric abnormalities in bipolar disorder.

Author

Hibar DP, Westlye LT, van Erp TG, Rasmussen J, Leonardo CD, Faskowitz J, Haukvik UK, Hartberg CB, Doan NT, Agartz I, Dale AM, Gruber O, Krämer B, Trost S, Liberg B, Abé C, Ekman CJ, Ingvar M, Landén M, Fears SC, Freimer NB, Bearden CE, Sprooten E, Glahn DC, Pearlson GD, Emsell L, Kenney J, Scanlon C, McDonald C, Cannon DM, Almeida J, Versace A, Caseras X, Lawrence NS, Phillips ML, Dima D, Delvecchio G, Frangou S, Satterthwaite TD, Wolf D, Houenou J, Henry C, Malt UF, Bøen E, Elvsåshagen T, Young AH, Lloyd AJ, Goodwin GM, Mackay CE, Bourne C, Bilderbeck A, Abramovic L, Boks MP, van Haren NE, Ophoff RA, Kahn RS, Bauer M, Pfennig A, Alda M, Hajek T, Mwangi B, Soares JC, Nickson T, Dimitrova R, Sussmann JE, Hagenaars S, Whalley HC, McIntosh AM, Thompson PM, and Andreassen OA

Subjects
Adult, Brain anatomy & histology, Case-Control Studies, Female, Humans, Magnetic Resonance Imaging methods, Male, Middle Aged, Organ Size physiology, Retrospective Studies, Bipolar Disorder physiopathology, Brain physiopathology
Abstract

Considerable uncertainty exists about the defining brain changes associated with bipolar disorder (BD). Understanding and quantifying the sources of uncertainty can help generate novel clinical hypotheses about etiology and assist in the development of biomarkers for indexing disease progression and prognosis. Here we were interested in quantifying case-control differences in intracranial volume (ICV) and each of eight subcortical brain measures: nucleus accumbens, amygdala, caudate, hippocampus, globus pallidus, putamen, thalamus, lateral ventricles. In a large study of 1710 BD patients and 2594 healthy controls, we found consistent volumetric reductions in BD patients for mean hippocampus (Cohen's d=-0.232; P=3.50 × 10 -7 ) and thalamus (d=-0.148; P=4.27 × 10 -3 ) and enlarged lateral ventricles (d=-0.260; P=3.93 × 10 -5 ) in patients. No significant effect of age at illness onset was detected. Stratifying patients based on clinical subtype (BD type I or type II) revealed that BDI patients had significantly larger lateral ventricles and smaller hippocampus and amygdala than controls. However, when comparing BDI and BDII patients directly, we did not detect any significant differences in brain volume. This likely represents similar etiology between BD subtype classifications. Exploratory analyses revealed significantly larger thalamic volumes in patients taking lithium compared with patients not taking lithium. We detected no significant differences between BDII patients and controls in the largest such comparison to date. Findings in this study should be interpreted with caution and with careful consideration of the limitations inherent to meta-analyzed neuroimaging comparisons.

Published
2016
Full Text
View/download PDF

5. White matter microstructural abnormalities in families multiply affected with bipolar I disorder: a diffusion tensor tractography study.

Author

Emsell L, Chaddock C, Forde N, Van Hecke W, Barker GJ, Leemans A, Sunaert S, Walshe M, Bramon E, Cannon D, Murray R, and McDonald C

Subjects
Adult, Bipolar Disorder genetics, Family, Female, Humans, Male, Middle Aged, Pedigree, Young Adult, Bipolar Disorder pathology, Diffusion Tensor Imaging methods, Endophenotypes, White Matter pathology
Abstract

Background: White matter (WM) abnormalities are proposed as potential endophenotypic markers of bipolar disorder (BD). In a diffusion tensor imaging (DTI) voxel-based analysis (VBA) study of families multiply affected with BD, we previously reported that widespread abnormalities of fractional anisotropy (FA) are associated with both BD and genetic liability for illness. In the present study, we further investigated the endophenotypic potential of WM abnormalities by applying DTI tractography to specifically investigate tracts implicated in the pathophysiology of BD., Method: Diffusion magnetic resonance imaging (MRI) data were acquired from 19 patients with BD type I from multiply affected families, 21 of their unaffected first-degree relatives and 18 healthy volunteers. DTI tractography was used to identify the cingulum, uncinate fasciculus (UF), arcuate portion of the superior longitudinal fasciculus (SLF), inferior longitudinal fasciculus (ILF), corpus callosum, and the anterior limb of the internal capsule (ALIC). Regression analyses were conducted to investigate the effect of participant group and genetic liability on FA and radial diffusivity (RD) in each tract., Results: We detected a significant effect of group on both FA and RD in the cingulum, SLF, callosal splenium and ILF driven by reduced FA and increased RD in patients compared to controls and relatives. Increasing genetic liability was associated with decreased FA and increased RD in the UF, and decreased FA in the SLF, among patients., Conclusions: WM microstructural abnormalities in limbic, temporal and callosal pathways represent microstructural abnormalities associated with BD whereas alterations in the SLF and UF may represent potential markers of endophenotypic risk.

Published
2014
Full Text
View/download PDF

6. Genetic variation in cholinergic muscarinic-2 receptor gene modulates M2 receptor binding in vivo and accounts for reduced binding in bipolar disorder.

Author

Cannon DM, Klaver JK, Gandhi SK, Solorio G, Peck SA, Erickson K, Akula N, Savitz J, Eckelman WC, Furey ML, Sahakian BJ, McMahon FJ, and Drevets WC

Subjects
Adolescent, Adult, Bipolar Disorder complications, Bipolar Disorder diagnostic imaging, Cognition Disorders diagnosis, Cognition Disorders etiology, Female, Fluorine Radioisotopes, Genome-Wide Association Study, Genotype, Humans, Male, Middle Aged, Neuropsychological Tests, Positron-Emission Tomography methods, Protein Binding drug effects, Protein Binding genetics, Psychiatric Status Rating Scales, Statistics, Nonparametric, Young Adult, Bipolar Disorder genetics, Brain diagnostic imaging, Brain metabolism, Polymorphism, Single Nucleotide genetics, Receptor, Muscarinic M2 genetics, Receptor, Muscarinic M2 metabolism
Abstract

Genetic variation in the cholinergic muscarinic-2 (M(2)) receptor gene (CHRM2) has been associated with the risk for developing depression. We previously reported that M(2)-receptor distribution volume (V(T)) was reduced in depressed subjects with bipolar disorder (BD) relative to depressed subjects with major depressive disorder (MDD) and healthy controls (HCs). In this study, we investigated the effects of six single-nucleotide polymorphisms (SNPs) for CHRM2 on M(2)-receptor binding to test the hypotheses that genetic variation in CHRM2 influences M(2)-receptor binding and that a CHRM2 polymorphism underlies the deficits in M(2)-receptor V(T) observed in BD. The M(2)-receptor V(T) was measured using positron emission tomography and [(18)F]FP-TZTP in unmedicated, depressed subjects with BD (n=16) or MDD (n=24) and HCs (n=25), and the effect of genotype on V(T) was assessed. In the controls, one SNP (with identifier rs324650, in which the ancestral allele adenine (A) is replaced with one or two copies of thymine (T), showed a significant allelic effect on V(T) in the pregenual and subgenual anterior cingulate cortices in the direction AA

Published
2011
Full Text
View/download PDF

7. The Association between familial risk and brain abnormalities Is disease specific: an ENIGMA-relatives study of schizophrenia and bipolar disorder

Author

Zwarte, S. M. C., Brouwer, R. M., Agartz, I., Alda, M., Aleman, A., Alpert, K. I., Bearden, C. E., Bertolino, A., Bois, C., Bonvino, A., Bramon, E., Buimer, E., Cahn, W., Cannon, D. M., Cannon, T. D., Caseras, X., Castro-Fornieles, J., Chen, Q., Serna, E., Giorgio, A. D., Doucet, G., Eker, M. C., Erk, S., Fears, S., Foley, S., Frangou, S., Frankland, A., Fullerton, J., Glahn, D., Goghari, V., Goldman, A., Gonul, A., Gruber, O., Haan, L., Hajek, T., Hawkins, E., Heinz, A., Hillegers, M., Pol, H., Hultman, C., Ingvar, M., Johansson, V., Jönsson, E., Kane, K., Kempton, M., Koenis, M., Kopecek, M., Krabbendam, L., Krämer, B., Lawrie, S., Lenroot, R., Marcelis, M., Marsman, J-B, Mattay, V., McDonald, C., Meyer-Lindenberg, A., Michielse, S., Mitchell, P., Moreno, D., Murray, R., Mwangi, B., Najt, P., Neilson, E., Newport, J., Os, J., Overs, B., Özerdem, A., Picchioni, M., Richter, A., Roberts, G., Aydoğan, A. S., Schofield, P., Şimşek, F., Soares, J., Sugranyes, G., Toulopoulou, Timothea, Tronchin, G., Walter, H., Wang, L., Weinberger, D., Whalley, H., Yalın, N., Andreassen, O., Ching, C., Erp, T., Turner, J., Jahanshad, N., Thompson, P., Kahn, R., Haren, N., and Toulopoulou, Timothea

Subjects
Meta-analysis, Familial riskImaging, Bipolar disorder, Neurodevelopment, Schizophrenia
Abstract

Background Schizophrenia and bipolar disorder share genetic liability, and some structural brain abnormalities are common to both conditions. First-degree relatives of patients with schizophrenia (FDRs-SZ) show similar brain abnormalities to patients, albeit with smaller effect sizes. Imaging findings in first-degree relatives of patients with bipolar disorder (FDRs-BD) have been inconsistent in the past, but recent studies report regionally greater volumes compared with control subjects. Methods We performed a meta-analysis of global and subcortical brain measures of 6008 individuals (1228 FDRs-SZ, 852 FDRs-BD, 2246 control subjects, 1016 patients with schizophrenia, 666 patients with bipolar disorder) from 34 schizophrenia and/or bipolar disorder family cohorts with standardized methods. Analyses were repeated with a correction for intracranial volume (ICV) and for the presence of any psychopathology in the relatives and control subjects. Results FDRs-BD had significantly larger ICV (d = +0.16, q < .05 corrected), whereas FDRs-SZ showed smaller thalamic volumes than control subjects (d = −0.12, q < .05 corrected). ICV explained the enlargements in the brain measures in FDRs-BD. In FDRs-SZ, after correction for ICV, total brain, cortical gray matter, cerebral white matter, cerebellar gray and white matter, and thalamus volumes were significantly smaller; the cortex was thinner (d < −0.09, q < .05 corrected); and third ventricle was larger (d = +0.15, q < .05 corrected). The findings were not explained by psychopathology in the relatives or control subjects. Conclusions Despite shared genetic liability, FDRs-SZ and FDRs-BD show a differential pattern of structural brain abnormalities, specifically a divergent effect in ICV. This may imply that the neurodevelopmental trajectories leading to brain anomalies in schizophrenia or bipolar disorder are distinct.

Published
2019

8. Positive symptoms associate with cortical thinning in the superior temporal gyrus via the enigma schizophrenia consortium

Author

Walton, E., Hibar, D. P., van Erp, T. G M, Potkin, S. G., Roiz-Santiañez, R., Crespo-Facorro, B., Suarez-Pinilla, P., Van Haren, N. E M, de Zwarte, S. M C, Kahn, R. S., Cahn, W., Doan, N. T., Jørgensen, K. N., Gurholt, T. P., Agartz, I., Andreassen, O. A., Westlye, L. T., Melle, I., Berg, A. O., Mørch-Johnsen, L., Færden, A., Flyckt, L., Fatouros-Bergman, H., Jönsson, E. G., Hashimoto, R., Yamamori, H., Fukunaga, M., Preda, A., De Rossi, P., Piras, F., Banaj, N., Ciullo, V., Spalletta, G., Gur, R. E., Gur, R. C., Wolf, D. H., Satterthwaite, T. D., Beard, L. M., Sommer, I. E., Koops, S., Gruber, O., Richter, A., Krämer, B., Kelly, S., Donohoe, G., McDonald, C., Cannon, D. M., Corvin, A., Gill, M., Di Giorgio, A., Bertolino, A., Lawrie, S., Nickson, T., Whalley, H. C., Neilson, E., Calhoun, V. D., Thompson, P. M., Turner, J. A., Ehrlich, S., Farde, L., Engberg, G., Erhardt, S., Cervenka, S., Schwieler, L., Piehl, F., Ikonen, P., Collste, K., Orhan, F., Malmqvist, A., and Hedberg, M.

Subjects
Male, genetic structures, Planum temporale, FreeSurfer, Audiology, Brain mapping, Superior temporal gyrus, 0302 clinical medicine, enigma, Prospective Studies, psychosis, bipolar disorder, Brain Mapping, Positive and Negative Syndrome Scale, positive and negative syndrome scale, ENIGMA, Magnetic Resonance Imaging, Temporal Lobe, Multicenter Study, Psychiatry and Mental health, superior temporal gyrus, Schizophrenia, cerebral-cortex, Female, Schizophrenic Psychology, auditory verbal hallucinations, Psychology, comprehension, MRI, freesurfer, metaanalysis, Adult, medicine.medical_specialty, Psychosis, cortical thickness, positive symptoms, scale for the assessment of positive symptoms, schizophrenia, Humans, Psychiatric Status Rating Scales, Psychiatry and Mental Health, 1st-episode schizophrenia, behavioral disciplines and activities, Article, Temporal lobe, 03 medical and health sciences, Journal Article, medicine, Bipolar disorder, Psychiatry, mri, medicine.disease, thickness, 030227 psychiatry, planum temporale, 1st episode schizophrenia, 030217 neurology & neurosurgery, Meta-Analysis
Abstract

OBJECTIVE: Based on the role of the superior temporal gyrus (STG) in auditory processing, language comprehension and self-monitoring, this study aimed to investigate the relationship between STG cortical thickness and positive symptom severity in schizophrenia.METHOD: This prospective meta-analysis includes data from 1987 individuals with schizophrenia collected at seventeen centres around the world that contribute to the ENIGMA Schizophrenia Working Group. STG thickness measures were extracted from T1-weighted brain scans using FreeSurfer. The study performed a meta-analysis of effect sizes across sites generated by a model predicting left or right STG thickness with a positive symptom severity score (harmonized SAPS or PANSS-positive scores), while controlling for age, sex and site. Secondary models investigated relationships between antipsychotic medication, duration of illness, overall illness severity, handedness and STG thickness.RESULTS: Positive symptom severity was negatively related to STG thickness in both hemispheres (left: βstd = -0.052; P = 0.021; right: βstd = -0.073; P = 0.001) when statistically controlling for age, sex and site. This effect remained stable in models including duration of illness, antipsychotic medication or handedness.CONCLUSION: Our findings further underline the important role of the STG in hallmark symptoms in schizophrenia. These findings can assist in advancing insight into symptom-relevant pathophysiological mechanisms in schizophrenia.

Published
2017
Full Text
View/download PDF

9. The 5-ht1a receptor and 5-ht transporter in temporal lobe epilepsy

Author

Martinez, A., Finegersh, A., Cannon, D. M., Dustin, I., Nugent, A., Herscovitch, P., and Theodore, W. H.

Subjects
bipolar disorder, binding, nervous system, pet, serotonin transporter, episodes, major depression, gene, human brain, positron-emission-tomography, seizures
Abstract

Objective: To study 5-HT transport and 5-HT1A receptors in temporal lobe epilepsy (TLE) and depression. Methods: Thirteen patients had PET with [C-11]DASB for 5-HTT and [F-18]FCWAY for 5-HT1A receptor binding, MRI, and psychiatric assessment. Sixteen healthy volunteers had [C-11]DASB, 19 had [F-18]FCWAY, and 6 had both PET studies. We used a reference tissue model to estimate [C-11]DASB binding. [F-18]FCWAY volume of distribution was corrected for plasma-free fraction. Images were normalized to common space. The main outcome was the regional asymmetry index. Positive asymmetry indicates relative reduced binding (reflecting transporter activity) ipsilateral to epileptic foci. Results: Mean regional [C-11]DASB binding and asymmetry did not differ between patients and controls. [F-18]FCWAY asymmetry was significantly greater for patients than controls in hippocampus, amygdala, and fusiform gyrus. On analysis of variance with region as a repeated measure, depression diagnosis had a significant effect on [C-11]DASB asymmetry, with significantly higher [C-11]DASB asymmetry in insular cortex (trend for fusiform gyrus). In insular cortex, patients had a significant correlation between [F-18]FCWAY asymmetry and [C-11]DASB asymmetry. Conclusions: Our study showed increased [C-11]DASB asymmetry in insula and fusiform gyrus, and relatively reduced transporter activity, in subjects with both TLE and depression, as compared to subjects with TLE alone, implying reduced reuptake and thus increased synaptic 5-HT availability. This finding may represent a compensatory mechanism for 5-HT1A receptor loss. Altered serotonergic mechanisms have an important role in TLE and concomitant depression.

Published
2013

10. 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
Full Text
View/download PDF

11. 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
Full Text
View/download PDF

12. 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
Full Text
View/download PDF

13. 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
Full Text
View/download PDF

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

Author

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

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

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

Published
2021
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results