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Exploring the genetics of lithium response in bipolar disorders
M. Herrera-Rivero, M. Adli, K. Akiyama, N. Akula, AT. Amare, R. Ardau, B. Arias, JM. Aubry, L. Backlund, F. Bellivier, A. Benabarre, S. Bengesser, AK. Bhattacharjee, JM. Biernacka, A. Birner, M. Cearns, P. Cervantes, HC. Chen, C. Chillotti, S....
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Document type Journal Article
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- Journal Article MeSH
BACKGROUND: Lithium (Li) remains the treatment of choice for bipolar disorders (BP). Its mood-stabilizing effects help reduce the long-term burden of mania, depression and suicide risk in patients with BP. It also has been shown to have beneficial effects on disease-associated conditions, including sleep and cardiovascular disorders. However, the individual responses to Li treatment vary within and between diagnostic subtypes of BP (e.g. BP-I and BP-II) according to the clinical presentation. Moreover, long-term Li treatment has been linked to adverse side-effects that are a cause of concern and non-adherence, including the risk of developing chronic medical conditions such as thyroid and renal disease. In recent years, studies by the Consortium on Lithium Genetics (ConLiGen) have uncovered a number of genetic factors that contribute to the variability in Li treatment response in patients with BP. Here, we leveraged the ConLiGen cohort (N = 2064) to investigate the genetic basis of Li effects in BP. For this, we studied how Li response and linked genes associate with the psychiatric symptoms and polygenic load for medical comorbidities, placing particular emphasis on identifying differences between BP-I and BP-II. RESULTS: We found that clinical response to Li treatment, measured with the Alda scale, was associated with a diminished burden of mania, depression, substance and alcohol abuse, psychosis and suicidal ideation in patients with BP-I and, in patients with BP-II, of depression only. Our genetic analyses showed that a stronger clinical response to Li was modestly related to lower polygenic load for diabetes and hypertension in BP-I but not BP-II. Moreover, our results suggested that a number of genes that have been previously linked to Li response variability in BP differentially relate to the psychiatric symptomatology, particularly to the numbers of manic and depressive episodes, and to the polygenic load for comorbid conditions, including diabetes, hypertension and hypothyroidism. CONCLUSIONS: Taken together, our findings suggest that the effects of Li on symptomatology and comorbidity in BP are partially modulated by common genetic factors, with differential effects between BP-I and BP-II.
Centre for Healthy Brain Ageing School of Psychiatry University of New South Wales Sydney Australia
Centro de Investigación Biomédica en Red de Salud Mental Instituto de Salud Carlos 3 Madrid Spain
Department of Adult Psychiatry Poznan University of Medical Sciences Poznań Poland
Department of Biomedical Sciences University of Cagliari Cagliari Italy
Department of Clinical Neurosciences Karolinska Institutet Stockholm Sweden
Department of Health Sciences Research Mayo Clinic Rochester USA
Department of Medical Epidemiology and Biostatistics Karolinska Institutet Stockholm Sweden
Department of Mental Health Johns Hopkins Bloomberg School of Public Health Baltimore USA
Department of Pharmacology Dalhousie University Halifax Canada
Department of Psychiatry and Behavioral Sciences Johns Hopkins University Baltimore USA
Department of Psychiatry and Psychology Mayo Clinic Rochester USA
Department of Psychiatry and Psychotherapy Ludwig Maximilian University Munich Munich Germany
Department of Psychiatry Dalhousie University Halifax Canada
Department of Psychiatry Dokkyo Medical University School of Medicine Mibu Japan
Department of Psychiatry Hokkaido University Graduate School of Medicine Sapporo Japan
Department of Psychiatry Lindner Center of Hope University of Cincinnati Cincinnati USA
Department of Psychiatry University of California San Diego San Diego USA
Department of Psychiatry University of Campania 'Luigi Vanvitelli' Caserta Italy
Department of Psychiatry University of Perugia Perugia Italy
Department of Psychiatry VA San Diego Healthcare System San Diego CA USA
Discipline of Psychiatry School of Medicine University of Adelaide Adelaide SA Australia
Douglas Mental Health University Institute McGill University Montreal Canada
Faculty of Medicine University of Geneva Geneva Switzerland
Fliedner Klinik Berlin Berlin Germany
Human Genomics Research Group Department of Biomedicine University Hospital Basel Basel Switzerland
Institute of Medical Genetics and Pathology University Hospital Basel Basel Switzerland
Institute of Neuroscience and Medicine Research Center Jülich Jülich Germany
Institute of Psychiatric Phenomics and Genomics University Hospital LMU Munich Munich Germany
Medical Faculty Bipolar Center Wiener Neustadt Sigmund Freud University Vienna Austria
Mental Health Research Group IMIM Hospital del Mar Barcelona Spain
Montreal Neurological Institute and Hospital McGill University Montreal Canada
Mood Disorders Center of Ottawa Ottawa Canada
National Institute of Mental Health Klecany Czech Republic
Northern Adelaide Local Health Network Mental Health Services Adelaide Australia
Office of Mental Health VA San Diego Healthcare System California USA
Psychiatric Genetic Unit Poznan University of Medical Sciences Poznań Poland
School of Psychiatry University of New South Wales Sydney Australia
Service de Psychiatrie Hôpital Charles Perrens Bordeaux France
The Neuromodulation Unit McGill University Health Centre Montreal Canada
Unit of Clinical Pharmacology Hospital University Agency of Cagliari Cagliari Italy
Unitat de Zoologia i Antropologia Biològica University of Barcelona CIBERSAM Barcelona Spain
References provided by Crossref.org
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- $a Herrera-Rivero, Marisol $u Department of Psychiatry, University of Münster and Joint Institute for Individualisation in a Changing Environment (JICE), University of Münster and Bielefeld University, Albert-Schweitzer-Campus 1, Building A9, 48149, Münster, Germany
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- $a Exploring the genetics of lithium response in bipolar disorders / $c M. Herrera-Rivero, M. Adli, K. Akiyama, N. Akula, AT. Amare, R. Ardau, B. Arias, JM. Aubry, L. Backlund, F. Bellivier, A. Benabarre, S. Bengesser, AK. Bhattacharjee, JM. Biernacka, A. Birner, M. Cearns, P. Cervantes, HC. Chen, C. Chillotti, S. Cichon, SR. Clark, F. Colom, C. Cruceanu, PM. Czerski, N. Dalkner, F. Degenhardt, M. Del Zompo, JR. DePaulo, B. Etain, P. Falkai, E. Ferensztajn-Rochowiak, AJ. Forstner, J. Frank, L. Frisén, MA. Frye, JM. Fullerton, C. Gallo, S. Gard, JS. Garnham, FS. Goes, M. Grigoroiu-Serbanescu, P. Grof, R. Hashimoto, R. Hasler, J. Hauser, U. Heilbronner, S. Herms, P. Hoffmann, L. Hou, YH. Hsu, S. Jamain, E. Jiménez, JP. Kahn, L. Kassem, T. Kato, J. Kelsoe, S. Kittel-Schneider, PH. Kuo, I. Kusumi, B. König, G. Laje, M. Landén, C. Lavebratt, M. Leboyer, SG. Leckband, M. Maj, M. Manchia, C. Marie-Claire, L. Martinsson, MJ. McCarthy, SL. McElroy, V. Millischer, M. Mitjans, FM. Mondimore, P. Monteleone, CM. Nievergelt, T. Novák, MM. Nöthen, C. O'Donovan, N. Ozaki, S. Papiol, A. Pfennig, C. Pisanu, JB. Potash, A. Reif, E. Reininghaus, H. Richard-Lepouriel, G. Roberts, GA. Rouleau, JK. Rybakowski, M. Schalling, PR. Schofield, KO. Schubert, EC. Schulte, BW. Schweizer, G. Severino, T. Shekhtman, PD. Shilling, K. Shimoda, C. Simhandl, CM. Slaney, A. Squassina, T. Stamm, P. Stopkova, F. Streit, F. Tekola-Ayele, A. Thalamuthu, A. Tortorella, G. Turecki, J. Veeh, E. Vieta, B. Viswanath, SH. Witt, PP. Zandi, M. Alda, M. Bauer, FJ. McMahon, PB. Mitchell, M. Rietschel, TG. Schulze, BT. Baune
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- $a BACKGROUND: Lithium (Li) remains the treatment of choice for bipolar disorders (BP). Its mood-stabilizing effects help reduce the long-term burden of mania, depression and suicide risk in patients with BP. It also has been shown to have beneficial effects on disease-associated conditions, including sleep and cardiovascular disorders. However, the individual responses to Li treatment vary within and between diagnostic subtypes of BP (e.g. BP-I and BP-II) according to the clinical presentation. Moreover, long-term Li treatment has been linked to adverse side-effects that are a cause of concern and non-adherence, including the risk of developing chronic medical conditions such as thyroid and renal disease. In recent years, studies by the Consortium on Lithium Genetics (ConLiGen) have uncovered a number of genetic factors that contribute to the variability in Li treatment response in patients with BP. Here, we leveraged the ConLiGen cohort (N = 2064) to investigate the genetic basis of Li effects in BP. For this, we studied how Li response and linked genes associate with the psychiatric symptoms and polygenic load for medical comorbidities, placing particular emphasis on identifying differences between BP-I and BP-II. RESULTS: We found that clinical response to Li treatment, measured with the Alda scale, was associated with a diminished burden of mania, depression, substance and alcohol abuse, psychosis and suicidal ideation in patients with BP-I and, in patients with BP-II, of depression only. Our genetic analyses showed that a stronger clinical response to Li was modestly related to lower polygenic load for diabetes and hypertension in BP-I but not BP-II. Moreover, our results suggested that a number of genes that have been previously linked to Li response variability in BP differentially relate to the psychiatric symptomatology, particularly to the numbers of manic and depressive episodes, and to the polygenic load for comorbid conditions, including diabetes, hypertension and hypothyroidism. CONCLUSIONS: Taken together, our findings suggest that the effects of Li on symptomatology and comorbidity in BP are partially modulated by common genetic factors, with differential effects between BP-I and BP-II.
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