What is bipolar disorder? A disease model of dysregulated energy expenditure
Advances in the understanding and management of bipolar disorder (BD) have been slow to emerge. Despite notable recent developments in neurosciences, our conceptualization of the nature of this mental disorder has not meaningfully progressed. One of the key reasons for this scenario is the continuin...
Ausführliche Beschreibung
Autor*in: |
Mansur, Rodrigo B. [verfasserIn] Lee, Yena [verfasserIn] McIntyre, Roger S. [verfasserIn] Brietzke, Elisa [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2020 |
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Schlagwörter: |
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Übergeordnetes Werk: |
Enthalten in: Neuroscience & biobehavioral reviews - Amsterdam [u.a.] : Elsevier Science, 1978, 113, Seite 529-545 |
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Übergeordnetes Werk: |
volume:113 ; pages:529-545 |
DOI / URN: |
10.1016/j.neubiorev.2020.04.006 |
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Katalog-ID: |
ELV004069641 |
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245 | 1 | 0 | |a What is bipolar disorder? A disease model of dysregulated energy expenditure |
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520 | |a Advances in the understanding and management of bipolar disorder (BD) have been slow to emerge. Despite notable recent developments in neurosciences, our conceptualization of the nature of this mental disorder has not meaningfully progressed. One of the key reasons for this scenario is the continuing lack of a comprehensive disease model. Within the increasing complexity of modern research methods, there is a clear need for an overarching theoretical framework, in which findings are assimilated and predictions are generated. In this review and hypothesis article, we propose such a framework, one in which dysregulated energy expenditure is a primary, sufficient cause for BD. Our proposed model is centered on the disruption of the molecular and cellular network regulating energy production and expenditure, as well its potential secondary adaptations and compensatory mechanisms. We also focus on the putative longitudinal progression of this pathological process, considering its most likely periods for onset, such as critical periods that challenges energy homeostasis (e.g. neurodevelopment, social isolation), and the resulting short and long-term phenotypical manifestations. | ||
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700 | 1 | |a Lee, Yena |e verfasserin |4 aut | |
700 | 1 | |a McIntyre, Roger S. |e verfasserin |4 aut | |
700 | 1 | |a Brietzke, Elisa |e verfasserin |4 aut | |
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10.1016/j.neubiorev.2020.04.006 doi (DE-627)ELV004069641 (ELSEVIER)S0149-7634(19)31129-7 DE-627 ger DE-627 rda eng 150 610 DE-600 BIODIV DE-30 fid 77.50 bkl 44.90 bkl Mansur, Rodrigo B. verfasserin aut What is bipolar disorder? A disease model of dysregulated energy expenditure 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Advances in the understanding and management of bipolar disorder (BD) have been slow to emerge. Despite notable recent developments in neurosciences, our conceptualization of the nature of this mental disorder has not meaningfully progressed. One of the key reasons for this scenario is the continuing lack of a comprehensive disease model. Within the increasing complexity of modern research methods, there is a clear need for an overarching theoretical framework, in which findings are assimilated and predictions are generated. In this review and hypothesis article, we propose such a framework, one in which dysregulated energy expenditure is a primary, sufficient cause for BD. Our proposed model is centered on the disruption of the molecular and cellular network regulating energy production and expenditure, as well its potential secondary adaptations and compensatory mechanisms. We also focus on the putative longitudinal progression of this pathological process, considering its most likely periods for onset, such as critical periods that challenges energy homeostasis (e.g. neurodevelopment, social isolation), and the resulting short and long-term phenotypical manifestations. Bipolar disorder pathophysiology energy homeostasis reward cognition mitochondria dopamine insulin Lee, Yena verfasserin aut McIntyre, Roger S. verfasserin aut Brietzke, Elisa verfasserin aut Enthalten in Neuroscience & biobehavioral reviews Amsterdam [u.a.] : Elsevier Science, 1978 113, Seite 529-545 Online-Ressource (DE-627)306588706 (DE-600)1498433-7 (DE-576)105430552 1873-7528 nnns volume:113 pages:529-545 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-BIODIV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 77.50 Psychophysiologie 44.90 Neurologie AR 113 529-545 |
spelling |
10.1016/j.neubiorev.2020.04.006 doi (DE-627)ELV004069641 (ELSEVIER)S0149-7634(19)31129-7 DE-627 ger DE-627 rda eng 150 610 DE-600 BIODIV DE-30 fid 77.50 bkl 44.90 bkl Mansur, Rodrigo B. verfasserin aut What is bipolar disorder? A disease model of dysregulated energy expenditure 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Advances in the understanding and management of bipolar disorder (BD) have been slow to emerge. Despite notable recent developments in neurosciences, our conceptualization of the nature of this mental disorder has not meaningfully progressed. One of the key reasons for this scenario is the continuing lack of a comprehensive disease model. Within the increasing complexity of modern research methods, there is a clear need for an overarching theoretical framework, in which findings are assimilated and predictions are generated. In this review and hypothesis article, we propose such a framework, one in which dysregulated energy expenditure is a primary, sufficient cause for BD. Our proposed model is centered on the disruption of the molecular and cellular network regulating energy production and expenditure, as well its potential secondary adaptations and compensatory mechanisms. We also focus on the putative longitudinal progression of this pathological process, considering its most likely periods for onset, such as critical periods that challenges energy homeostasis (e.g. neurodevelopment, social isolation), and the resulting short and long-term phenotypical manifestations. Bipolar disorder pathophysiology energy homeostasis reward cognition mitochondria dopamine insulin Lee, Yena verfasserin aut McIntyre, Roger S. verfasserin aut Brietzke, Elisa verfasserin aut Enthalten in Neuroscience & biobehavioral reviews Amsterdam [u.a.] : Elsevier Science, 1978 113, Seite 529-545 Online-Ressource (DE-627)306588706 (DE-600)1498433-7 (DE-576)105430552 1873-7528 nnns volume:113 pages:529-545 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-BIODIV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 77.50 Psychophysiologie 44.90 Neurologie AR 113 529-545 |
allfields_unstemmed |
10.1016/j.neubiorev.2020.04.006 doi (DE-627)ELV004069641 (ELSEVIER)S0149-7634(19)31129-7 DE-627 ger DE-627 rda eng 150 610 DE-600 BIODIV DE-30 fid 77.50 bkl 44.90 bkl Mansur, Rodrigo B. verfasserin aut What is bipolar disorder? A disease model of dysregulated energy expenditure 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Advances in the understanding and management of bipolar disorder (BD) have been slow to emerge. Despite notable recent developments in neurosciences, our conceptualization of the nature of this mental disorder has not meaningfully progressed. One of the key reasons for this scenario is the continuing lack of a comprehensive disease model. Within the increasing complexity of modern research methods, there is a clear need for an overarching theoretical framework, in which findings are assimilated and predictions are generated. In this review and hypothesis article, we propose such a framework, one in which dysregulated energy expenditure is a primary, sufficient cause for BD. Our proposed model is centered on the disruption of the molecular and cellular network regulating energy production and expenditure, as well its potential secondary adaptations and compensatory mechanisms. We also focus on the putative longitudinal progression of this pathological process, considering its most likely periods for onset, such as critical periods that challenges energy homeostasis (e.g. neurodevelopment, social isolation), and the resulting short and long-term phenotypical manifestations. Bipolar disorder pathophysiology energy homeostasis reward cognition mitochondria dopamine insulin Lee, Yena verfasserin aut McIntyre, Roger S. verfasserin aut Brietzke, Elisa verfasserin aut Enthalten in Neuroscience & biobehavioral reviews Amsterdam [u.a.] : Elsevier Science, 1978 113, Seite 529-545 Online-Ressource (DE-627)306588706 (DE-600)1498433-7 (DE-576)105430552 1873-7528 nnns volume:113 pages:529-545 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-BIODIV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 77.50 Psychophysiologie 44.90 Neurologie AR 113 529-545 |
allfieldsGer |
10.1016/j.neubiorev.2020.04.006 doi (DE-627)ELV004069641 (ELSEVIER)S0149-7634(19)31129-7 DE-627 ger DE-627 rda eng 150 610 DE-600 BIODIV DE-30 fid 77.50 bkl 44.90 bkl Mansur, Rodrigo B. verfasserin aut What is bipolar disorder? A disease model of dysregulated energy expenditure 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Advances in the understanding and management of bipolar disorder (BD) have been slow to emerge. Despite notable recent developments in neurosciences, our conceptualization of the nature of this mental disorder has not meaningfully progressed. One of the key reasons for this scenario is the continuing lack of a comprehensive disease model. Within the increasing complexity of modern research methods, there is a clear need for an overarching theoretical framework, in which findings are assimilated and predictions are generated. In this review and hypothesis article, we propose such a framework, one in which dysregulated energy expenditure is a primary, sufficient cause for BD. Our proposed model is centered on the disruption of the molecular and cellular network regulating energy production and expenditure, as well its potential secondary adaptations and compensatory mechanisms. We also focus on the putative longitudinal progression of this pathological process, considering its most likely periods for onset, such as critical periods that challenges energy homeostasis (e.g. neurodevelopment, social isolation), and the resulting short and long-term phenotypical manifestations. Bipolar disorder pathophysiology energy homeostasis reward cognition mitochondria dopamine insulin Lee, Yena verfasserin aut McIntyre, Roger S. verfasserin aut Brietzke, Elisa verfasserin aut Enthalten in Neuroscience & biobehavioral reviews Amsterdam [u.a.] : Elsevier Science, 1978 113, Seite 529-545 Online-Ressource (DE-627)306588706 (DE-600)1498433-7 (DE-576)105430552 1873-7528 nnns volume:113 pages:529-545 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-BIODIV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 77.50 Psychophysiologie 44.90 Neurologie AR 113 529-545 |
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What is bipolar disorder? A disease model of dysregulated energy expenditure |
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What is bipolar disorder? A disease model of dysregulated energy expenditure |
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Mansur, Rodrigo B. |
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Neuroscience & biobehavioral reviews |
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Mansur, Rodrigo B. Lee, Yena McIntyre, Roger S. Brietzke, Elisa |
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what is bipolar disorder? a disease model of dysregulated energy expenditure |
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What is bipolar disorder? A disease model of dysregulated energy expenditure |
abstract |
Advances in the understanding and management of bipolar disorder (BD) have been slow to emerge. Despite notable recent developments in neurosciences, our conceptualization of the nature of this mental disorder has not meaningfully progressed. One of the key reasons for this scenario is the continuing lack of a comprehensive disease model. Within the increasing complexity of modern research methods, there is a clear need for an overarching theoretical framework, in which findings are assimilated and predictions are generated. In this review and hypothesis article, we propose such a framework, one in which dysregulated energy expenditure is a primary, sufficient cause for BD. Our proposed model is centered on the disruption of the molecular and cellular network regulating energy production and expenditure, as well its potential secondary adaptations and compensatory mechanisms. We also focus on the putative longitudinal progression of this pathological process, considering its most likely periods for onset, such as critical periods that challenges energy homeostasis (e.g. neurodevelopment, social isolation), and the resulting short and long-term phenotypical manifestations. |
abstractGer |
Advances in the understanding and management of bipolar disorder (BD) have been slow to emerge. Despite notable recent developments in neurosciences, our conceptualization of the nature of this mental disorder has not meaningfully progressed. One of the key reasons for this scenario is the continuing lack of a comprehensive disease model. Within the increasing complexity of modern research methods, there is a clear need for an overarching theoretical framework, in which findings are assimilated and predictions are generated. In this review and hypothesis article, we propose such a framework, one in which dysregulated energy expenditure is a primary, sufficient cause for BD. Our proposed model is centered on the disruption of the molecular and cellular network regulating energy production and expenditure, as well its potential secondary adaptations and compensatory mechanisms. We also focus on the putative longitudinal progression of this pathological process, considering its most likely periods for onset, such as critical periods that challenges energy homeostasis (e.g. neurodevelopment, social isolation), and the resulting short and long-term phenotypical manifestations. |
abstract_unstemmed |
Advances in the understanding and management of bipolar disorder (BD) have been slow to emerge. Despite notable recent developments in neurosciences, our conceptualization of the nature of this mental disorder has not meaningfully progressed. One of the key reasons for this scenario is the continuing lack of a comprehensive disease model. Within the increasing complexity of modern research methods, there is a clear need for an overarching theoretical framework, in which findings are assimilated and predictions are generated. In this review and hypothesis article, we propose such a framework, one in which dysregulated energy expenditure is a primary, sufficient cause for BD. Our proposed model is centered on the disruption of the molecular and cellular network regulating energy production and expenditure, as well its potential secondary adaptations and compensatory mechanisms. We also focus on the putative longitudinal progression of this pathological process, considering its most likely periods for onset, such as critical periods that challenges energy homeostasis (e.g. neurodevelopment, social isolation), and the resulting short and long-term phenotypical manifestations. |
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title_short |
What is bipolar disorder? A disease model of dysregulated energy expenditure |
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