Basal ganglia circuits changes in Parkinson's disease patients
► We studied the causal connectivity of basal ganglia networks in Parkinson's disease. ► The dopaminergic system exerts influences on widespread brain networks. ► The pattern of basal ganglia network connectivity is abnormal in Parkinson's disease. ► fMRI appears to be a useful method to d...
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Published in | Neuroscience letters Vol. 524; no. 1; pp. 55 - 59 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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Elsevier Ireland Ltd
22.08.2012
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ISSN | 0304-3940 1872-7972 1872-7972 |
DOI | 10.1016/j.neulet.2012.07.012 |
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Abstract | ► We studied the causal connectivity of basal ganglia networks in Parkinson's disease. ► The dopaminergic system exerts influences on widespread brain networks. ► The pattern of basal ganglia network connectivity is abnormal in Parkinson's disease. ► fMRI appears to be a useful method to demonstrate basal ganglia pathways.
Functional changes in basal ganglia circuitry are responsible for the major clinical features of Parkinson's disease (PD). Current models of basal ganglia circuitry can only partially explain the cardinal symptoms in PD. We used functional MRI to investigate the causal connectivity of basal ganglia networks from the substantia nigra pars compacta (SNc) in PD in the movement and resting state. In controls, SNc activity predicted increased activity in the supplementary motor area, the default mode network, and dorsolateral prefrontal cortex, but, in patients, activity predicted decreases in the same structures. The SNc had decreased connectivity with the striatum, globus pallidus, subthalamic nucleus, thalamus, supplementary motor area, dorsolateral prefrontal cortex, insula, default mode network, temporal lobe, cerebellum, and pons in patients compared to controls. Levodopa administration partially normalized the pattern of connectivity. Our findings show how the dopaminergic system exerts influences on widespread brain networks, including motor and cognitive networks. The pattern of basal ganglia network connectivity is abnormal in PD secondary to dopamine depletion, and is more deviant in more severe disease. Use of functional MRI with network analysis appears to be a useful method to demonstrate basal ganglia pathways in vivo in human subjects. |
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AbstractList | Functional changes in basal ganglia circuitry are responsible for the major clinical features of Parkinson's disease (PD). Current models of basal ganglia circuitry can only partially explain the cardinal symptoms in PD. We used functional MRI to investigate the causal connectivity of basal ganglia networks from the substantia nigra pars compacta (SNc) in PD in the movement and resting state. In controls, SNc activity predicted increased activity in the supplementary motor area, the default mode network, and dorsolateral prefrontal cortex, but, in patients, activity predicted decreases in the same structures. The SNc had decreased connectivity with the striatum, globus pallidus, subthalamic nucleus, thalamus, supplementary motor area, dorsolateral prefrontal cortex, insula, default mode network, temporal lobe, cerebellum, and pons in patients compared to controls. Levodopa administration partially normalized the pattern of connectivity. Our findings show how the dopaminergic system exerts influences on widespread brain networks, including motor and cognitive networks. The pattern of basal ganglia network connectivity is abnormal in PD secondary to dopamine depletion, and is more deviant in more severe disease. Use of functional MRI with network analysis appears to be a useful method to demonstrate basal ganglia pathways in vivo in human subjects. ► We studied the causal connectivity of basal ganglia networks in Parkinson's disease. ► The dopaminergic system exerts influences on widespread brain networks. ► The pattern of basal ganglia network connectivity is abnormal in Parkinson's disease. ► fMRI appears to be a useful method to demonstrate basal ganglia pathways. Functional changes in basal ganglia circuitry are responsible for the major clinical features of Parkinson's disease (PD). Current models of basal ganglia circuitry can only partially explain the cardinal symptoms in PD. We used functional MRI to investigate the causal connectivity of basal ganglia networks from the substantia nigra pars compacta (SNc) in PD in the movement and resting state. In controls, SNc activity predicted increased activity in the supplementary motor area, the default mode network, and dorsolateral prefrontal cortex, but, in patients, activity predicted decreases in the same structures. The SNc had decreased connectivity with the striatum, globus pallidus, subthalamic nucleus, thalamus, supplementary motor area, dorsolateral prefrontal cortex, insula, default mode network, temporal lobe, cerebellum, and pons in patients compared to controls. Levodopa administration partially normalized the pattern of connectivity. Our findings show how the dopaminergic system exerts influences on widespread brain networks, including motor and cognitive networks. The pattern of basal ganglia network connectivity is abnormal in PD secondary to dopamine depletion, and is more deviant in more severe disease. Use of functional MRI with network analysis appears to be a useful method to demonstrate basal ganglia pathways in vivo in human subjects. Functional changes in basal ganglia circuitry are responsible for the major clinical features of Parkinson's disease (PD). Current models of basal ganglia circuitry can only partially explain the cardinal symptoms in PD. We used functional MRI to investigate the causal connectivity of basal ganglia networks from the substantia nigra pars compacta (SNc) in PD in the movement and resting state. In controls, SNc activity predicted increased activity in the supplementary motor area, the default mode network, and dorsolateral prefrontal cortex, but, in patients, activity predicted decreases in the same structures. The SNc had decreased connectivity with the striatum, globus pallidus, subthalamic nucleus, thalamus, supplementary motor area, dorsolateral prefrontal cortex, insula, default mode network, temporal lobe, cerebellum, and pons in patients compared to controls. Levodopa administration partially normalized the pattern of connectivity. Our findings show how the dopaminergic system exerts influences on widespread brain networks, including motor and cognitive networks. The pattern of basal ganglia network connectivity is abnormal in PD secondary to dopamine depletion, and is more deviant in more severe disease. Use of functional MRI with network analysis appears to be a useful method to demonstrate basal ganglia pathways in vivo in human subjects.Functional changes in basal ganglia circuitry are responsible for the major clinical features of Parkinson's disease (PD). Current models of basal ganglia circuitry can only partially explain the cardinal symptoms in PD. We used functional MRI to investigate the causal connectivity of basal ganglia networks from the substantia nigra pars compacta (SNc) in PD in the movement and resting state. In controls, SNc activity predicted increased activity in the supplementary motor area, the default mode network, and dorsolateral prefrontal cortex, but, in patients, activity predicted decreases in the same structures. The SNc had decreased connectivity with the striatum, globus pallidus, subthalamic nucleus, thalamus, supplementary motor area, dorsolateral prefrontal cortex, insula, default mode network, temporal lobe, cerebellum, and pons in patients compared to controls. Levodopa administration partially normalized the pattern of connectivity. Our findings show how the dopaminergic system exerts influences on widespread brain networks, including motor and cognitive networks. The pattern of basal ganglia network connectivity is abnormal in PD secondary to dopamine depletion, and is more deviant in more severe disease. Use of functional MRI with network analysis appears to be a useful method to demonstrate basal ganglia pathways in vivo in human subjects. |
Author | Wu, Tao Wang, Jue Hallett, Mark Zang, Yufeng Chan, Piu Wu, Xiaoli Wang, Chaodong |
AuthorAffiliation | 3 Human Motor Control Section, Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA 2 Center for Cognition and Brain Disorders, Affiliated Hospital, Hangzhou Normal University, China 1 Department of Neurobiology, Key Laboratory on Neurodegenerative Disorders of Ministry of Education, Beijing Institute of Geriatrics, Xuanwu Hospital, Capital Medical University, Beijing, China |
AuthorAffiliation_xml | – name: 3 Human Motor Control Section, Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA – name: 2 Center for Cognition and Brain Disorders, Affiliated Hospital, Hangzhou Normal University, China – name: 1 Department of Neurobiology, Key Laboratory on Neurodegenerative Disorders of Ministry of Education, Beijing Institute of Geriatrics, Xuanwu Hospital, Capital Medical University, Beijing, China |
Author_xml | – sequence: 1 givenname: Tao surname: Wu fullname: Wu, Tao email: wutao69@gmail.com, wutao69@163.com organization: Department of Neurobiology, Key Laboratory on Neurodegenerative Disorders of Ministry of Education, Beijing Institute of Geriatrics, Xuanwu Hospital, Capital Medical University, Beijing 100053, China – sequence: 2 givenname: Jue surname: Wang fullname: Wang, Jue organization: Center for Cognition and Brain Disorders, Affiliated Hospital, Hangzhou Normal University, China – sequence: 3 givenname: Chaodong surname: Wang fullname: Wang, Chaodong organization: Department of Neurobiology, Key Laboratory on Neurodegenerative Disorders of Ministry of Education, Beijing Institute of Geriatrics, Xuanwu Hospital, Capital Medical University, Beijing 100053, China – sequence: 4 givenname: Mark surname: Hallett fullname: Hallett, Mark organization: Human Motor Control Section, Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA – sequence: 5 givenname: Yufeng surname: Zang fullname: Zang, Yufeng organization: Center for Cognition and Brain Disorders, Affiliated Hospital, Hangzhou Normal University, China – sequence: 6 givenname: Xiaoli surname: Wu fullname: Wu, Xiaoli organization: Department of Neurobiology, Key Laboratory on Neurodegenerative Disorders of Ministry of Education, Beijing Institute of Geriatrics, Xuanwu Hospital, Capital Medical University, Beijing 100053, China – sequence: 7 givenname: Piu surname: Chan fullname: Chan, Piu organization: Department of Neurobiology, Key Laboratory on Neurodegenerative Disorders of Ministry of Education, Beijing Institute of Geriatrics, Xuanwu Hospital, Capital Medical University, Beijing 100053, China |
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Keywords | Granger causality analysis Dopaminergic deficits Parkinson's disease Basal ganglia circuits Substantia nigra |
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Snippet | ► We studied the causal connectivity of basal ganglia networks in Parkinson's disease. ► The dopaminergic system exerts influences on widespread brain... Functional changes in basal ganglia circuitry are responsible for the major clinical features of Parkinson's disease (PD). Current models of basal ganglia... Functional changes in basal ganglia circuitry are responsible for the major clinical features of Parkinson’s disease (PD). Current models of basal ganglia... |
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SubjectTerms | Adult Basal ganglia Basal Ganglia - physiopathology Basal ganglia circuits Brain Cerebellum Cognitive ability Cortex (prefrontal) Dopamine Dopaminergic deficits Female Functional magnetic resonance imaging Globus pallidus Granger causality analysis Humans Magnetic Resonance Imaging Male Middle Aged Movement disorders Neostriatum Nerve Net - physiopathology Neural networks Neurodegenerative diseases Parkinson Disease - physiopathology Parkinson's disease Pons Substantia nigra subthalamic nucleus supplementary motor area Temporal lobe Thalamus |
Title | Basal ganglia circuits changes in Parkinson's disease patients |
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