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Behavioral neurobiology of Huntingto...
~
Cenci, M. Angela.
Behavioral neurobiology of Huntington's disease and Parkinson's disease[electronic resource] /
紀錄類型:
書目-電子資源 : Monograph/item
杜威分類號:
616.8
書名/作者:
Behavioral neurobiology of Huntington's disease and Parkinson's disease/ edited by Hoa Huu Phuc Nguyen, M. Angela Cenci.
其他作者:
Nguyen, Hoa Huu Phuc.
出版者:
Berlin, Heidelberg : : Springer Berlin Heidelberg :, 2015.
面頁冊數:
xiii, 397 p. : : ill., digital ;; 24 cm.
Contained By:
Springer eBooks
標題:
Nervous system - Diseases.
標題:
Huntington's disease.
標題:
Parkinson's disease.
標題:
Biomedicine.
標題:
Neurosciences.
標題:
Human Genetics.
標題:
Neurobiology.
標題:
Cell Biology.
ISBN:
9783662463444 (electronic bk.)
ISBN:
9783662463437 (paper)
內容註:
Clinical Aspects of Huntington's Disease -- The Neuropathology of Huntington's Disease -- Neurobiology of Huntington's Disease -- Mouse Models of Huntington's Disease -- Transgenic Rat Models of Huntington's Disease -- Large Animal Models of Huntington's Disease -- Therapeutic Strategies for Huntington's Disease -- Clinical and Pathological Features of Parkinson's Disease -- Symptomatic Models of Parkinson's Disease and L-DOPA-Induced Dyskinesia in Non-human Primates -- Neuroinflammation in Parkinson's Disease Animal Models: A Cell Stress Response or a Step in Neurodegeneration? -- Viral Vector-Based Models of Parkinson's Disease -- Transgenic Rodent Models to Study Alpha-Synuclein Pathogenesis, with a Focus on Cognitive Deficits -- Modeling LRRK2 Pathobiology in Parkinson's Disease: From Yeast to Rodents -- Models of Multiple System Atrophy.
摘要、提要註:
Motor dysfunction and cognitive impairment are major symptoms in both Huntington's Disease (HD) and Parkinson's Disease (PD) A breakthrough in HD research occurred in 1993, with the identification of the gene causing this devastating monogenetic illness. Since 1996, several genes were reported to cause familial forms of PD. Following these genetic discoveries, a variety of genetic disease models were generated, providing completely novel opportunities to explore the neurobiological basis of HD and PD. Genetic models allow us to study the earliest manifestations of the diseases both behaviorally and neuropathologically, and provide tools to probe molecular pathways of neurodegeneration. Additionally, neurotoxic animal models allow us to reproduce neurochemical and cellular events of great pathophysiological importance. In the PD field, neurotoxic animal models remain the preferred option to reproduce symptomatic features of the human disease that are responsive to dopaminergic pharmacotherapies. In addition, neurotoxic PD models are often used to investigate pathways of mitochondrial dysfunction, oxidative stress, and neuroinflammation. This book provides up-to-date reviews on current animal models of both HD and PD. These animal models are essential to investigate links between the pathobiology and the behavioral abnormalities associated with these disorders.
電子資源:
http://dx.doi.org/10.1007/978-3-662-46344-4
Behavioral neurobiology of Huntington's disease and Parkinson's disease[electronic resource] /
Behavioral neurobiology of Huntington's disease and Parkinson's disease
[electronic resource] /edited by Hoa Huu Phuc Nguyen, M. Angela Cenci. - Berlin, Heidelberg :Springer Berlin Heidelberg :2015. - xiii, 397 p. :ill., digital ;24 cm. - Current topics in behavioral neurosciences,v.221866-3370 ;. - Current topics in behavioral neurosciences ;9..
Clinical Aspects of Huntington's Disease -- The Neuropathology of Huntington's Disease -- Neurobiology of Huntington's Disease -- Mouse Models of Huntington's Disease -- Transgenic Rat Models of Huntington's Disease -- Large Animal Models of Huntington's Disease -- Therapeutic Strategies for Huntington's Disease -- Clinical and Pathological Features of Parkinson's Disease -- Symptomatic Models of Parkinson's Disease and L-DOPA-Induced Dyskinesia in Non-human Primates -- Neuroinflammation in Parkinson's Disease Animal Models: A Cell Stress Response or a Step in Neurodegeneration? -- Viral Vector-Based Models of Parkinson's Disease -- Transgenic Rodent Models to Study Alpha-Synuclein Pathogenesis, with a Focus on Cognitive Deficits -- Modeling LRRK2 Pathobiology in Parkinson's Disease: From Yeast to Rodents -- Models of Multiple System Atrophy.
Motor dysfunction and cognitive impairment are major symptoms in both Huntington's Disease (HD) and Parkinson's Disease (PD) A breakthrough in HD research occurred in 1993, with the identification of the gene causing this devastating monogenetic illness. Since 1996, several genes were reported to cause familial forms of PD. Following these genetic discoveries, a variety of genetic disease models were generated, providing completely novel opportunities to explore the neurobiological basis of HD and PD. Genetic models allow us to study the earliest manifestations of the diseases both behaviorally and neuropathologically, and provide tools to probe molecular pathways of neurodegeneration. Additionally, neurotoxic animal models allow us to reproduce neurochemical and cellular events of great pathophysiological importance. In the PD field, neurotoxic animal models remain the preferred option to reproduce symptomatic features of the human disease that are responsive to dopaminergic pharmacotherapies. In addition, neurotoxic PD models are often used to investigate pathways of mitochondrial dysfunction, oxidative stress, and neuroinflammation. This book provides up-to-date reviews on current animal models of both HD and PD. These animal models are essential to investigate links between the pathobiology and the behavioral abnormalities associated with these disorders.
ISBN: 9783662463444 (electronic bk.)
Standard No.: 10.1007/978-3-662-46344-4doiSubjects--Topical Terms:
401867
Nervous system
--Diseases.
LC Class. No.: RC346
Dewey Class. No.: 616.8
Behavioral neurobiology of Huntington's disease and Parkinson's disease[electronic resource] /
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Clinical Aspects of Huntington's Disease -- The Neuropathology of Huntington's Disease -- Neurobiology of Huntington's Disease -- Mouse Models of Huntington's Disease -- Transgenic Rat Models of Huntington's Disease -- Large Animal Models of Huntington's Disease -- Therapeutic Strategies for Huntington's Disease -- Clinical and Pathological Features of Parkinson's Disease -- Symptomatic Models of Parkinson's Disease and L-DOPA-Induced Dyskinesia in Non-human Primates -- Neuroinflammation in Parkinson's Disease Animal Models: A Cell Stress Response or a Step in Neurodegeneration? -- Viral Vector-Based Models of Parkinson's Disease -- Transgenic Rodent Models to Study Alpha-Synuclein Pathogenesis, with a Focus on Cognitive Deficits -- Modeling LRRK2 Pathobiology in Parkinson's Disease: From Yeast to Rodents -- Models of Multiple System Atrophy.
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Motor dysfunction and cognitive impairment are major symptoms in both Huntington's Disease (HD) and Parkinson's Disease (PD) A breakthrough in HD research occurred in 1993, with the identification of the gene causing this devastating monogenetic illness. Since 1996, several genes were reported to cause familial forms of PD. Following these genetic discoveries, a variety of genetic disease models were generated, providing completely novel opportunities to explore the neurobiological basis of HD and PD. Genetic models allow us to study the earliest manifestations of the diseases both behaviorally and neuropathologically, and provide tools to probe molecular pathways of neurodegeneration. Additionally, neurotoxic animal models allow us to reproduce neurochemical and cellular events of great pathophysiological importance. In the PD field, neurotoxic animal models remain the preferred option to reproduce symptomatic features of the human disease that are responsive to dopaminergic pharmacotherapies. In addition, neurotoxic PD models are often used to investigate pathways of mitochondrial dysfunction, oxidative stress, and neuroinflammation. This book provides up-to-date reviews on current animal models of both HD and PD. These animal models are essential to investigate links between the pathobiology and the behavioral abnormalities associated with these disorders.
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