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Behavioral Neurobiology of ...
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
Monografía
monografia Rebiun15295539 https://catalogo.rebiun.org/rebiun/record/Rebiun15295539 cr nn 008mamaa 150523s2015 gw | s |||| 0|eng d 9783662463444 UEM 81567 CBUC 991027188279706706 CBUC 991011468619706708 UNAV 612.8 23 Behavioral Neurobiology of Huntington's Disease and Parkinson's Disease Recurso electrónico] edited by Hoa Huu Phuc Nguyen, M. Angela Cenci Berlin Heidelberg Springer Berlin Heidelberg 2015 Berlin Heidelberg Berlin Heidelberg Springer Berlin Heidelberg XIII, 397 p. 95 il., 25 il. col XIII, 397 p. Current Topics in Behavioral Neurosciences 22 Springer eBooks 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 Forma de acceso: World Wide Web Nguyen, Hoa Huu Phuc Cenci, M. Angela SpringerLink