Read more
Motor dysfunction and cognitive impairment are major symptoms in both Huntington's Disease (HD) and Parkinson's Disease (PD). A breakthrough in HD research was the identification of the gene that causes this devastating monogenetic illness. Similarly, several genes were found to cause familial forms of PD. With their identification, a plethora of genetic animal models has been generated and has revolutionized the understanding of the pathobiology and pathophysiology of these disorders. The models allow us to study the earliest manifestations of the diseases behaviorally and neuropathologically and help us understand how they progress over time. Additionally, neurotoxic animal models are still of high interest to the PD field, as they are being used to study e.g. mitochondrial dysfunction in PD. This book focuses on animal models of both diseases and how they have helped and will continue to help understand the behavioral neurobiology in these disorders.
List of contents
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.
Summary
Motor dysfunction and cognitive impairment are major symptoms in both Huntington’s Disease (HD) and Parkinson’s Disease (PD). A breakthrough in HD research was the identification of the gene that causes this devastating monogenetic illness. Similarly, several genes were found to cause familial forms of PD. With their identification, a plethora of genetic animal models has been generated and has revolutionized the understanding of the pathobiology and pathophysiology of these disorders. The models allow us to study the earliest manifestations of the diseases behaviorally and neuropathologically and help us understand how they progress over time. Additionally, neurotoxic animal models are still of high interest to the PD field, as they are being used to study e.g. mitochondrial dysfunction in PD. This book focuses on animal models of both diseases and how they have helped and will continue to help understand the behavioral neurobiology in these disorders.
