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020 _a9783662463444
_9978-3-662-46344-4
024 7 _a10.1007/978-3-662-46344-4
_2doi
035 _ato000561746
040 _aSpringer
_cSpringer
_dRU-ToGU
050 4 _aRC321-580
072 7 _aPSAN
_2bicssc
072 7 _aMED057000
_2bisacsh
082 0 4 _a612.8
_223
245 1 0 _aBehavioral Neurobiology of Huntington's Disease and Parkinson's Disease
_helectronic resource
_cedited by Hoa Huu Phuc Nguyen, M. Angela Cenci.
260 _aBerlin, Heidelberg :
_bSpringer Berlin Heidelberg :
_bImprint: Springer,
_c2015.
300 _aXIII, 397 p. 95 illus., 25 illus. in color.
_bonline resource.
336 _atext
_btxt
_2rdacontent
337 _acomputer
_bc
_2rdamedia
338 _aonline resource
_bcr
_2rdacarrier
490 1 _aCurrent Topics in Behavioral Neurosciences,
_x1866-3370 ;
_v22
505 0 _aClinical 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.
520 _aMotor 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.
650 0 _amedicine.
_9566220
650 0 _aHuman genetics.
_9566248
650 0 _aNeurosciences.
_9302217
650 0 _aCell Biology.
_9302220
650 0 _aNeurobiology.
_9303649
650 1 4 _aBiomedicine.
_9566246
650 2 4 _aNeurosciences.
_9302217
650 2 4 _aHuman Genetics.
_9566249
650 2 4 _aNeurobiology.
_9303649
650 2 4 _aCell Biology.
_9302220
700 1 _aNguyen, Hoa Huu Phuc.
_eeditor.
_9470260
700 1 _aCenci, M. Angela.
_eeditor.
_9470261
710 2 _aSpringerLink (Online service)
_9143950
773 0 _tSpringer eBooks
830 0 _aCurrent Topics in Behavioral Neurosciences,
_9412800
856 4 0 _uhttp://dx.doi.org/10.1007/978-3-662-46344-4
912 _aZDB-2-SBL
999 _c416958