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008			150523s2015 gw | s |||| 0|eng d
020			_a9783662463444
024	7		_a10.1007/978-3-662-46344-4 _2doi
050		4	_aRC346 _b.B44 2015 EB
082	0	4	_a612.8
245	1	0	_aBehavioral Neurobiology of Huntington's Disease and Parkinson's Disease _cedited by Hoa Huu Phuc Nguyen, M. Angela Cenci.
264		1	_aBerlin, Heidelberg _bSpringer _c2015
300			_a1 recurso en línea (XIII, 397 páginas) _b95 ilustraciones, 25 ilustraciones en color
336			_aTexto (visual) _btxt _2rdacontent
337			_aelectrónico _bc _2rdamedia
338			_arecurso electrónico _bcr _2rdacarrier
490	0		_aCurrent Topics in Behavioral Neurosciences _x1866-3370 _v22
505	0		_aClinical Aspects of Huntingtonâ€{u3804}isease -- The Neuropathology of Huntingtonâ€{u3804}isease -- Neurobiology of Huntingtonâ€{u3804}isease -- Mouse Models of Huntingtonâ€{u3804}isease -- Transgenic Rat Models of Huntingtonâ€{u3804}isease -- Large Animal Models of Huntingtonâ€{u3804}isease -- Therapeutic Strategies for Huntingtonâ€{u3804}isease -- Clinical and Pathological Features of Parkinsonâ€{u3804}isease -- Symptomatic Models of Parkinsonâ€{u3804}isease and L-DOPA-Induced Dyskinesia in Non-human Primates -- Neuroinflammation in Parkinsonâ€{u3804}isease Animal Models: A Cell Stress Response or a Step in Neurodegeneration? -- Viral Vector-Based Models of Parkinsonâ€{u3804}isease -- Transgenic Rodent Models to Study Alpha-Synuclein Pathogenesis, with a Focus on Cognitive Deficits -- Modeling LRRK2 Pathobiology in Parkinsonâ€{u3804}isease: From Yeast to Rodents -- Models of Multiple System Atrophy.
520			_aMotor dysfunction and cognitive impairment are major symptoms in both Huntingtonâ€{u3804}isease (HD) and Parkinsonâ€{u3804}isease (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		7	_aNeurología _2embne _9139040
650		7	_aParkinson, Enfermedad de _2embne _9141804
700	1		_aCenci, M. Angela _eeditor literario _994051 _0Local _0http://id.loc.gov/authorities/names/nb2010024617 _1http://viaf.org/viaf/152711975
700	1		_aNguyen, Hoa Huu Phuc _eeditor literario _994050 _0Local _0http://id.loc.gov/authorities/names/n2015189220 _1http://viaf.org/viaf/243144782712282545533
710	2		_aSpringerLink (Online service) _0Local _0http://id.loc.gov/authorities/names/no2005046756 _1http://viaf.org/viaf/148105729 _9106996
856	4	0	_uhttps://go.openathens.net/redirector/universidadeuropea.es?url=https://link.springer.com/book/10.1007/978-3-662-46344-4 _zAcceso a este recurso digital (usuarios Universidad Europea de Madrid)
907			_a.b1290157x _b10-10-17 _c18-01-16
942			_2lcc _cLE
945			_aRC321-580 EB _g1 _ieBOOK _j0 _lmae _o- _pEUR0.00 _q- _r- _sb _t15 _u0 _v0 _w0 _x0 _y.i11571196 _z06-04-17
988	0	0	_aEBOOK, EBSPRINGER, GOBI_sep2018
988			_aEbook_one2one
998			_aSI _a_alco _a_vill _b10/2018 _cm _dz _ef _feng _ggw _h0
999			_c81567 _d81567 _x1