000			03554nam a22004095i 4500
001			293496
003			MX-SnUAN
005			20181024133115.0
007			cr nn 008mamaa
008			150903s2005 gw | o |||| 0|eng d
020			_a9783540265221 _99783540265221
024	7		_a10.1007/b137738 _2doi
035			_avtls000346637
039		9	_a201509030419 _bVLOAD _c201405070508 _dVLOAD _y201402070902 _zstaff
040			_aMX-SnUAN _bspa _cMX-SnUAN _erda
050		4	_aRC321-580
100	1		_9414856 _aCummings, Jeffrey L., _d1948- _eeditor.
245	1	0	_aGenotype — Proteotype — Phenotype Relationships in Neurodegenerative Diseases / _cedited by Jeffrey L. Cummings, Michel Poncet, John Hardy, Yves Christen.
264		1	_aBerlin, Heidelberg : _bSpringer Berlin Heidelberg, _c2005.
300			_axiii, 166 páginas 20 ilustraciones _brecurso en línea.
336			_atexto _btxt _2rdacontent
337			_acomputadora _bc _2rdamedia
338			_arecurso en línea _bcr _2rdacarrier
347			_aarchivo de texto _bPDF _2rda
490	0		_aResearch and Perspectives in Alzheimer's Disease, _x0945-6066
500			_aSpringer eBooks
505	0		_aNeurodegenerative Disorders as Proteinopathies: Phenotypic Relationships -- Towards a Molecular Classification of Neurodegenerative Disease -- Racial and Ethnic Influences on the Expression of the Genotype in Neurodegenerative Diseases -- Causes and Consequences of Oxidative Stress in Neurodegenerative Diseases -- Early Onset Familial Alzheimer's Disease: Is a Mutation Predictive of Pathology? -- Identification of Genes that Modify the Age of Onset in a Large Familial Alzheimer's Disease Kindred -- Variable Phenotype of Alzheimer's Disease with Spastic Paraparesis -- Presenilin Mutations: Variations in the Behavioral Phenotype with an Emphasis on the Frontotemporal Dementia Phenotype -- Frontotemporal Dementias: Genotypes and Phenotypes -- Chromosome 17-linked Frontotemporal dementia with Ubiquitin-Positive, Tau-Negative Inclusions -- Variations of the Phenotype in Frontotemporal Dementias -- Phenotype/genotype correlations in Parkinson's disease.
520			_aProtein misfolding and other abnormalities of protein metabolism are increasingly recognized as central mechanisms in the pathophysiology of neurodegenerative disorders. Amyloid beta protein disturbances in Alzheimer’s disease, tau and ubiquitin protein abnormalities in frontotemporal dementias, proteasome and alpha-synuclein disorders in Parkinson’s disease and dementia with Lewy bodies comprise central elements in these common neurodegenerative diseases. Improved understanding of role of protein dysmetabolism in neurodegeneration promises to improve diagnoses, facilitate the development of biological markers relevant to disease pathophysiology, and provide tractable therapeutic targets. This Fondation IPSEN conference summary provides an update on the latest advances of the role of protein misfolding in the pathophysiology of neurodegenerative diseases.
590			_aPara consulta fuera de la UANL se requiere clave de acceso remoto.
700	1		_aPoncet, Michel. _eeditor. _9326126
700	1		_aHardy, John. _eeditor. _9326127
700	1		_aChristen, Yves. _eeditor. _9326128
710	2		_aSpringerLink (Servicio en línea) _9299170
776	0	8	_iEdición impresa: _z9783540248354
856	4	0	_uhttp://remoto.dgb.uanl.mx/login?url=http://dx.doi.org/10.1007/b137738 _zConectar a Springer E-Books (Para consulta externa se requiere previa autentificación en Biblioteca Digital UANL)
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999			_c293496 _d293496