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336			_aTexto _btxt _2rdacontent
710	2		_aSpringerLink (Online service) _0http://id.loc.gov/authorities/names/no2005046756 _1http://viaf.org/viaf/148105729 _9106996
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008			180209s2018 gw | s |||| 0|eng d
020			_a9783319717791
024	7		_a10.1007/978-3-319-71779-1 _2doi
050		4	_aRC346.4 _b2018 EB
245	1	0	_aPolyglutamine Disorders _cedited by Clévio Nóbrega, Luís Pereira de Almeida.
264		1	_aCham, Switzerland _bSpringer International Publishing _c2018
300			_a1 recurso en línea (VIII, 469 páginas 41 ilustraciones,39 ilustraciones a color)
337			_2rdamedia _aelectrónico _bc
338			_2rdacarrier _arecurso electrónico _bcr
347			_atext file _bPDF
490	0		_aAdvances in Experimental Medicine and Biology _x0065-2598 _v1049
490	0		_aBiomedical and Life Sciences (Springer-11642)
520	3		_aThis book provides a cutting-edge review of polyglutamine disorders. It primarily focuses on two main aspects: (1) the mechanisms underlying the pathologies' development and progression, and (2) the therapeutic strategies that are currently being explored to stop or delay disease progression.  Polyglutamine (polyQ) disorders are a group of inherited neurodegenerative diseases with a fatal outcome that are caused by an abnormal expansion of a coding trinucleotide repeat (CAG), which is then translated in an abnormal protein with an elongated glutamine tract (Q). To date, nine polyQ disorders have been identified and described: dentatorubral-pallidoluysian atrophy (DRPLA); Huntington's disease (HD); spinal-bulbar muscular atrophy (SBMA); and six spinocerebellar ataxias (SCA 1, 2, 3, 6, 7, and 17). The genetic basis of polyQ disorders is well established and described, and despite important advances that have opened up the possibility of generating genetic models of the disease, the mechanisms that cause neuronal degeneration are still largely unknown and there is currently no treatment available for these disorders. Further, it is believed that the different polyQ may share some mechanisms and pathways contributing to neurodegeneration and disease progression.
650		7	_aNeurociencias _2embne _9158907
650		7	_aSistema nervioso _2embne _9138462
650		7	_aNeurología _2embne _9139040
650		7	_aGenética _2embne _9138044
700	1		_aNóbrega, Clévio _eeditor literario _4edt _4http://id.loc.gov/vocabulary/relators/edt _0http://id.loc.gov/authorities/names/n2015182366
700	1		_aPereira de Almeida, Luís _eeditor literario _4edt _4http://id.loc.gov/vocabulary/relators/edt
776	0	8	_iEdición impresa: _z9783319717784
776	0	8	_iEdición impresa: _z9783319717807
776	0	8	_iEdición impresa: _z9783319891033
856	4	0	_uhttps://go.openathens.net/redirector/universidadeuropea.es?url=https://doi.org/10.1007/978-3-319-71779-1 _zAcceso a este recurso digital (usuarios Universidad Europea de Madrid)
942			_2lcc _cLE
998			_aSI _b03/2019 _cm _dz _ep _feng _ggw _h0