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008			160913s2016 gw | s |||| 0|eng d
020			_a9783319421391
040			_aES-MaUEC
050		4	_aRC382 _b.M586 2016 EB
082	0	4	_a612.8042
090			_aRC382 _b.M586 2016
245	1	0	_aMitochondrial Mechanisms of Degeneration and Repair in Parkinson's Disease _cedited by Lori M Buhlman
260			_aCham _bSpringer International Publishing _c2016
300			_a1 recurso en línea (XII, 275 p.) _b28 ilustraciones, 23 ilustraciones en color
336			_aTexto (visual) _btxt _2rdacontent
337			_aelectrónico _bc _2rdamedia
338			_arecurso electrónico _bcr _2rdacarrier
505	0		_aMitochondrial ROS and Apoptosis -- Dopamine Metabolism and Reactive Oxygen Species Production -- The Consequences of Damaged Mitochondrial DNA -- The role of chronic inflammation in the etiology of Parkinson�s disease -- Ion-Catalyzed Reactive Oxygen Species in Sporadic Models of Parkinson's Disease -- Toxin Mediated Complex I Inhibition and Parkinson�s Disease -- Parkinson Disease-Associated Mutations Affect Mitochondrial Function -- PARKIN/PINK1 Pathway for the Selective Isolation and Degradation of Impaired Mitochondria -- Mitochondrial Therapeutic approaches in Parkinson's Disease -- Altering Mitochondrial Fusion and Fission Protein Levels Rescues Parkin and PINK1 Loss-of-Function Phenotypes -- Early Nicotine Exposure is Protective in Familial and Idiopathic Models of Parkinson�s Disease -- Transcription Modulation of Mitochondrial Function and Related Pathways as a Therapeutic Opportunity in Parkinson�s Disease -- Delivery of Biologically Active Molecules to Mitochondria.
520			_aThis volume brings together various theories of how aberrations in mitochondrial function and morphology contribute to neurodegeneration in idiopathic and familial forms of Parkinson�s disease. Moreover, it comprehensively reviews the current search for therapies, and proposes how molecules are involved in specific functions as attractive therapeutic targets. It is expected to facilitate critical thought and discussion about the fundamental aspects of neurodegeneration in Parkinson�s disease and foster the development of therapeutic strategies among researchers and graduate students. Theories of idiopathic Parkinson�s etiology support roles for chronic inflammation and exposure to heavy metals or pesticides. Interestingly, as this project proposes, a case can be made that abnormalities in mitochondrial morphology and function are at the core of each of these theories. In fact, the most common approach to the generation of animal and cell-culture models of idiopathic Parkinson�s disease involves exposure to mitochondrial toxins. Even more compelling is the fact that most familial patients harbor genetic mutations that cause disruptions in normal mitochondrial morphology and function. While there remains to be no effective treatment for Parkinson�s disease, efforts to postpone, prevent and zcurey onset mitochondrial aberrations and neurodegeneration associated with Parkinson�s disease in various models are encouraging. While only about ten percent of Parkinson�s patients inherit disease-causing mutations, discovering common mechanisms by which familial forms of Parkinson�s disease manifest will likely shed light on the pathophysiology of the more common idiopathic form and provide insight to the general process of neurodegeneration, thus revealing therapeutic targets that will become more and more accessible as technology improves.
710	2		_aSpringerLink (Online service) _0Local _9106996
942			_2lcc _cLE
988	0	0	_aEBOOK, EBSPRINGER
650		7	_aMedicina _0comprobar BNE19900959047 _2embne _9405021
650		7	_9146728 _aNeuroquímica _0comprobar BNE19923784923 _2embne
650		7	_aNeurología _0comprobar BNE19900967585 _2embne _9139040
700	1		_aBuhlman, Lori M. _eeditor literario _999856 _0Local
856	4	0	_uhttps://go.openathens.net/redirector/universidadeuropea.es?url=https://link.springer.com/book/10.1007/978-3-319-42139-1 _zAcceso a este recurso digital (usuarios Universidad Europea de Madrid)
901			_ai9783319421391
907			_a.b12955437 _b10-10-17 _c21-11-16
998			_am _a_alco _a_vill _b - - _cm _dz _e- _feng _ggw _h0
945			_aRC382 .M586 2016 EB _g1 _ieBOOK _j0 _lmae _o- _pEUR0.00 _q- _r- _sb _t15 _u0 _v0 _w0 _x0 _y.i11615278 _z30-06-17
999			_c86265 _d86265 _x1