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003			ES-MaUEC
005			20230207040151.0
008			160707s2006 mau| s |||| 0|eng d
020			_a9780387301723
040			_aES-MaUEC
050		4	_aQP562.A8 _bN33 2006 EB
245	0	0	_aN-Acetylaspartate : _ba unique neuronal molecule in the central nervous system _cedited by John R. Moffet... [et al.]
260			_aBoston _bSpringer International Publishing _c2006
300			_a1 recurso en línea (XVII, 375 p.) _b114 il.
336			_aTexto (visual) _btxt _2rdacontent
337			_aelectrónico _bc _2rdamedia
338			_arecurso electrónico _bcr _2rdacarrier
338			_aonline resource _bcr _2rdacarrier
490	1		_aAdvances in Experimental Medicine and Biology _v576
520			_aN-acetylaspartate, or NAA, is the acetylated form of the amino acid aspartate, and it is present exclusively in the nervous system. Indeed, NAA is one of the most highly concentrated chemicals found in the brain of humans and animals, and yet the functions served by this brain-specific metabolite remain elusive, and controversial. Despite the uncertainties surrounding the functions of NAA in the development and operation of the nervous system, this molecule has attracted the attention of researchers and clinicians for two distinct reasons. First, the acetyl proton on NAA gives off a very prominent signal in water-suppressed, proton magnetic resonance spectroscopy (MRS), which permits clinicians to monitor levels of NAA in the brains of patients in a non-invasive manner. Because NAA is found primarily in neurons, and because the levels in the brain have been found to change rapidly after injury, or slowly during neurodegenerative diseases, MRS has become a preferred method of analyzing nerve cell dysfunction and death without surgical intervention. The second reason that NAA has attracted attention in recent years is that a congenital genetic disorder of NAA metabolism has been found to be the cause of the neurodegenerative disorder known as Canavanâ Disease. Canavanâ Disease is an inherited leukodystrophy that involves myelination pathologies of cortical white matter, leading to death within 10 years of birth. The genetic mutation results in a defective enzyme that de-acetylates NAA in the brain, resulting in a significant rise in NAA levels in the brain and urine. This enzyme, known as aspartoacylase (ASPA), appears to be involved in the process of myelination, such that a defective enzyme results in a disruption of the myelination of nerve fibers during development. The purpose of this symposium is to bring together investigators from around the world who are interested in the study of NAA, and the roles it plays in neuronal development and functioning. It is hoped that bringing researchers and clinicians together in such a forum will facilitate rapid progress in this emerging field, and will help lead to discoveries that can alleviate the suffering caused by a deadly, inheritable infantile disease.
650		7	_aAminoácidos _2embne _9138424
700	1		_aMoffett, John R _eeditor literario _984133 _0Local
856	4	0	_uhttps://go.openathens.net/redirector/universidadeuropea.es?url=https://link.springer.com/book/10.1007/0-387-30172-0 _zAcceso a este recurso digital (usuarios Universidad Europea de Madrid)
901			_ai9780387301723
907			_a.b12812456 _b10-10-17 _c01-10-14
942			_2lcc _cLE
945			_aQP562.A8 N33 2006 EB _g1 _ieBOOK _j0 _lmae _o- _pEUR0.00 _q- _r- _sb _t15 _u0 _v0 _w0 _x0 _y.i11541830 _z06-04-17
988			_aEBOOK, EBSPRINGERrevisado
998			_am _a_alco _a_vill _b07-07-16 _cm _dz _ef _feng _gmau _h0