000			04039nam a22004817a 4500
001			sulb-eb0024509
003			BD-SySUS
005			20160413122443.0
007			cr nn 008mamaa
008			130328s2013 gw | s |||| 0|eng d
020			_a9783642354915 _9978-3-642-35491-5
024	7		_a10.1007/978-3-642-35491-5 _2doi
050		4	_aRC321-580
072		7	_aPSAN _2bicssc
072		7	_aMED057000 _2bisacsh
082	0	4	_a612.8 _223
245	1	0	_aProteopathic Seeds and Neurodegenerative Diseases _h[electronic resource] / _cedited by Mathias Jucker, Yves Christen.
264		1	_aBerlin, Heidelberg : _bSpringer Berlin Heidelberg : _bImprint: Springer, _c2013.
300			_aXII, 156 p. _bonline resource.
336			_atext _btxt _2rdacontent
337			_acomputer _bc _2rdamedia
338			_aonline resource _bcr _2rdacarrier
347			_atext file _bPDF _2rda
490	1		_aResearch and Perspectives in Alzheimer's Disease, _x0945-6066
505	0		_aPreface -- Widening Spectrum of Prions Causing Neurodegenerative Diseases (Stanley B. Prusiner).- b-Amyloid Fibril Structures, In Vitro and In Vivo (Robert Tycko).- Structure-Activity Relationship of Amyloids (Jason Greenwald and Roland Riek).- Seeding and Cross-seeding in Amyloid Diseases (Per Westermark and Gunilla T. Westermark).- The Prion-like Aspect of Alzheimer Pathology (Sarah K. Fritschi, Bahareh Eftekharzadeh, Giusi Manfredi, Tsuyoshi Hamaguchi, Götz Heilbronner, Amudha Nagarathinam, Franziska Langer, Yvonne S. Eisele, Lary Walker, Mathias Jucker).- Amyloid-β Transmissibility (Duran-Aniotz C, Morales R, Moreno-Gonzalez I, Soto C).- Prion-like Properties of Assembled Tau Protein (Florence Clavaguera, Markus Tolnay, and Michel Goedert).- Accumulating Evidence Suggests that Parkinson´s Disease is a Prion-like Disorder -- Nolwen L. Rey, Elodie Angot, Christopher Dunning, Jennifer A. Steiner, Patrik Brundin).- Propagation and Replication of Misfolded SOD1: Implications for Amyotrophic Lateral Sclerosis (Anne Bertolotti) -- Development of Drugs that Target Proteopathic Seeds Will Require Measurement of Drug Mechanism in Human Brain (Peter T. Lansbury).- The Role of Functional Prions in the Persistence of Memory Storage (Eric R. Kandel, Irina Derkatch, Elias Pavlopoulos) -- Subject Index.
520			_aThe misfolding and aggregation of specific proteins is an early and obligatory event in many of the age-related neurodegenerative diseases of humans, and appears to occur many years before the onset of clinical symptoms. The initial cause of this pathogenic cascade and the means whereby disease spreads through the nervous system, remain uncertain. A recent surge of research, first instigated by pathologic similarities between prion disease and Alzheimer’s disease, has increasingly implicated corruptive protein templating, or seeding, as a prime factor in the neurodegenerative process. The prion-like corruption of proteins also characterizes such clinically and etiologically diverse neurological disorders as Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, and frontotemporal lobar degeneration. Understanding the misfolding, aggregation, trafficking and pathogenicity of affected proteins thus could reveal universal principles and common therapeutic targets for some of the most devastating and intractable human brain disorders.
650		0	_aMedicine.
650		0	_aNeurosciences.
650		0	_aPharmacology.
650	1	4	_aBiomedicine.
650	2	4	_aNeurosciences.
650	2	4	_aPharmacology/Toxicology.
700	1		_aJucker, Mathias. _eeditor.
700	1		_aChristen, Yves. _eeditor.
710	2		_aSpringerLink (Online service)
773	0		_tSpringer eBooks
776	0	8	_iPrinted edition: _z9783642354908
830		0	_aResearch and Perspectives in Alzheimer's Disease, _x0945-6066
856	4	0	_uhttp://dx.doi.org/10.1007/978-3-642-35491-5
912			_aZDB-2-SBL
942			_2Dewey Decimal Classification _ceBooks
999			_c46601 _d46601