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1 on with a single strain of the agent (bovine spongiform encephalopathy).
2 chronic wasting disease, scrapie, and bovine spongiform encephalopathy.
3 disease, a naturally occurring transmissible spongiform encephalopathy.
4 st system to study this cervid transmissible spongiform encephalopathy.
5 nts including Alzheimer's disease and bovine spongiform encephalopathy.
6 cluding Creutzfeldt-Jakob disease and bovine spongiform encephalopathy.
7 otes PrP amyloidogenesis in the absence of a spongiform encephalopathy.
8 transgenic mice (Tg PrP101LL), resulting in spongiform encephalopathy.
9 om sheep with scrapie and cattle with bovine spongiform encephalopathy.
10 such as Creutzfeld-Jacob Disease and Bovine Spongiform Encephalopathy.
11 rom sheep with scrapie or cattle with bovine spongiform encephalopathy.
12 not previously examined in any transmissible spongiform encephalopathy.
13 mum global risk for human exposure to bovine spongiform encephalopathy.
14 degenerative diseases known as transmissible spongiform encephalopathy.
15 evention of human dietary exposure to bovine spongiform encephalopathy.
16 nisms and/or at the onset of a transmissible spongiform encephalopathy.
17 shown to develop a spontaneous transmissible spongiform encephalopathy.
18 is responsible for a range of transmissible spongiform encephalopathies.
19 generative diseases called the transmissible spongiform encephalopathies.
20 confer this high resistance to transmissible spongiform encephalopathies.
21 e devastating neurological diseases known as spongiform encephalopathies.
22 onformation is associated with transmissible spongiform encephalopathies.
23 he prevention of the spread of transmissible spongiform encephalopathies.
24 s of yet exists for any of the transmissible spongiform encephalopathies.
25 ng Alzheimer's disease and the transmissible spongiform encephalopathies.
26 gy resembling that observed in transmissible spongiform encephalopathies.
27 is the major event leading to transmissible spongiform encephalopathies.
28 at accumulates in mammals with transmissible spongiform encephalopathies.
29 s may be exploited in the diagnosis of these spongiform encephalopathies.
30 rotein responsible for the neurodegenerative spongiform encephalopathies.
31 degenerative diseases known as transmissible spongiform encephalopathies.
32 are clinically associated with transmissible spongiform encephalopathies.
33 a prion that causes the fatal transmissible spongiform encephalopathies.
34 s to the infectious prion protein (PrPsc) in spongiform encephalopathies.
35 egenerative disorders known as transmissible spongiform encephalopathies.
38 e (CWD) is a universally fatal transmissible spongiform encephalopathy affecting cervids, and natural
41 Cross-species infection with transmissible spongiform encephalopathy agents may lead to subclinical
43 ronic wasting disease of cervids, and bovine spongiform encephalopathy) all seem to be laterally tran
44 ges in the prion protein cause transmissible spongiform encephalopathies, also referred to as prion d
45 raperitoneal, or oral); all groups developed spongiform encephalopathy, although the oral route requi
47 roinvasion in many prion diseases, in bovine spongiform encephalopathy and atypical cases of sheep sc
48 al host systems, including strains of bovine spongiform encephalopathy and chronic wasting disease.
49 nfluence the susceptibility to transmissible spongiform encephalopathy and determine the characterist
50 T treatment also inhibits the development of spongiform encephalopathy and gliosis in the central ner
52 ecific, and early diagnosis of transmissible spongiform encephalopathy and to further understand the
53 oxidative stress such as Friedreich ataxia, spongiform encephalopathies, and Alzheimer's and Parkins
55 nds their lifespan by threefold, rescues the spongiform encephalopathy, and attenuates mitochondrial
56 seases that include scrapie in sheep, bovine spongiform encephalopathy, and Creutzfeldt-Jakob disease
57 g PrP-101L with neurological disease, severe spongiform encephalopathy, and formation of proteinase K
58 were fed brain of (eleven) cows with bovine spongiform encephalopathy, and some were euthanized befo
59 herited prion disease; sheep scrapie; bovine spongiform encephalopathy; and chronic wasting disease.
62 nd systemic amyloidoses and prion-associated spongiform encephalopathies are acquired or inherited pr
64 generative diseases induced by transmissible spongiform encephalopathies are associated with prions.
72 overy that devastating brain diseases called spongiform encephalopathies are transmissible to new hos
74 ions, the infectious agents of transmissible spongiform encephalopathies, are composed primarily of a
75 Prion diseases, also known as transmissible spongiform encephalopathies, are fatal neurodegenerative
76 onic wasting disease and other transmissible spongiform encephalopathies, are misfolded proteins that
77 ) strains, notably those derived from bovine spongiform encephalopathy, are highly resistant to total
78 (PRNP) region in patients with transmissible spongiform encephalopathy associated with the PRNP D178N
80 Two atypical BSE strains, bovine amyloidotic spongiform encephalopathy (BASE, also named BSE-L) and B
81 ldt-Jakob disease (CJD), scrapie, and bovine spongiform encephalopathy because they express high leve
84 transmission efficiencies of vCJD and bovine spongiform encephalopathy (BSE) and an assessment of the
86 this has to be added the backwash of bovine spongiform encephalopathy (BSE) and foot-and-mouth disea
87 rodegenerative disorders that include bovine spongiform encephalopathy (BSE) and scrapie in animals a
88 l and neuropathological properties of bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-
89 , endemic sheep scrapie, and epidemic bovine spongiform encephalopathy (BSE) are caused by a related
91 illions of people possibly exposed to bovine spongiform encephalopathy (BSE) by consumption of BSE-in
95 -Jakob disease, following on from the bovine spongiform encephalopathy (BSE) epidemic, led to concern
96 n transmission was reported after the bovine spongiform encephalopathy (BSE) epidemic, when >200 case
97 dily distinguished experimental sheep bovine spongiform encephalopathy (BSE) from classical scrapie.
98 n protein PrP(C), such as PrP(BSE) in bovine spongiform encephalopathy (BSE) in cattle and PrP(CJD) i
99 wasting disease (CWD) in cervids and bovine spongiform encephalopathy (BSE) in cattle are prion dise
106 ethionine 129, inoculated with either bovine spongiform encephalopathy (BSE) or variant CJD prions, m
107 Creutzfeldt-Jakob disease (vCJD) and bovine spongiform encephalopathy (BSE) prions are two of the pr
108 ef products from cattle infected with bovine spongiform encephalopathy (BSE) prions causes new varian
109 sing concern over the extent to which bovine spongiform encephalopathy (BSE) prions have been transmi
110 ter the extensive dietary exposure to bovine spongiform encephalopathy (BSE) prions in the UK, has le
112 on protein (BoPrP) serially propagate bovine spongiform encephalopathy (BSE) prions without posing a
113 little about human susceptibility to bovine spongiform encephalopathy (BSE) prions, the causal agent
114 c mouse line, Tg(CerPrP)1536(+/-), to bovine spongiform encephalopathy (BSE) prions, which have the a
119 fection, it remains uncertain whether bovine spongiform encephalopathy (BSE) was transmitted to sheep
120 ob disease (vCJD), experimental ovine bovine spongiform encephalopathy (BSE), and natural sheep scrap
123 hat sheep and goats consumed the same bovine spongiform encephalopathy (BSE)-contaminated meat and bo
128 iciency syndrome (AIDS), hepatitis C, bovine spongiform encephalopathy (BSE)/variant Creutzfeldt-Jako
129 e for neurodegenerative diseases like bovine spongiform encephalopathy (BSE; "mad cow" disease) and C
130 are infected with prions from cattle (bovine spongiform encephalopathy [BSE]), both PrP variants occu
131 eases of cattle include the classical bovine spongiform encephalopathy (C-BSE) and the atypical H-typ
133 Some animal prion diseases, such as bovine spongiform encephalopathy, can infect humans; however, h
134 ditary and apparently sporadic transmissible spongiform encephalopathy cases associated with the D178
135 wild-type mice and was also found in bovine spongiform encephalopathy cattle brain, indicating that
138 21 overlap with QTLs associated with Bovine spongiform encephalopathy, clinical mastitis or somatic
139 ectious agents responsible for transmissible spongiform encephalopathies, consist mainly of the misfo
140 ught to be acquired by consumption of bovine spongiform encephalopathy-contaminated food products.
142 re the safety of processed meats from bovine spongiform encephalopathy contamination, and could also
143 n to replicate many aspects of transmissible spongiform encephalopathy disease to investigate the cel
147 ons, the etiological agents in transmissible spongiform encephalopathies, exhibit remarkable resistan
148 ted sheep and cattle, and cattle with bovine spongiform encephalopathy failed to identify patterns ca
149 have been shown to be susceptible to feline spongiform encephalopathy (FSE), almost certainly caused
151 specimens for the diagnosis of transmissible spongiform encephalopathies has been described in sheep,
152 nto the causative agent of the transmissible spongiform encephalopathies, has previously been shown t
153 risks posed by prion zoonoses such as bovine spongiform encephalopathy, has focused much attention on
154 an form of a prion disease of cattle, bovine spongiform encephalopathy-have been reported from 12 cou
160 tion proportional to the incidence of bovine spongiform encephalopathy in the United Kingdom and acco
161 n, we show that prions causing transmissible spongiform encephalopathy in wild-type hamsters can be g
162 diagnosis and understanding of transmissible spongiform encephalopathies, including transmission mech
163 ntified as causative agents of transmissible spongiform encephalopathies, increasing evidence now sug
164 ritical goal of discriminating transmissible spongiform encephalopathy-infected from healthy uninfect
166 als in feedstuffs in order to prevent Bovine Spongiform Encephalopathy infection and diffusion, howev
167 significant removal of rodent transmissible spongiform encephalopathy infections by filtration of re
169 t the infectious agent causing transmissible spongiform encephalopathies is a conformational isomer o
170 t the infectious agent causing transmissible spongiform encephalopathies is a conformational isomer o
173 equired for the infectivity of transmissible spongiform encephalopathies is central to the debate abo
174 t blood in naturally occurring transmissible spongiform encephalopathies is not infectious has implod
175 y event in the pathogenesis of transmissible spongiform encephalopathies is the conversion of PrP-sen
176 the protein-only hypothesis of transmissible spongiform encephalopathies is the link between inherite
177 ation and neurotoxicity during transmissible spongiform encephalopathies is undisputed, the physiolog
178 sceptible to the prion causing L-type bovine spongiform encephalopathy (L-BSE), although RQ171 sheep
179 affected by C-BSE and atypical L-type bovine spongiform encephalopathy (L-type BSE or L-BSE) with the
180 e UK population has been exposed to a bovine spongiform encephalopathy-like prion strain and are at r
184 e of its abnormal conformer in transmissible spongiform encephalopathies, normal PrP(C) may be implic
186 ronic wasting disease (CWD), a transmissible spongiform encephalopathy of cervids, was first document
187 ronic wasting disease (CWD), a transmissible spongiform encephalopathy of cervids, was first document
188 ronic wasting disease (CWD), a transmissible spongiform encephalopathy of deer, elk, and moose, is th
189 prevalent manifestation of the transmissible spongiform encephalopathies or prion diseases affecting
194 g approaches to the therapy of transmissible spongiform encephalopathies, or prion diseases, is beset
197 al step in the pathogenesis of transmissible spongiform encephalopathies (prion diseases) is the conv
198 imer's and Parkinson's and the transmissible spongiform encephalopathies (prion diseases), are charac
199 g disease (CWD) is an emerging transmissible spongiform encephalopathy (prion disease) of North Ameri
200 ep scrapie is the prototypical transmissible spongiform encephalopathy (prion disease), which has a f
202 ion strain resulting from exposure to bovine spongiform encephalopathy prions to which the Fore were
204 chronic waste disease (PrP(CWD)), and bovine spongiform encephalopathy (PrP(BSE)) in lab-scale compos
206 stant core identical to that found in bovine spongiform encephalopathy-specific scrapie-associated pr
210 Chronic wasting disease (CWD) is a fatal spongiform encephalopathy that is efficiently transmitte
211 imental challenge and the outbreak of bovine spongiform encephalopathy that occurred in the late 1980
212 ible to humans, as has been shown for bovine spongiform encephalopathy (the prion disease of cattle),
213 l as the interspecies transmission of bovine spongiform encephalopathy to humans in the form of varia
216 The risk of transmission of transmissible spongiform encephalopathies (TSE) between different spec
218 ectious agent of the mammalian transmissible spongiform encephalopathies (TSE) has long been consider
219 t current diagnostic tests for transmissible spongiform encephalopathies (TSE) rely on the presence o
223 form encephalopathy (BSE) is a transmissible spongiform encephalopathy (TSE) (or prion disease) that
225 Following oral exposure, some transmissible spongiform encephalopathy (TSE) agents accumulate first
226 n of tissue culture cells with transmissible spongiform encephalopathy (TSE) agents as a result of th
228 of many peripherally acquired transmissible spongiform encephalopathy (TSE) agents is less efficient
229 ection of cells with exogenous transmissible spongiform encephalopathy (TSE) agents, we examined the
231 presented here, using the same transmissible spongiform encephalopathy (TSE) animal model, our aim wa
233 protease-resistant PrP without transmissible spongiform encephalopathy (TSE) clinical signs or notabl
238 infectious agents (prions) of transmissible spongiform encephalopathy (TSE) diseases including chron
239 l infectious agents that cause transmissible spongiform encephalopathy (TSE) diseases, or prion disea
242 sly undetected sporadic bovine transmissible spongiform encephalopathy (TSE) have long been considere
245 nic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) of cervids now detected
247 the iatrogenic transmission of transmissible spongiform encephalopathy (TSE) or prion disease has bec
249 eared to be dependent upon the transmissible spongiform encephalopathy (TSE) strain, allowing discrim
252 discriminatory testing of all transmissible spongiform encephalopathy (TSE)-positive small ruminant
255 se of the similarities between transmissible spongiform encephalopathies (TSEs) and other protein mis
256 pecies were not susceptible to transmissible spongiform encephalopathies (TSEs) and therefore represe
262 zheimer's, Parkinson's and the transmissible spongiform encephalopathies (TSEs) are characterized by
263 ions responsible for mammalian transmissible spongiform encephalopathies (TSEs) are due primarily to
269 ess studied, pregnancy-related transmissible spongiform encephalopathies (TSEs) have been implicated
278 s about the possible spread of transmissible spongiform encephalopathies (TSEs) via blood products.
280 lassical scrapie is one of the transmissible spongiform encephalopathies (TSEs), a group of fatal inf
281 on diseases, also known as the transmissible spongiform encephalopathies (TSEs), are a group of fatal
283 ions, the infectious agents of transmissible spongiform encephalopathies (TSEs), have defied full cha
286 The agents responsible for transmissible spongiform encephalopathies (TSEs), or prion diseases, c
287 iginally formulated to explain transmissible spongiform encephalopathies (TSEs), the prion hypothesis
293 about the iatrogenic spread of transmissible spongiform encephalopathies (TSEs)/prion diseases throug
294 ission of the prion disorders (transmissible spongiform encephalopathies, TSEs) are mediated by a mod
296 linical signs, neuropathology (transmissible spongiform encephalopathy vacuolation and prion protein
297 several patients with various transmissible spongiform encephalopathies (variant and sporadic Creutz
298 sight into the molecular basis of hereditary spongiform encephalopathies, we have characterized the b
299 degenerative diseases known as transmissible spongiform encephalopathies, which affect humans, deer,
300 ectious agents responsible for transmissible spongiform encephalopathies, which appear to be composed