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1 on with a single strain of the agent (bovine spongiform encephalopathy).
2 disease, a naturally occurring transmissible spongiform encephalopathy.
3 st system to study this cervid transmissible spongiform encephalopathy.
4 nts including Alzheimer's disease and bovine spongiform encephalopathy.
5 cluding Creutzfeldt-Jakob disease and bovine spongiform encephalopathy.
6 otes PrP amyloidogenesis in the absence of a spongiform encephalopathy.
7 transgenic mice (Tg PrP101LL), resulting in spongiform encephalopathy.
8 mum global risk for human exposure to bovine spongiform encephalopathy.
9 degenerative diseases known as transmissible spongiform encephalopathy.
10 om sheep with scrapie and cattle with bovine spongiform encephalopathy.
11 such as Creutzfeld-Jacob Disease and Bovine Spongiform Encephalopathy.
12 rom sheep with scrapie or cattle with bovine spongiform encephalopathy.
13 not previously examined in any transmissible spongiform encephalopathy.
14 ible for diseases such as scrapie and bovine 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 chronic wasting disease, scrapie, and bovine spongiform encephalopathy.
19 is responsible for a range of transmissible spongiform encephalopathies.
20 generative diseases called the transmissible spongiform encephalopathies.
21 e devastating neurological diseases known as spongiform encephalopathies.
22 onformation is associated with transmissible spongiform encephalopathies.
23 degenerative diseases known as transmissible spongiform encephalopathies.
24 he prevention of the spread of transmissible spongiform encephalopathies.
25 s of yet exists for any of the transmissible spongiform encephalopathies.
26 ng Alzheimer's disease and the transmissible spongiform encephalopathies.
27 gy resembling that observed in transmissible spongiform encephalopathies.
28 is the major event leading to transmissible spongiform encephalopathies.
29 at accumulates in mammals with transmissible spongiform encephalopathies.
30 s may be exploited in the diagnosis of these spongiform encephalopathies.
31 rotein responsible for the neurodegenerative spongiform encephalopathies.
32 genesis of orally communicated transmissible spongiform encephalopathies.
33 tential therapeutic agents for transmissible spongiform encephalopathies.
34 confer this high resistance to transmissible spongiform encephalopathies.
35 a prion that causes the fatal transmissible spongiform encephalopathies.
36 s to the infectious prion protein (PrPsc) in spongiform encephalopathies.
37 egenerative disorders known as transmissible spongiform encephalopathies.
40 e (CWD) is a universally fatal transmissible spongiform encephalopathy affecting cervids, and natural
43 Cross-species infection with transmissible spongiform encephalopathy agents may lead to subclinical
45 ronic wasting disease of cervids, and bovine spongiform encephalopathy) all seem to be laterally tran
46 ges in the prion protein cause transmissible spongiform encephalopathies, also referred to as prion d
47 raperitoneal, or oral); all groups developed spongiform encephalopathy, although the oral route requi
49 roinvasion in many prion diseases, in bovine spongiform encephalopathy and atypical cases of sheep sc
50 al host systems, including strains of bovine spongiform encephalopathy and chronic wasting disease.
51 nfluence the susceptibility to transmissible spongiform encephalopathy and determine the characterist
52 T treatment also inhibits the development of spongiform encephalopathy and gliosis in the central ner
54 ecific, and early diagnosis of transmissible spongiform encephalopathy and to further understand the
55 oxidative stress such as Friedreich ataxia, spongiform encephalopathies, and Alzheimer's and Parkins
57 nds their lifespan by threefold, rescues the spongiform encephalopathy, and attenuates mitochondrial
58 seases that include scrapie in sheep, bovine spongiform encephalopathy, and Creutzfeldt-Jakob disease
59 g PrP-101L with neurological disease, severe spongiform encephalopathy, and formation of proteinase K
60 were fed brain of (eleven) cows with bovine spongiform encephalopathy, and some were euthanized befo
63 nd systemic amyloidoses and prion-associated spongiform encephalopathies are acquired or inherited pr
65 generative diseases induced by transmissible spongiform encephalopathies are associated with prions.
73 overy that devastating brain diseases called spongiform encephalopathies are transmissible to new hos
75 ions, the infectious agents of transmissible spongiform encephalopathies, are composed primarily of a
76 Prion diseases, also known as transmissible spongiform encephalopathies, are fatal neurodegenerative
77 onic wasting disease and other transmissible spongiform encephalopathies, are misfolded proteins that
78 ) strains, notably those derived from bovine spongiform encephalopathy, are highly resistant to total
79 (PRNP) region in patients with transmissible spongiform encephalopathy associated with the PRNP D178N
81 Two atypical BSE strains, bovine amyloidotic spongiform encephalopathy (BASE, also named BSE-L) and B
82 ldt-Jakob disease (CJD), scrapie, and bovine spongiform encephalopathy because they express high leve
83 transmission efficiencies of vCJD and bovine spongiform encephalopathy (BSE) and an assessment of the
85 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 ldt-Jakob disease (CJD) in humans and bovine spongiform encephalopathy (BSE) and scrapie in animals.
89 l and neuropathological properties of bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-
91 , endemic sheep scrapie, and epidemic bovine spongiform encephalopathy (BSE) are caused by a related
93 illions of people possibly exposed to bovine spongiform encephalopathy (BSE) by consumption of BSE-in
96 -Jakob disease, following on from the bovine spongiform encephalopathy (BSE) epidemic, led to concern
97 n transmission was reported after the bovine spongiform encephalopathy (BSE) epidemic, when >200 case
98 dily distinguished experimental sheep bovine spongiform encephalopathy (BSE) from classical scrapie.
99 n protein PrP(C), such as PrP(BSE) in bovine spongiform encephalopathy (BSE) in cattle and PrP(CJD) i
100 wasting disease (CWD) in cervids and bovine spongiform encephalopathy (BSE) in cattle are prion dise
101 iseases and include scrapie in sheep, bovine spongiform encephalopathy (BSE) in cattle, chronic wasti
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
148 ons, the etiological agents in transmissible spongiform encephalopathies, exhibit remarkable resistan
149 ted sheep and cattle, and cattle with bovine spongiform encephalopathy failed to identify patterns ca
150 have been shown to be susceptible to feline spongiform encephalopathy (FSE), almost certainly caused
152 specimens for the diagnosis of transmissible spongiform encephalopathies has been described in sheep,
153 nto the causative agent of the transmissible spongiform encephalopathies, has previously been shown t
154 risks posed by prion zoonoses such as bovine spongiform encephalopathy, has focused much attention on
155 an form of a prion disease of cattle, bovine spongiform encephalopathy-have been reported from 12 cou
161 tion proportional to the incidence of bovine spongiform encephalopathy in the United Kingdom and acco
162 n, we show that prions causing transmissible spongiform encephalopathy in wild-type hamsters can be g
163 diagnosis and understanding of transmissible spongiform encephalopathies, including transmission mech
164 ntified as causative agents of transmissible spongiform encephalopathies, increasing evidence now sug
165 ritical goal of discriminating transmissible spongiform encephalopathy-infected from healthy uninfect
167 als in feedstuffs in order to prevent Bovine Spongiform Encephalopathy infection and diffusion, howev
168 significant removal of rodent transmissible spongiform encephalopathy infections by filtration of re
170 t the infectious agent causing transmissible spongiform encephalopathies is a conformational isomer o
171 t the infectious agent causing transmissible spongiform encephalopathies is a conformational isomer o
174 equired for the infectivity of transmissible spongiform encephalopathies is central to the debate abo
175 in protein structure may be at the basis of spongiform encephalopathies is changing our views of tra
176 t blood in naturally occurring transmissible spongiform encephalopathies is not infectious has implod
177 y event in the pathogenesis of transmissible spongiform encephalopathies is the conversion of PrP-sen
178 the protein-only hypothesis of transmissible spongiform encephalopathies is the link between inherite
179 ation and neurotoxicity during transmissible spongiform encephalopathies is undisputed, the physiolog
180 sceptible to the prion causing L-type bovine spongiform encephalopathy (L-BSE), although RQ171 sheep
181 affected by C-BSE and atypical L-type bovine spongiform encephalopathy (L-type BSE or L-BSE) with the
182 e UK population has been exposed to a bovine spongiform encephalopathy-like prion strain and are at r
186 e of its abnormal conformer in transmissible spongiform encephalopathies, normal PrP(C) may be implic
188 ronic wasting disease (CWD), a transmissible spongiform encephalopathy of cervids, was first document
189 ronic wasting disease (CWD), a transmissible spongiform encephalopathy of cervids, was first document
190 ronic wasting disease (CWD), a transmissible spongiform encephalopathy of deer, elk, and moose, is th
191 prevalent manifestation of the transmissible spongiform encephalopathies or prion diseases affecting
196 g approaches to the therapy of transmissible spongiform encephalopathies, or prion diseases, is beset
199 al step in the pathogenesis of transmissible spongiform encephalopathies (prion diseases) is the conv
200 imer's and Parkinson's and the transmissible spongiform encephalopathies (prion diseases), are charac
201 g disease (CWD) is an emerging transmissible spongiform encephalopathy (prion disease) of North Ameri
202 ep scrapie is the prototypical transmissible spongiform encephalopathy (prion disease), which has a f
204 ion strain resulting from exposure to bovine spongiform encephalopathy prions to which the Fore were
206 chronic waste disease (PrP(CWD)), and bovine spongiform encephalopathy (PrP(BSE)) in lab-scale compos
208 stant core identical to that found in bovine spongiform encephalopathy-specific scrapie-associated pr
212 Chronic wasting disease (CWD) is a fatal spongiform encephalopathy that is efficiently transmitte
213 imental challenge and the outbreak of bovine spongiform encephalopathy that occurred in the late 1980
214 ible to humans, as has been shown for bovine spongiform encephalopathy (the prion disease of cattle),
215 l as the interspecies transmission of bovine spongiform encephalopathy to humans in the form of varia
220 The risk of transmission of transmissible spongiform encephalopathies (TSE) between different spec
222 ectious agent of the mammalian transmissible spongiform encephalopathies (TSE) has long been consider
223 t current diagnostic tests for transmissible spongiform encephalopathies (TSE) rely on the presence o
226 form encephalopathy (BSE) is a transmissible spongiform encephalopathy (TSE) (or prion disease) that
228 Following oral exposure, some transmissible spongiform encephalopathy (TSE) agents accumulate first
229 n of tissue culture cells with transmissible spongiform encephalopathy (TSE) agents as a result of th
231 of many peripherally acquired transmissible spongiform encephalopathy (TSE) agents is less efficient
232 ection of cells with exogenous transmissible spongiform encephalopathy (TSE) agents, we examined the
234 presented here, using the same transmissible spongiform encephalopathy (TSE) animal model, our aim wa
236 protease-resistant PrP without transmissible spongiform encephalopathy (TSE) clinical signs or notabl
241 infectious agents (prions) of transmissible spongiform encephalopathy (TSE) diseases including chron
242 l infectious agents that cause transmissible spongiform encephalopathy (TSE) diseases, or prion disea
245 sly undetected sporadic bovine transmissible spongiform encephalopathy (TSE) have long been considere
248 nic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) of cervids now detected
250 the iatrogenic transmission of transmissible spongiform encephalopathy (TSE) or prion disease has bec
252 eared to be dependent upon the transmissible spongiform encephalopathy (TSE) strain, allowing discrim
255 discriminatory testing of all transmissible spongiform encephalopathy (TSE)-positive small ruminant
258 pecies were not susceptible to transmissible spongiform encephalopathies (TSEs) and therefore represe
264 zheimer's, Parkinson's and the transmissible spongiform encephalopathies (TSEs) are characterized by
265 ions responsible for mammalian transmissible spongiform encephalopathies (TSEs) are due primarily to
271 ess studied, pregnancy-related transmissible spongiform encephalopathies (TSEs) have been implicated
280 s about the possible spread of transmissible spongiform encephalopathies (TSEs) via blood products.
282 lassical scrapie is one of the transmissible spongiform encephalopathies (TSEs), a group of fatal inf
283 on diseases, also known as the transmissible spongiform encephalopathies (TSEs), are a group of fatal
285 ions, the infectious agents of transmissible spongiform encephalopathies (TSEs), have defied full cha
288 The agents responsible for transmissible spongiform encephalopathies (TSEs), or prion diseases, c
289 iginally formulated to explain transmissible spongiform encephalopathies (TSEs), the prion hypothesis
294 about the iatrogenic spread of transmissible spongiform encephalopathies (TSEs)/prion diseases throug
295 ission of the prion disorders (transmissible spongiform encephalopathies, TSEs) are mediated by a mod
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
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