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1 class of neurodegenerative diseases known as transmissible spongiform encephalopathy.
2 0 transcripts not previously examined in any transmissible spongiform encephalopathy.
3 notype influences the phenotypic features of transmissible spongiform encephalopathy.
4 rity onset diabetes, Alzheimer's disease and transmissible spongiform encephalopathy.
5 n healthy organisms and/or at the onset of a transmissible spongiform encephalopathy.
6 has also been shown to develop a spontaneous transmissible spongiform encephalopathy.
7 ronic wasting disease, a naturally occurring transmissible spongiform encephalopathy.
8 odel as a robust system to study this cervid transmissible spongiform encephalopathy.
9 a-sheet rich conformation is associated with transmissible spongiform encephalopathies.
10 group of neurodegenerative diseases known as transmissible spongiform encephalopathies.
11 ng tools for the prevention of the spread of transmissible spongiform encephalopathies.
12 No cure as of yet exists for any of the transmissible spongiform encephalopathies.
13 itions including Alzheimer's disease and the transmissible spongiform encephalopathies.
14 biting pathology resembling that observed in transmissible spongiform encephalopathies.
15 crapie (PrPSc) is the major event leading to transmissible spongiform encephalopathies.
16 t aggregate that accumulates in mammals with transmissible spongiform encephalopathies.
17 d in the pathogenesis of orally communicated transmissible spongiform encephalopathies.
18 s models of potential therapeutic agents for transmissible spongiform encephalopathies.
19 P(Sc) conformation, which is associated with transmissible spongiform encephalopathies.
20 ars to be a key event in the pathogenesis of transmissible spongiform encephalopathies.
21 Alzheimer's disease, type 2 diabetes and the transmissible spongiform encephalopathies.
22 central to the control of development of all transmissible spongiform encephalopathies.
23 rugs have favorably influenced the course of transmissible spongiform encephalopathies.
24 mule deer, and elk with naturally occurring transmissible spongiform encephalopathies.
25 a potential source of therapeutic agents for transmissible spongiform encephalopathies.
26 ng prion protein (PrP-null) are resistant to transmissible spongiform encephalopathies.
27 or Creutzfeldt-Jakob disease and the related transmissible spongiform encephalopathies.
28 PSc) is a central event in scrapie and other transmissible spongiform encephalopathies.
29 otein can form a prion that causes the fatal transmissible spongiform encephalopathies.
30 rminants that confer this high resistance to transmissible spongiform encephalopathies.
31 roup of neurodegenerative disorders known as transmissible spongiform encephalopathies.
32 hen misfolded, is responsible for a range of transmissible spongiform encephalopathies.
33 oup of neurodegenerative diseases called the transmissible spongiform encephalopathies.
35 wasting disease (CWD) is a universally fatal transmissible spongiform encephalopathy affecting cervid
36 l PrP-sen-expressing cells appear to support transmissible spongiform encephalopathy agent replicatio
37 , the species specificity in transmission of transmissible spongiform encephalopathy agents in vivo.
40 rmational changes in the prion protein cause transmissible spongiform encephalopathies, also referred
41 mic amyloidosis, Alzheimer's disease and the transmissible spongiform encephalopathies always contain
42 rP, has a key role in the development of the transmissible spongiform encephalopathies and the level
43 seen in neurodegenerative diseases, such as transmissible spongiform encephalopathy and Alzheimer di
44 n of PrP can influence the susceptibility to transmissible spongiform encephalopathy and determine th
45 sensitive, specific, and early diagnosis of transmissible spongiform encephalopathy and to further u
46 heimer's disease, type II diabetes mellitus, transmissible spongiform encephalopathies, and prion dis
64 f scrapie, chronic wasting disease and other transmissible spongiform encephalopathies, are misfolded
65 protein gene (PRNP) region in patients with transmissible spongiform encephalopathy associated with
67 ence that hereditary and apparently sporadic transmissible spongiform encephalopathy cases associated
68 rions, the infectious agents responsible for transmissible spongiform encephalopathies, consist mainl
70 nce of the PrP protein in the development of transmissible spongiform encephalopathies, despite the f
71 reviously shown to replicate many aspects of transmissible spongiform encephalopathy disease to inves
78 AMALT) biopsy specimens for the diagnosis of transmissible spongiform encephalopathies has been descr
79 d to misfold into the causative agent of the transmissible spongiform encephalopathies, has previousl
80 t of infectious prions that cause a group of transmissible spongiform encephalopathies in animals and
82 n diagnostic and pathogenesis studies of the transmissible spongiform encephalopathies in these rumin
83 ation variation, we show that prions causing transmissible spongiform encephalopathy in wild-type ham
85 vances in the diagnosis and understanding of transmissible spongiform encephalopathies, including tra
86 Originally identified as causative agents of transmissible spongiform encephalopathies, increasing ev
87 achieved the critical goal of discriminating transmissible spongiform encephalopathy-infected from he
88 not the source of blood-borne infectivity in transmissible spongiform encephalopathy-infected hamster
89 demonstrating significant removal of rodent transmissible spongiform encephalopathy infections by fi
90 fore not necessarily be a reliable marker of transmissible spongiform encephalopathy infectivity.
92 sis states that the infectious agent causing transmissible spongiform encephalopathies is a conformat
93 esis holds that the infectious agent causing transmissible spongiform encephalopathies is a conformat
94 hat the critical step in the pathogenesis of transmissible spongiform encephalopathies is a transitio
97 leic acid is required for the infectivity of transmissible spongiform encephalopathies is central to
98 The idea that blood in naturally occurring transmissible spongiform encephalopathies is not infecti
100 at the critical event in the pathogenesis of transmissible spongiform encephalopathies is the convers
101 s in favor of the protein-only hypothesis of transmissible spongiform encephalopathies is the link be
102 n prion replication and neurotoxicity during transmissible spongiform encephalopathies is undisputed,
103 s of kuru, the only other orally transmitted transmissible spongiform encephalopathy, might be instru
106 ion to the role of its abnormal conformer in transmissible spongiform encephalopathies, normal PrP(C)
110 rly understood, steps in the pathogenesis of transmissible spongiform encephalopathies or prion disea
111 A central aspect of pathogenesis in the transmissible spongiform encephalopathies or prion disea
112 ) is the most prevalent manifestation of the transmissible spongiform encephalopathies or prion disea
114 ) is a required factor for susceptibility to transmissible spongiform encephalopathy or prion disease
117 euroinflammatory response may play a role in transmissible spongiform encephalopathy pathogenesis.
118 ncluding Alzheimer's and Parkinson's and the transmissible spongiform encephalopathies (prion disease
119 The critical step in the pathogenesis of transmissible spongiform encephalopathies (prion disease
120 Chronic wasting disease (CWD) is an emerging transmissible spongiform encephalopathy (prion disease)
131 A fundamental event in the pathogenesis of transmissible spongiform encephalopathies (TSE) is the c
137 Bovine spongiform encephalopathy (BSE) is a transmissible spongiform encephalopathy (TSE) (or prion
140 f contamination of tissue culture cells with transmissible spongiform encephalopathy (TSE) agents as
142 e pathogenesis of many peripherally acquired transmissible spongiform encephalopathy (TSE) agents is
143 he initial infection of cells with exogenous transmissible spongiform encephalopathy (TSE) agents, we
144 tures strikingly similar to those induced by transmissible spongiform encephalopathy (TSE) agents.
145 In the study presented here, using the same transmissible spongiform encephalopathy (TSE) animal mod
147 activity and protease-resistant PrP without transmissible spongiform encephalopathy (TSE) clinical s
149 exerts a major influence over the outcome of transmissible spongiform encephalopathy (TSE) disease, b
150 this mutation (101LL) showed no spontaneous transmissible spongiform encephalopathy (TSE) disease, b
154 to translocate infectious agents (prions) of transmissible spongiform encephalopathy (TSE) diseases i
156 unconventional infectious agents that cause transmissible spongiform encephalopathy (TSE) diseases,
157 nventional infectious agents responsible for transmissible spongiform encephalopathy (TSE) diseases.
158 feature of the pathogenesis associated with transmissible spongiform encephalopathy (TSE) diseases.
159 ission via blood transfusion exists for many transmissible spongiform encephalopathy (TSE) diseases.
160 e or a previously undetected sporadic bovine transmissible spongiform encephalopathy (TSE) have long
161 a novel and advantageous model for studying transmissible spongiform encephalopathy (TSE) infection.
166 Bovine spongiform encephalopathy (BSE) is a transmissible spongiform encephalopathy (TSE) or prion d
167 e of blood in the iatrogenic transmission of transmissible spongiform encephalopathy (TSE) or prion d
169 ellum also appeared to be dependent upon the transmissible spongiform encephalopathy (TSE) strain, al
170 ime strategy in the development of potential transmissible spongiform encephalopathy (TSE) therapeuti
171 Creutzfeldt-Jakob disease (CJD), the first transmissible spongiform encephalopathy (TSE) to be desc
172 of Creutzfeldt-Jakob disease (CJD), a human transmissible spongiform encephalopathy (TSE), emerged i
174 ations require discriminatory testing of all transmissible spongiform encephalopathy (TSE)-positive s
177 s has focused intense interest on all of the transmissible spongiform encephalopathies (TSEs) and how
178 that certain species were not susceptible to transmissible spongiform encephalopathies (TSEs) and the
184 ses such as Alzheimer's, Parkinson's and the transmissible spongiform encephalopathies (TSEs) are cha
197 tively leucoreduction reduced infectivity of transmissible spongiform encephalopathies (TSEs) in bloo
202 ral in the pathogenesis of scrapie and other transmissible spongiform encephalopathies (TSEs) or 'pri
203 re are many strains of the agents that cause transmissible spongiform encephalopathies (TSEs) or 'pri
208 isting concerns about the possible spread of transmissible spongiform encephalopathies (TSEs) via blo
209 rescence spectra of the eye for diagnosis of transmissible spongiform encephalopathies (TSEs) was exa
226 new concerns about the iatrogenic spread of transmissible spongiform encephalopathies (TSEs)/prion d
227 sis and transmission of the prion disorders (transmissible spongiform encephalopathies, TSEs) are med
228 e samples from several patients with various transmissible spongiform encephalopathies (variant and s
229 iseases caused by PRNP mutations or in human transmissible spongiform encephalopathies; we propose to
230 of fatal neurodegenerative diseases known as transmissible spongiform encephalopathies, which affect
231 nventional infectious agents responsible for transmissible spongiform encephalopathies, which appear
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