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1 0 transcripts not previously examined in any transmissible spongiform encephalopathy.
2 class of neurodegenerative diseases known as 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 ng tools for the prevention of the spread of transmissible spongiform encephalopathies.
11 No cure as of yet exists for any of the transmissible spongiform encephalopathies.
12 itions including Alzheimer's disease and the transmissible spongiform encephalopathies.
13 biting pathology resembling that observed in transmissible spongiform encephalopathies.
14 crapie (PrPSc) is the major event leading to transmissible spongiform encephalopathies.
15 t aggregate that accumulates in mammals with transmissible spongiform encephalopathies.
16 group of neurodegenerative diseases known as 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 prion protein are clinically associated with transmissible spongiform encephalopathies.
30 otein can form a prion that causes the fatal 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 rminants that confer this high resistance to transmissible spongiform encephalopathies.
34 oup of neurodegenerative diseases called the transmissible spongiform encephalopathies.
36 wasting disease (CWD) is a universally fatal transmissible spongiform encephalopathy affecting cervid
37 l PrP-sen-expressing cells appear to support transmissible spongiform encephalopathy agent replicatio
38 , the species specificity in transmission of transmissible spongiform encephalopathy agents in vivo.
41 rmational changes in the prion protein cause transmissible spongiform encephalopathies, also referred
42 mic amyloidosis, Alzheimer's disease and the transmissible spongiform encephalopathies always contain
43 rP, has a key role in the development of the transmissible spongiform encephalopathies and the level
44 seen in neurodegenerative diseases, such as transmissible spongiform encephalopathy and Alzheimer di
45 n of PrP can influence the susceptibility to transmissible spongiform encephalopathy and determine th
46 sensitive, specific, and early diagnosis of transmissible spongiform encephalopathy and to further u
47 heimer's disease, type II diabetes mellitus, transmissible spongiform encephalopathies, and prion dis
65 f scrapie, chronic wasting disease and other transmissible spongiform encephalopathies, are misfolded
66 protein gene (PRNP) region in patients with transmissible spongiform encephalopathy associated with
68 ence that hereditary and apparently sporadic transmissible spongiform encephalopathy cases associated
69 Prions are infectious agents that initiate transmissible spongiform encephalopathies, causing devas
70 rions, the infectious agents responsible for transmissible spongiform encephalopathies, consist mainl
72 nce of the PrP protein in the development of transmissible spongiform encephalopathies, despite the f
73 reviously shown to replicate many aspects of transmissible spongiform encephalopathy disease to inves
80 AMALT) biopsy specimens for the diagnosis of transmissible spongiform encephalopathies has been descr
81 d to misfold into the causative agent of the transmissible spongiform encephalopathies, has previousl
82 or its involvement as a misfolded isoform in transmissible spongiform encephalopathies, has recently
83 t of infectious prions that cause a group of transmissible spongiform encephalopathies in animals and
85 ns were discovered as the cause of the fatal transmissible spongiform encephalopathies in mammals, bu
86 n diagnostic and pathogenesis studies of the transmissible spongiform encephalopathies in these rumin
87 ation variation, we show that prions causing transmissible spongiform encephalopathy in wild-type ham
89 vances in the diagnosis and understanding of transmissible spongiform encephalopathies, including tra
90 Originally identified as causative agents of transmissible spongiform encephalopathies, increasing ev
91 achieved the critical goal of discriminating transmissible spongiform encephalopathy-infected from he
92 not the source of blood-borne infectivity in transmissible spongiform encephalopathy-infected hamster
93 demonstrating significant removal of rodent transmissible spongiform encephalopathy infections by fi
94 fore not necessarily be a reliable marker of transmissible spongiform encephalopathy infectivity.
96 sis states that the infectious agent causing transmissible spongiform encephalopathies is a conformat
97 esis holds that the infectious agent causing transmissible spongiform encephalopathies is a conformat
98 hat the critical step in the pathogenesis of transmissible spongiform encephalopathies is a transitio
101 leic acid is required for the infectivity of transmissible spongiform encephalopathies is central to
102 The idea that blood in naturally occurring transmissible spongiform encephalopathies is not infecti
104 at the critical event in the pathogenesis of transmissible spongiform encephalopathies is the convers
105 s in favor of the protein-only hypothesis of transmissible spongiform encephalopathies is the link be
106 n prion replication and neurotoxicity during transmissible spongiform encephalopathies is undisputed,
107 s of kuru, the only other orally transmitted transmissible spongiform encephalopathy, might be instru
110 ion to the role of its abnormal conformer in transmissible spongiform encephalopathies, normal PrP(C)
114 rly understood, steps in the pathogenesis of transmissible spongiform encephalopathies or prion disea
115 A central aspect of pathogenesis in the transmissible spongiform encephalopathies or prion disea
116 ) is the most prevalent manifestation of the transmissible spongiform encephalopathies or prion disea
117 ) is a required factor for susceptibility to transmissible spongiform encephalopathy or prion disease
122 euroinflammatory response may play a role in transmissible spongiform encephalopathy pathogenesis.
123 ncluding Alzheimer's and Parkinson's and the transmissible spongiform encephalopathies (prion disease
124 The critical step in the pathogenesis of transmissible spongiform encephalopathies (prion disease
125 Chronic wasting disease (CWD) is an emerging transmissible spongiform encephalopathy (prion disease)
136 A fundamental event in the pathogenesis of transmissible spongiform encephalopathies (TSE) is the c
143 Bovine spongiform encephalopathy (BSE) is a transmissible spongiform encephalopathy (TSE) (or prion
146 f contamination of tissue culture cells with transmissible spongiform encephalopathy (TSE) agents as
148 e pathogenesis of many peripherally acquired transmissible spongiform encephalopathy (TSE) agents is
149 he initial infection of cells with exogenous transmissible spongiform encephalopathy (TSE) agents, we
150 tures strikingly similar to those induced by transmissible spongiform encephalopathy (TSE) agents.
151 In the study presented here, using the same transmissible spongiform encephalopathy (TSE) animal mod
153 activity and protease-resistant PrP without transmissible spongiform encephalopathy (TSE) clinical s
155 exerts a major influence over the outcome of transmissible spongiform encephalopathy (TSE) disease, b
156 this mutation (101LL) showed no spontaneous transmissible spongiform encephalopathy (TSE) disease, b
160 to translocate infectious agents (prions) of transmissible spongiform encephalopathy (TSE) diseases i
162 unconventional infectious agents that cause transmissible spongiform encephalopathy (TSE) diseases,
163 nventional infectious agents responsible for transmissible spongiform encephalopathy (TSE) diseases.
164 feature of the pathogenesis associated with transmissible spongiform encephalopathy (TSE) diseases.
165 ission via blood transfusion exists for many transmissible spongiform encephalopathy (TSE) diseases.
166 e or a previously undetected sporadic bovine transmissible spongiform encephalopathy (TSE) have long
167 a novel and advantageous model for studying transmissible spongiform encephalopathy (TSE) infection.
172 Bovine spongiform encephalopathy (BSE) is a transmissible spongiform encephalopathy (TSE) or prion d
173 e of blood in the iatrogenic transmission of transmissible spongiform encephalopathy (TSE) or prion d
175 ellum also appeared to be dependent upon the transmissible spongiform encephalopathy (TSE) strain, al
176 ime strategy in the development of potential transmissible spongiform encephalopathy (TSE) therapeuti
177 Creutzfeldt-Jakob disease (CJD), the first transmissible spongiform encephalopathy (TSE) to be desc
178 of Creutzfeldt-Jakob disease (CJD), a human transmissible spongiform encephalopathy (TSE), emerged i
180 ations require discriminatory testing of all transmissible spongiform encephalopathy (TSE)-positive s
183 s has focused intense interest on all of the transmissible spongiform encephalopathies (TSEs) and how
185 that certain species were not susceptible to transmissible spongiform encephalopathies (TSEs) and the
191 ses such as Alzheimer's, Parkinson's and the transmissible spongiform encephalopathies (TSEs) are cha
204 tively leucoreduction reduced infectivity of transmissible spongiform encephalopathies (TSEs) in bloo
209 ral in the pathogenesis of scrapie and other transmissible spongiform encephalopathies (TSEs) or 'pri
210 re are many strains of the agents that cause transmissible spongiform encephalopathies (TSEs) or 'pri
215 isting concerns about the possible spread of transmissible spongiform encephalopathies (TSEs) via blo
216 rescence spectra of the eye for diagnosis of transmissible spongiform encephalopathies (TSEs) was exa
236 new concerns about the iatrogenic spread of transmissible spongiform encephalopathies (TSEs)/prion d
237 sis and transmission of the prion disorders (transmissible spongiform encephalopathies, TSEs) are med
238 mbination of clinical signs, neuropathology (transmissible spongiform encephalopathy vacuolation and
239 e samples from several patients with various transmissible spongiform encephalopathies (variant and s
240 iseases caused by PRNP mutations or in human transmissible spongiform encephalopathies; we propose to
241 of fatal neurodegenerative diseases known as transmissible spongiform encephalopathies, which affect
242 nventional infectious agents responsible for transmissible spongiform encephalopathies, which appear