ライフサイエンスコーパス: scrapie

1 rt on strong genetic resistance to classical scrapie.

2 ociated with susceptibility or resistance to scrapie.

3 ble prions in the horizontal transmission of scrapie.

4 urine prion protein mice infected with mouse scrapie.

5 elates with their propensities for classical scrapie.

6 ge, using the 263K strain of hamster-adapted scrapie.

7 ion of some neurological pathologies such as scrapie.

8 ted to experimental strains of mouse-adapted scrapie.

9 139H, and drowsy strains of hamster-adapted scrapie.

10 rless PrP-sen are not directly infected with scrapie.

11 on 171 in sheep, which confers resistance to scrapie.

12 ically resistant to development of classical scrapie.

13 prevent dendritic degeneration in mice with scrapie.

14 es by transfusion of 36% for BSE and 43% for scrapie.

15 ongiform encephalopathy (BSE) from classical scrapie.

16 seases such as Creutzfeldt-Jakob disease and scrapie.

17 g Disease of deer and elk and atypical/Nor98 scrapie.

18 cess (>95%) VRQ-PrP fraction found in PrP in scrapie.

19 crapie, or may be masked by coinfection with scrapie.

20 ssing the genetic susceptibility of goats to scrapie.

21 in (PrP(Sc) [Sc superscript stands for sheep scrapie]).

22 /10 mice intracerebrally inoculated with 22L scrapie, abnormal protease-resistant prion protein (PrPr

23 tural, synthetic porphyrins have potent anti-scrapie activity and can interact with normal prion prot

24 mulation of PrP(d) in the adrenal medulla of scrapie affected sheep using light and electron microsco

25 rP(Sc)) in brain, spleen, blood and urine of scrapie-affected hamsters.

26 Here we report that a scrapie-affected sheep farm has a widespread environment

27 Comparisons of scrapie-affected wild-type mice and transgenic mice expr

28 ples were tested with the IDEXX HerdChek BSE-Scrapie Ag Kit to detect the abnormal prion protein, PrP

29 ally and orally infected sheep with clinical scrapie agent and orally infected preclinical and infect

30 In addition, sheep with no exposure to the scrapie agent did not contain any measurable prions with

31 play a key role in the translocation of the scrapie agent from the gut lumen to the GALT from which

32 icating that PrP expression was required for scrapie agent induction of other cytokines detected.

33 rodegenerative disease by 160 days after RML scrapie agent infection.

34 n vivo in GPI(-/-) PrP tg mice infected with scrapie agent may likely involve the GABAergic pathway.

35 stigated the contribution of CD11c(+) DCs in scrapie agent neuroinvasion through use of CD11c-dipther

36 Using two distinct scrapie agent strains (ME7 and 139A scrapie agents), we

37 After infection with RML murine scrapie agent, transgenic (tg) mice expressing prion pro

38 PrP(sc) was detected in the blood of 55% of scrapie agent-infected animals (n = 80) and 71% of anima

39 nses, primary glial cultures were exposed to scrapie agent-infected brain homogenates.

40 to analyze protein levels of 24 cytokines in scrapie agent-infected C57BL/10 mouse brains, we observe

41 e the onset of clinical signs in a subset of scrapie agent-infected sheep, followed from 3 months of

42 Scrapie agent-infected wild-type mice and transgenic mic

43 oradic CJD and BSE agents and representative scrapie agents were clearly different from kuru in incub

44 distinct scrapie agent strains (ME7 and 139A scrapie agents), we show that when CD11c(+) DCs were tra

45 ested as the mode of transmission of CWD and scrapie among herbivores susceptible to these prion dise

46 ding Creutzfeldt-Jakob disease in humans and scrapie and bovine spongiform encephalopathy in animals.

47 Ovine scrapie and cervine chronic wasting disease show conside

48 lay an important role in the transmission of scrapie and chronic wasting disease (CWD) via the enviro

49 ny neurodegenerative diseases, and arguably, scrapie and Creutzfeldt-Jakob disease prions represent t

50 mination between two experimental strains of scrapie and grouping of natural scrapie isolates into tw

51 amplification (PMCA), by using experimental scrapie and human prion strains as seeds and specific br

52 h implications for the transmission of ovine scrapie and very likely other prion diseases.

53 diseases including chronic wasting disease, scrapie, and bovine spongiform encephalopathy.

54 utzfeldt-Jakob disease (sCJD), endemic sheep scrapie, and epidemic bovine spongiform encephalopathy (

55 in which ovine BSE and distinct isolates of scrapie are mixed at various ratios ranging from 99% to

56 Prion diseases, including sheep scrapie, are neurodegenerative diseases with the fundame

57 tion with the same isolates of natural sheep scrapie as detected by SSCA.

58 from two different strains of mouse-passaged scrapie as seed.

59 astoma cells infected with the 22L strain of scrapie as well as hypothalamic GT cells infected with t

60 ed material were not subclinical carriers of scrapie, as no PrP(Sc) was detected in brains or spleen

61 is is the first detailed description of such scrapie-associated fragments within a natural host.

62 Scrapie brain dilutions up to 10(-8) and 10(-13) were de

63 t glial stimulation was induced by clarified scrapie brain homogenates lacking PrPres.

64 s used to estimate the infectious titer of a scrapie brain pool (RBP1) and proved to be more sensitiv

65 Previous studies that examined scrapie brains reported that both sialo- and asialo-GPIs

66 -175) markedly influences infection by sheep scrapie, BSE, mouse-adapted scrapie, deer chronic wastin

67 survival of mice infected with mouse-adapted scrapie but also resulted in the emergence of a drug-res

68 strating the transmission of BSE and natural scrapie by blood transfusion in sheep.

69 lts of experimental challenges of goats with scrapie by both the intracerebral (i.c.) and oral routes

70 f mononucleated cell populations to transmit scrapie by the transfusion route.

71 o what extent natural and experimental ovine scrapie can be detected ex vivo.

72 Classical scrapie can transmit laterally from ewe to lamb perinata

73 As hamster scrapie cannot infect mice, due to sequence differences

74 efined CNS regions, compared between BSE and scrapie cases and also between two experimental scrapie

75 have been significantly underrepresented in scrapie cases though present in scrapie-exposed flocks,

76 advances in this area, namely, the standard scrapie cell assay (SSCA) and the Rov9 and MovS6 cell li

77 in vitro within 2 weeks, using the standard scrapie cell assay (SSCA).

78 eased elk, we describe a modification of the scrapie cell assay allowing evaluation of prions causing

79 by in vivo strain typing and by the standard scrapie cell assay in vitro.

80 An in vitro prion bioassay, the scrapie cell assay, uses a neuroblastoma-derived cell li

81 s prion strains, as measured by the standard scrapie cell assay.

82 ell depletion reduced susceptibility to oral scrapie challenge indicating that TSE agent neuroinvasio

83 istent exposure, we performed the first oral scrapie challenge of goats singly heterozygous for eithe

84 Prions, the infectious agent of scrapie, chronic wasting disease and other transmissible

85 ormal prion protein (PrP) into a pathogenic "scrapie" conformation.

86 fection by sheep scrapie, BSE, mouse-adapted scrapie, deer chronic wasting disease, and hamster-adapt

87 ferent prion strains, including RML, another scrapie-derived prion strain ME7, and chronic wasting di

88 th Rocky Mountain Laboratory (RML) prions, a scrapie-derived strain, and treated with IND24 eventuall

89 s offers a noninvasive methodology to detect scrapie during preclinical/subclinical disease.

90 s contigs (RNAs over- or underrepresented in scrapie) emerged, representing <4 kb from the transcript

91 encephalopathy (TSE) of sheep and goats, and scrapie eradication in sheep is based in part on strong

92 gest longer relevant trace-back histories in scrapie-eradication programs for animals bearing these a

93 examined the association of survival time of scrapie-exposed ARQ sheep with variation elsewhere in th

94 presented in scrapie cases though present in scrapie-exposed flocks, and have demonstrated low cell-f

95 from clinically affected animals as well as scrapie-exposed sheep at least 20 months before clinical

96 with an additional 687 days of survival for scrapie-exposed sheep compared to M112 sheep (odds ratio

97 Prions were detected in buccal swabs from scrapie-exposed sheep of genotypes linked to high (VRQ/V

98 licular dendritic cells, were susceptible to scrapie following intratongue and intranasal inoculation

99 ease-resistant counterpart of the pathogenic scrapie form (PrP(Sc)) of PrP.

100 l prion protein (PrP(C)) into its pathogenic scrapie form (PrP(Sc)).

101 resented with accumulation of the aggregated scrapie form of PrP in brain tissue, and the mouse/elk h

102 ur findings for the structural model for the scrapie form of PrP(C) are discussed.

103 s required for propagation of the infectious scrapie form of the protein, one therapeutic strategy is

104 ed into amyloid aggregates representing the "scrapie form" of the protein ([Formula: see text]).

105 rm (denoted PrP(C)) to a disease-associated "scrapie" form (PrP(Sc)).

106 PrP(C) misfolding leading to neurotoxic PrP-scrapie formation (PrP(SC)).

107 enotype absent from similar flies exposed to scrapie-free material.

108 motor activity than similar flies exposed to scrapie-free material.

109 The variant susceptible to classical scrapie has a larger population of the intermediate stat

110 -ranging cervid populations that, similar to scrapie, has been shown to involve the immune system, wh

111 spongiform encephalopathies (TSEs) including scrapie have been attributed to an infectious protein or

112 ide range of prion diseases, including sheep scrapie, human Creutzfeldt-Jakob disease, and cervid chr

113 e bovine spongiform encephalopathy (BSE) and scrapie in animals and Creutzfeldt-Jakob disease (CJD) i

114 cantly, the toxic phenotype induced by ovine scrapie in cytosolic PrP transgenic Drosophila was trans

115 tration of 10(5) WBCs is sufficient to cause scrapie in recipient sheep.

116 pongiform encephalopathies (TSEs), including scrapie in sheep (Ovis aries), are fatal neurodegenerati

117 cluding Creutzfeldt-Jakob disease in humans, scrapie in sheep and bovine spongiform encephalopathy in

118 sgenic mice infected with prions that caused scrapie in sheep or prions that caused chronic wasting d

119 onic wasting disease (CWD) in cervids and in scrapie in sheep, prions appear to be transmitted horizo

120 with differing susceptibilities to classical scrapie in sheep.

121 n the hosts, as has been shown for classical scrapie in sheep.

122 potent compounds that effected clearance of scrapie in the low nanomolar range.

123 m fetal brain, were developed to study sheep scrapie in the natural host and to investigate potential

124 nmethylated CpG DNA was shown to prolong the scrapie incubation period in mice, suggesting that innat

125 roglial PrP expression might be required for scrapie-induced retinal microglial activation and damage

126 Significantly, the scrapie-induced toxic phenotype in cytosolic transgenic

127 rticipate in the generation of transmissible scrapie-induced toxicity.

128 100 mul of blood collected from asymptomatic scrapie infected animals can transmit the disease.

129 peptides, we investigated brain tissues from scrapie-infected "anchorless PrP" Tg mice and wild type

130 RNA preparations from eight normal and eight scrapie-infected (strain 263K) hamster brains were rando

131 ique to total nucleic acid preparations from scrapie-infected and control brain.

132 This assay could discriminate between scrapie-infected and uninfected hamsters using 2-microl

133 rst described in 1968 in synaptic regions of scrapie-infected brain and subsequently identified in ma

134 sensitivity when BSE agent was diluted into scrapie-infected brain homogenates at 1% (vol/vol).

135 lia and astroglia similar to that induced by scrapie-infected brain homogenates, whereas purified ful

136 Subclones of scrapie-infected C2C12 cells produced high levels of PrP

137 Terminal differentiation of scrapie-infected C2C12 myoblasts into myotubes resulted

138 Consistent with the in vitro data, scrapie-infected cells expressing anchored PrP-sen trans

139 fresh whole blood collected in asymptomatic scrapie-infected donor sheep can transmit the disease.

140 hich was obtained by propagating prions from scrapie-infected goat brain in mice.

141 (CSF), we measured the activity over time in scrapie-infected hamsters by real-time quaking-induced c

142 Neuropathological analysis of scrapie-infected hamsters using the fluorescent dye acri

143 d genes that were increased in the brains of scrapie-infected mice and were associated with inflammat

144 In brains of scrapie-infected mice at pre- and postclinical stages, w

145 In scrapie-infected mice deficient in or overexpressing IL-

146 ne response in the brains of clinically sick scrapie-infected mice was restricted to a small group of

147 1 also inhibits mouse prion propagation in a scrapie-infected mouse cell line.

148 fected human and mouse brain homogenates and scrapie-infected mouse neuroblastoma cells results in 4-

149 Scrapie-infected N2a cells were capable of accumulating

150 otubes was comparable to the levels found in scrapie-infected N2A cells, indicating that a high level

151 conversion to PrP(res) when transfected into scrapie-infected N2a neuroblastoma cells, likely due to

152 al cell lines (ScGT1 and ScN2a cells) and in scrapie-infected primary cortical neurons was increased

153 issue from heterozygous (ARQ/VRQ or ARH/ARQ) scrapie-infected Rasa Aragonesa sheep was analyzed using

154 ht chain immunoglobulin G (IgG) fragments in scrapie-infected sheep but not in infected CWD-infected

155 uccal swab samples obtained from preclinical scrapie-infected sheep by concentrating the collected pr

156 Heterozygous scrapie-infected sheep that produce two PrP variants ass

157 PrP(res)) from brain of heterozygous ARR/VRQ scrapie-infected sheep was compared with that of BSE-inf

158 turally and experimentally infected clinical scrapie-infected sheep were independent of their genotyp

159 observed at the fetal-maternal interface of scrapie-infected sheep.

160 rions from feces of CWD-infected cervids and scrapie-infected sheep.

161 ic acid patterns were generally identical in scrapie-infected versus control brain, some rare bands w

162 lenic or gut-associated lymph node cDCs with scrapie-infected whole brain homogenate in the presence

163 , but infection of the LRS was found only in scrapie-infected wild-type mice and HY TME-infected hams

164 ND24 and IND81 doubled the survival times of scrapie-infected, wild-type mice.

165 In this model, scrapie infection and protease-resistant PrP deposition

166 Scrapie infection causes PrP(Sc) accumulation and microg

167 ease penetrance, indicating that subclinical scrapie infection is likely to be a common occurrence.

168 nical signs might be involved in controlling scrapie infection or in facilitating damage to host tiss

169 imes more sensitive than Rov9 to SSBP/1-like scrapie infection were isolated, but all the subclones m

170 ted genes was increased preclinically during scrapie infection, suggesting early activation of the ST

171 h a VRQ/VRQ PRNP genotype during preclinical scrapie infection.

172 activation via TLR signaling interferes with scrapie infection.

173 uction in mouse brain at various times after scrapie infection.

174 The amount of scrapie infectivity or PrP(Sc) in C2C12 myotubes was com

175 The susceptibility to classical scrapie inocula could be assessed in Drosophila transgen

176 oded by a second transgene) become ill after scrapie inoculation, but with a dramatically delayed tim

177 irst detected at 40 days after intracerebral scrapie inoculation.

178 ing scrapie samples, including a fast-acting scrapie inoculum for which incubation time is highly dep

179 y or intraperitoneally with various doses of scrapie inoculum.

180 Prion diseases such as scrapie involve the accumulation of disease-specific pri

181 Scrapie is a prion (PrP(Sc)) disease of sheep.

182 ence that in utero transmission of classical scrapie is also possible.

183 Classical scrapie is one of the transmissible spongiform encephalo

184 The incubation period of sheep scrapie is strongly influenced by polymorphisms at posit

185 Sheep scrapie is the prototypical transmissible spongiform enc

186 Scrapie is the transmissible spongiform encephalopathy (

187 Scrapie is thus actually transmissible to primates with

188 prion protein (PrP(C)) into the pathological scrapie isoform (PrP(Sc)) in the brain.

189 entally different from that of authentic PrP scrapie isoform (PrP(Sc)).

190 cultured slices and decreased the amount of scrapie isoform of PrP(C) (PrP(Sc)) oligomers that could

191 ties to those of a host-stabilized reference scrapie isolate (NADC 13-7) in order to assess the stabi

192 e direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant

193 Biological strain typing of ovine scrapie isolates by serial passage in conventional mice

194 l strains of scrapie and grouping of natural scrapie isolates into two profiles.

195 lum, and spinal cord samples allowed natural scrapie isolates to be separated into four distinct mole

196 ty of permissiveness and resistance to other scrapie isolates was maintained.

197 or the high levels of oxidized methionine in scrapie isolates.

198 riminate field cases of mouse-passaged ovine scrapie isolates.

199 ge excess of classical, atypical, and CH1641 scrapie isolates.

200 hat if BSE in sheep were to come to resemble scrapie it would lose its ability to affect humans.

201 ith time and in some sheep genotypes, become scrapie-like at the molecular level.

202 tion and accumulates into highly aggregated, scrapie-like conformers in transgenic flies.

203 iform degeneration and does not convert into scrapie-like conformers.

204 egeneration and accumulates small amounts of scrapie-like conformers.

205 iffers from both ovine classic BSE or CH1641 scrapie maintaining its specific strain properties after

206 Outside of scrapie-mediated prion disease, to our knowledge, this f

207 d mice showed that the zoonotic potential of scrapie might be similar to c-BSE.

208 ed by the report of an antiprion effect in a scrapie model and by ongoing international clinical tria

209 Previous experiments carried out in a sheep scrapie model demonstrated that the transfusion of 200 m

210 Using a scrapie mouse model of prion disease to assess various t

211 , but all S146 and K222 heterozygotes remain scrapie negative by both rectal biopsy and clinical sign

212 om scrapie-positive sheep were compared with scrapie-negative sheep using fluorescence spectroscopy,

213 verexpressor transgenic mice inoculated with scrapie, neither loss nor overexpression of IL-1Ra demon

214 (PRNP) is one of the major determinants for scrapie occurrence in sheep and goats.

215 Infectious prion diseases-scrapie of sheep and chronic wasting disease (CWD) of se

216 Here we investigate the effect of sheep scrapie on the morphology and the accumulation of PrP(d)

217 The most abundant scrapie-only ros sequence was homologous to a repetitive

218 ay be at subclinical levels, may manifest as scrapie, or may be masked by coinfection with scrapie.

219 rthermore, the results also suggest that the scrapie pathogen, or a component(s) thereof, is capable

220 y in our model and therefore might influence scrapie pathogenesis in vivo.

221 Q/VRQ) lymphoreticular system involvement in scrapie pathogenesis.

222 All N146-Q222 homozygotes became clinically scrapie positive by an average of 24months, but all S146

223 E agent which had been mixed into a range of scrapie-positive brain homogenates.

224 Retinas from scrapie-positive sheep were compared with scrapie-negati

225 expression exposed to classical or atypical scrapie prion inocula showed a faster decrease in locomo

226 The delay could relate to reduced scrapie prion protein (PrP(Sc)) accumulation on follicul

227 ave studied the modulation of the HSR by the scrapie prion protein (PrP(Sc)) and amyloid beta peptide

228 f either one of the two protease K-resistant scrapie prion protein (PrP(Sc)) types identified as 1 an

229 of a misfolded, beta-sheet-enriched isoform (scrapie prion protein (PrP(Sc))) of the cellular prion p

230 ive disorders characterized by deposition of scrapie prion protein (PrPSc) in the CNS.

231 The scrapie prion protein isoform, PrPSc, is a prion-associa

232 ally detect BSE, even within the presence of scrapie prion protein, are required.

233 n, PrP(c), to a pathogenic, amyloid isoform, scrapie prion protein, PrP(Sc) We examined the role of t

234 la are susceptible to classical and atypical scrapie prion strains and highlight the utility of this

235 n formation when seeded by minute amounts of scrapie prions in vitro Surprisingly, combination of the

236 These data demonstrate that orally available scrapie prions may be a common feature in sheep incubati

237 Tg(C1) mice inoculated with scrapie prions remain healthy and do not accumulate prot

238 isease when infected i.p. with mouse-adapted scrapie prions.

239 force-fed material infected with RML-strain scrapie prions.

240 ma cells that are persistently infected with scrapie prions.

241 ffect on the survival of those infected with scrapie prions.

242 chronic wasting disease, and hamster-adapted scrapie prions.

243 prion protein amino acid sequence influences scrapie progression, with sheep homozygous for A(136)R(1

244 ral prion protein in FFI, altered PrPres and Scrapie PrP (abnormal and pathogenic PrP) patterns and r

245 in gene and conformational properties of the scrapie PrP (PrP(Sc)) grossly identified types 1 and 2.

246 e conversion of the prion protein (PrP) into scrapie PrP (PrP(Sc)) is a central event in prion diseas

247 and proteinase K-resistant conformer, termed scrapie PrP (PrP(Sc)).

248 ulates propagation of the protease-resistant scrapie PrP (PrP(Sc)).

249 ed the degradation of prions associated with scrapie (PrP(263K)), chronic waste disease (PrP(CWD)), a

250 detection of abnormally folded prion protein scrapie (PrP(Sc)) in human brain and cerebrospinal fluid

251 ts normal conformation to an aggregated, PrP-scrapie (PrP(Sc)) isoform.

252 ed retinal degeneration is attributed to PrP-scrapie (PrP(Sc)), a misfolded isoform of prion protein

253 e cellular prion protein (PrP(C)) termed PrP-scrapie (PrP(Sc)).

254 may be a common feature in sheep incubating scrapie, regardless of the PRNP genotype and any associa

255 s form of prion protein (e.g. PrP(Sc) or PrP-Scrapie) remain poorly defined.

256 olic PrP, whereas susceptibility to atypical scrapie required ubiquitous PrP expression.

257 Goats may serve as a scrapie reservoir, and to date there has been no experim

258 ents in both homozygotes to assess potential scrapie resistance.

259 ction was significantly higher than that for scrapie-resistant ARR/ARR sheep which were kept in the s

260 own to produce the anti-apoptotic N1 and the scrapie-resistant C1 peptide fragments.

261 ty assay to characterize naturally occurring scrapie samples, including a fast-acting scrapie inoculu

262 incubation period as the input brain-derived scrapie samples, providing no evidence for generation of

263 amyloid formation was no longer slower than scrapie-seeded amyloid formation.

264 py revealed that PMCA of native hamster 263K scrapie seeds in hamster PrP(C) substrate caused conform

265 c PrP transgenic Drosophila exposed to ovine scrapie showed a toxic phenotype absent from similar fli

266 h forms of PrP-sen were exposed to the mouse scrapie strain 22L.

267 rly differing from ovine classic BSE or from scrapie strain CH1641.

268 also distinct from those of the hamster 263K scrapie strain.

269 Comparison of mice infected with two scrapie strains (22L and RML), which have dissimilar neu

270 e neuropathogenesis by using three different scrapie strains (22L, RML, 79A) to infect knockout mice

271 e brains with three different murine-adapted scrapie strains (Chandler, 22L, and Me7) and systematica

272 lammatory markers between mice infected with scrapie strains 22L and RML indicated that the inflammat

273 Our data show that mouse-adapted ovine scrapie strains can be discriminated by their distinct c

274 ies may reflect the natural heterogeneity of scrapie strains in the sheep population in the United Ki

275 r this purpose we compared the 263K and 139A scrapie strains in transgenic mice expressing P101L PrP(

276 s were strikingly similar, even though these scrapie strains infect different brain regions.

277 apie cases and also between two experimental scrapie strains, appeared to be largely dependent upon t

278 ween the 22L, ME7, and Chandler (RML) murine scrapie strains, most notably in bands attributed to bet

279 th two principal Prnp(a) mouse-adapted ovine scrapie strains, namely, RML and ME7, in order to establ

280 Contrary to laboratory-adapted mouse scrapie strains, the synthetic prion agents exhibited a

281 nic mice inoculated with 22L, 79A and/or RML scrapie strains.

282 y reacts differently to three murine-adapted scrapie strains.

283 kDa, similar to those observed in classical scrapie strains.

284 p homozygous for T112 (TARQ) did not develop scrapie, suggesting that the allelic effect may be addit

285 us goats have become naturally infected with scrapie, suggesting these alleles do not confer complete

286 ce two PrP variants associated with opposite scrapie susceptibilities (136V-PrP variant, high; 171R-P

287 dons 136, 154, and 171, respectively) sheep, scrapie susceptibility is reduced to near resistance in

288 Equivalent fractions from a second scrapie-susceptible cell line also stimulate conversion.

289 ns derived from gradient centrifugation of a scrapie-susceptible cell line.

290 Preclinical sheep with the highly scrapie-susceptible VRQ/VRQ PRNP genotype secrete prions

291 diseases caused by a pathogenic protein, PrP scrapie, that derives from misfolding of a normal form,

292 isease-related isoform (PrP(Sc), where Sc is scrapie), the accumulation of which is associated with s

293 en challenged with Rocky Mountain Laboratory scrapie, the onset of prion disease was delayed in Atp7a

294 (N-TAAP) of PrP(res) from sheep affected by scrapie, the prion disease of small ruminants, to rapidl

295 ygous for asparagine at codon 146 succumb to scrapie under natural conditions.IMPORTANCE In goats, li

296 s impaired by species barriers than is sheep scrapie, we find that some [URE3] prion variants are inf

297 et and dramatic elevation of IL-12p40 during scrapie, we investigated whether IL-12p40 contributed to

298 etinal samples from mice inoculated with RML scrapie were collected at 30, 60, 90, 105, and 120 days

299 rated PrP(Sc) molecules into hamsters caused scrapie, which was transmissible on second passage.

300 ich may have come to phenotypically resemble scrapie while maintaining its pathogenicity for humans.