ライフサイエンスコーパス: spongiform

1 d accumulation of activated microglia in the spongiform areas of the brain accompanied by an increase

2 nsfer ratios may be an in vivo surrogate for spongiform change and has potential utility as a therape

3 in mice with early prion infection reversed spongiform change and prevented clinical symptoms and ne

4 d increased interstitial space, vacuolation, spongiform change, and capillaries bent at amylin accumu

5 nation revealed neuronal loss, scant foci of spongiform change, and diffuse multicentric amyloid plaq

6 racterized by abundant PrP plaque formation, spongiform change, and gliosis.

7 deposition is accompanied by neuronal loss, spongiform change, astrogliosis, and conspicuous microgl

8 PrP(Sc), in the absence of neuronal loss or spongiform change, in the central nervous system corresp

9 Cerebral cortex spongiform change, one of the classical pathological fea

10 Spongiform changes and intense PrP(Sc) staining were pre

11 h long incubation periods and characteristic spongiform changes associated with neuronal loss in the

12 p75(NTR)), and sortilin in the areas showing spongiform changes.

13 in PrP amyloid deposition, in the absence of spongiform changes.

14 We recently showed that hamster PrP induces spongiform degeneration and accumulates into highly aggr

15 of sick transgenic mice exhibited widespread spongiform degeneration and contained abnormal prion pro

16 l features that define prion strains include spongiform degeneration and deposition patterns of PrP(S

17 We show now that rabbit PrP does not induce spongiform degeneration and does not convert into scrapi

18 6Q), we provide evidence that glycans reduce spongiform degeneration and hinder plaque formation in p

19 al inactivation of Fig4 in neurons developed spongiform degeneration and the full spectrum of neurolo

20 ish the contributions of neurons and glia to spongiform degeneration in the Fig4 null mouse, we expre

21 ull mutation of Fig4 in the mouse results in spongiform degeneration of brain and peripheral ganglia,

22 to the signaling lipid PI(3,5)P(2) result in spongiform degeneration of mouse brain and are associate

23 ne that results in tremor, hypopigmentation, spongiform degeneration of the brain, and juvenile letha

24 cinity in the absence of clinical disease or spongiform degeneration of the brain.

25 Deficiency in this activity leads to spongiform degeneration of the white matter of the brain

26 Spongiform degeneration only occurs in the entorhinal co

27 markers and microgliosis but did not prevent spongiform degeneration or lethality.

28 inoculation of tissue from the case with no spongiform degeneration resulted in almost complete abse

29 llular and neurological phenotypes including spongiform degeneration, gliosis and juvenile lethality.

30 n the cerebellum affected by prions includes spongiform degeneration, neuronal loss, and gliosis.

31 ed the hallmarks of prion disease, including spongiform degeneration, pronounced astrogliosis, and de

32 The type of spongiform degeneration, the PrP immunostaining pattern,

33 To confirm the neuronal origin of spongiform degeneration, we generated a floxed allele of

34 urons is necessary and sufficient to prevent spongiform degeneration.

35 Only one of the brains had spongiform degeneration.

36 of the prion protein, PrP-res, and displayed spongiform degeneration.

37 Transmissible spongiform encephalitis (TSE) is a lethal illness with n

38 sease phenotype compared to the induction of spongiform encephalomyelitis with a longer latency, as s

39 The progressive spongiform encephalomyelopathy caused by ts1, a neuropat

40 Since 2005, two cases of natural bovine spongiform encephalopathies (BSE) have been reported in

41 The risk of transmission of transmissible spongiform encephalopathies (TSE) between different spec

42 Transmissible spongiform encephalopathies (TSE) can be contracted thro

43 ectious agent of the mammalian transmissible spongiform encephalopathies (TSE) has long been consider

44 t current diagnostic tests for transmissible spongiform encephalopathies (TSE) rely on the presence o

45 In the transmissible spongiform encephalopathies (TSE), accumulation of the a

46 rotein that is responsible for transmissible spongiform encephalopathies (TSE).

47 The hallmark of transmissible spongiform encephalopathies (TSEs or prion diseases) is

48 se of the similarities between transmissible spongiform encephalopathies (TSEs) and other protein mis

49 pecies were not susceptible to transmissible spongiform encephalopathies (TSEs) and therefore represe

50 Transmissible spongiform encephalopathies (TSEs) are a family of invar

51 Transmissible spongiform encephalopathies (TSEs) are a family of invar

52 Transmissible spongiform encephalopathies (TSEs) are a group of neurod

53 Transmissible spongiform encephalopathies (TSEs) are associated with t

54 Many transmissible spongiform encephalopathies (TSEs) are believed to be ca

55 zheimer's, Parkinson's and the transmissible spongiform encephalopathies (TSEs) are characterized by

56 ions responsible for mammalian transmissible spongiform encephalopathies (TSEs) are due primarily to

57 Transmissible spongiform encephalopathies (TSEs) are fatal neurodegene

58 Transmissible spongiform encephalopathies (TSEs) are fatal neurologica

59 ess studied, pregnancy-related transmissible spongiform encephalopathies (TSEs) have been implicated

60 duction reduced infectivity of transmissible spongiform encephalopathies (TSEs) in blood.

61 The transmissible spongiform encephalopathies (TSEs) including scrapie hav

62 Human transmissible spongiform encephalopathies (TSEs) or prion diseases are

63 Transmissible spongiform encephalopathies (TSEs) or prion diseases are

64 Transmissible spongiform encephalopathies (TSEs) or prion diseases are

65 Transmissible spongiform encephalopathies (TSEs) represent a group of

66 s about the possible spread of transmissible spongiform encephalopathies (TSEs) via blood products.

67 ra of the eye for diagnosis of transmissible spongiform encephalopathies (TSEs) was examined.

68 lassical scrapie is one of the transmissible spongiform encephalopathies (TSEs), a group of fatal inf

69 on diseases, also known as the transmissible spongiform encephalopathies (TSEs), are a group of fatal

70 Prion diseases, or transmissible spongiform encephalopathies (TSEs), are a group of rare

71 ions, the infectious agents of transmissible spongiform encephalopathies (TSEs), have defied full cha

72 Transmissible spongiform encephalopathies (TSEs), including scrapie in

73 Transmissible spongiform encephalopathies (TSEs), or prion diseases, a

74 The agents responsible for transmissible spongiform encephalopathies (TSEs), or prion diseases, c

75 iginally formulated to explain transmissible spongiform encephalopathies (TSEs), the prion hypothesis

76 In transmissible spongiform encephalopathies (TSEs), which are lethal neu

77 s associated with the onset of transmissible spongiform encephalopathies (TSEs).

78 the etiological agents of the transmissible spongiform encephalopathies (TSEs).

79 ectious agents responsible for transmissible spongiform encephalopathies (TSEs).

80 about the iatrogenic spread of transmissible spongiform encephalopathies (TSEs)/prion diseases throug

81 several patients with various transmissible spongiform encephalopathies (variant and sporadic Creutz

82 Experiments on transmissible spongiform encephalopathies affecting rodents have led t

83 Transmissible spongiform encephalopathies are a class of fatal neurode

84 Transmissible spongiform encephalopathies are accompanied by the accum

85 nd systemic amyloidoses and prion-associated spongiform encephalopathies are acquired or inherited pr

86 Transmissible spongiform encephalopathies are associated with conforma

87 Spongiform encephalopathies are believed to be transmitt

88 Prion diseases or transmissible spongiform encephalopathies are characterized histopatho

89 Transmissible spongiform encephalopathies are fatal neurodegenerative

90 Transmissible spongiform encephalopathies are lethal neurodegenerative

91 Transmissible spongiform encephalopathies are neurodegenerative diseas

92 overy that devastating brain diseases called spongiform encephalopathies are transmissible to new hos

93 specimens for the diagnosis of transmissible spongiform encephalopathies has been described in sheep,

94 s prions that cause a group of transmissible spongiform encephalopathies in animals and humans.

95 associated with transmissible and hereditary spongiform encephalopathies in mammalian species.

96 Propagation of transmissible spongiform encephalopathies is associated with the conve

97 Propagation of transmissible spongiform encephalopathies is believed to involve the c

98 equired for the infectivity of transmissible spongiform encephalopathies is central to the debate abo

99 t blood in naturally occurring transmissible spongiform encephalopathies is not infectious has implod

100 the protein-only hypothesis of transmissible spongiform encephalopathies is the link between inherite

101 ation and neurotoxicity during transmissible spongiform encephalopathies is undisputed, the physiolog

102 prevalent manifestation of the transmissible spongiform encephalopathies or prion diseases affecting

103 , steps in the pathogenesis of transmissible spongiform encephalopathies or prion diseases.

104 Prion diseases (transmissible spongiform encephalopathies) are fatal neurodegenerative

105 For spongiform encephalopathies, a real prion can be transmi

106 ges in the prion protein cause transmissible spongiform encephalopathies, also referred to as prion d

107 se, type II diabetes mellitus, transmissible spongiform encephalopathies, and prion diseases.

108 Prion diseases, also known as transmissible spongiform encephalopathies, are fatal neurodegenerative

109 onic wasting disease and other transmissible spongiform encephalopathies, are misfolded proteins that

110 ectious agents responsible for transmissible spongiform encephalopathies, consist mainly of the misfo

111 ons, the etiological agents in transmissible spongiform encephalopathies, exhibit remarkable resistan

112 nto the causative agent of the transmissible spongiform encephalopathies, has previously been shown t

113 diagnosis and understanding of transmissible spongiform encephalopathies, including transmission mech

114 ntified as causative agents of transmissible spongiform encephalopathies, increasing evidence now sug

115 The transmissible spongiform encephalopathies, more commonly known as the

116 e of its abnormal conformer in transmissible spongiform encephalopathies, normal PrP(C) may be implic

117 Transmissible spongiform encephalopathies, or prion diseases, are caus

118 g approaches to the therapy of transmissible spongiform encephalopathies, or prion diseases, is beset

119 Prions, the agents of transmissible spongiform encephalopathies, require the expression of p

120 infected with prion diseases (transmissible spongiform encephalopathies, TSE).

121 ission of the prion disorders (transmissible spongiform encephalopathies, TSEs) are mediated by a mod

122 degenerative diseases known as transmissible spongiform encephalopathies, which affect humans, deer,

123 ectious agents responsible for transmissible spongiform encephalopathies, which appear to be composed

124 egenerative disorders known as transmissible spongiform encephalopathies.

125 is responsible for a range of transmissible spongiform encephalopathies.

126 generative diseases called the transmissible spongiform encephalopathies.

127 confer this high resistance to transmissible spongiform encephalopathies.

128 e devastating neurological diseases known as spongiform encephalopathies.

129 onformation is associated with transmissible spongiform encephalopathies.

130 he prevention of the spread of transmissible spongiform encephalopathies.

131 s of yet exists for any of the transmissible spongiform encephalopathies.

132 ng Alzheimer's disease and the transmissible spongiform encephalopathies.

133 gy resembling that observed in transmissible spongiform encephalopathies.

134 degenerative diseases known as transmissible spongiform encephalopathies.

135 are clinically associated with transmissible spongiform encephalopathies.

136 a prion that causes the fatal transmissible spongiform encephalopathies.

137 s to the infectious prion protein (PrPsc) in spongiform encephalopathies.

138 Two atypical BSE strains, bovine amyloidotic spongiform encephalopathy (BASE, also named BSE-L) and B

139 gh they were similarly exposed to the bovine spongiform encephalopathy (BSE) agent.

140 transmission efficiencies of vCJD and bovine spongiform encephalopathy (BSE) and an assessment of the

141 However, an association between bovine spongiform encephalopathy (BSE) and bovine PRNP exon 3 h

142 rodegenerative disorders that include bovine spongiform encephalopathy (BSE) and scrapie in animals a

143 l and neuropathological properties of bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-

144 , endemic sheep scrapie, and epidemic bovine spongiform encephalopathy (BSE) are caused by a related

145 An experimental oral bovine spongiform encephalopathy (BSE) challenge study was perf

146 However, since the bovine spongiform encephalopathy (BSE) crisis, their use has be

147 teins is strongly regulated since the bovine spongiform encephalopathy (BSE) crisis.

148 -Jakob disease, following on from the bovine spongiform encephalopathy (BSE) epidemic, led to concern

149 n transmission was reported after the bovine spongiform encephalopathy (BSE) epidemic, when >200 case

150 dily distinguished experimental sheep bovine spongiform encephalopathy (BSE) from classical scrapie.

151 n protein PrP(C), such as PrP(BSE) in bovine spongiform encephalopathy (BSE) in cattle and PrP(CJD) i

152 wasting disease (CWD) in cervids and bovine spongiform encephalopathy (BSE) in cattle are prion dise

153 Statutory surveillance of bovine spongiform encephalopathy (BSE) indicates that cattle ar

154 In bovine spongiform encephalopathy (BSE) infection, the polymorph

155 Bovine spongiform encephalopathy (BSE) is a transmissible spong

156 Bovine spongiform encephalopathy (BSE) is a TSE that occurs in

157 Bovine Spongiform Encephalopathy (BSE) is the only animal prion

158 samples in order to classify them as bovine spongiform encephalopathy (BSE) or non-BSE.

159 Creutzfeldt-Jakob disease (vCJD) and bovine spongiform encephalopathy (BSE) prions are two of the pr

160 ter the extensive dietary exposure to bovine spongiform encephalopathy (BSE) prions in the UK, has le

161 Bovine spongiform encephalopathy (BSE) prions were responsible

162 on protein (BoPrP) serially propagate bovine spongiform encephalopathy (BSE) prions without posing a

163 little about human susceptibility to bovine spongiform encephalopathy (BSE) prions, the causal agent

164 c mouse line, Tg(CerPrP)1536(+/-), to bovine spongiform encephalopathy (BSE) prions, which have the a

165 aused by dietary or other exposure to bovine spongiform encephalopathy (BSE) prions.

166 ause of the original case or cases of bovine spongiform encephalopathy (BSE) remains an enigma.

167 Foodborne transmission of bovine spongiform encephalopathy (BSE) to humans as variant Cre

168 However, its effect on bovine spongiform encephalopathy (BSE) transmission to goats is

169 ob disease (vCJD), experimental ovine bovine spongiform encephalopathy (BSE), and natural sheep scrap

170 Bovine spongiform encephalopathy (BSE), the prion disease in ca

171 Bovine spongiform encephalopathy (BSE)-associated prions were p

172 hat sheep and goats consumed the same bovine spongiform encephalopathy (BSE)-contaminated meat and bo

173 st certainly caused by consumption of bovine spongiform encephalopathy (BSE)-contaminated meat.

174 isease associated with infection with bovine spongiform encephalopathy (BSE)-like prions.

175 a zoonotic form of the cattle disease bovine spongiform encephalopathy (BSE).

176 iciency syndrome (AIDS), hepatitis C, bovine spongiform encephalopathy (BSE)/variant Creutzfeldt-Jako

177 e for neurodegenerative diseases like bovine spongiform encephalopathy (BSE; "mad cow" disease) and C

178 eases of cattle include the classical bovine spongiform encephalopathy (C-BSE) and the atypical H-typ

179 Classical bovine spongiform encephalopathy (c-BSE) is the only animal pri

180 c wasting disease (CWD) and classical bovine spongiform encephalopathy (cBSE) prions.

181 have been shown to be susceptible to feline spongiform encephalopathy (FSE), almost certainly caused

182 sceptible to the prion causing L-type bovine spongiform encephalopathy (L-BSE), although RQ171 sheep

183 affected by C-BSE and atypical L-type bovine spongiform encephalopathy (L-type BSE or L-BSE) with the

184 mals (n = 80) and 71% of animals with bovine spongiform encephalopathy (n = 7).

185 g disease (CWD) is an emerging transmissible spongiform encephalopathy (prion disease) of North Ameri

186 ep scrapie is the prototypical transmissible spongiform encephalopathy (prion disease), which has a f

187 chronic waste disease (PrP(CWD)), and bovine spongiform encephalopathy (PrP(BSE)) in lab-scale compos

188 ible to humans, as has been shown for bovine spongiform encephalopathy (the prion disease of cattle),

189 form encephalopathy (BSE) is a transmissible spongiform encephalopathy (TSE) (or prion disease) that

190 This is evidence that transmissible spongiform encephalopathy (TSE) agent properties alone,

191 Following oral exposure, some transmissible spongiform encephalopathy (TSE) agents accumulate first

192 As with viruses, transmissible spongiform encephalopathy (TSE) agents can adapt to new

193 of many peripherally acquired transmissible spongiform encephalopathy (TSE) agents is less efficient

194 presented here, using the same transmissible spongiform encephalopathy (TSE) animal model, our aim wa

195 Transmissible spongiform encephalopathy (TSE) can be induced in animal

196 protease-resistant PrP without transmissible spongiform encephalopathy (TSE) clinical signs or notabl

197 Diagnosis of transmissible spongiform encephalopathy (TSE) disease in humans and ru

198 Agents causing transmissible spongiform encephalopathy (TSE) diseases are resistant t

199 infectious agents (prions) of transmissible spongiform encephalopathy (TSE) diseases including chron

200 l infectious agents that cause transmissible spongiform encephalopathy (TSE) diseases, or prion disea

201 od transfusion exists for many transmissible spongiform encephalopathy (TSE) diseases.

202 ectious agents responsible for transmissible spongiform encephalopathy (TSE) diseases.

203 sly undetected sporadic bovine transmissible spongiform encephalopathy (TSE) have long been considere

204 dvantageous model for studying transmissible spongiform encephalopathy (TSE) infection.

205 Transmissible spongiform encephalopathy (TSE) infectivity naturally sp

206 nic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) of cervids now detected

207 Scrapie is the transmissible spongiform encephalopathy (TSE) of sheep and goats, and

208 the iatrogenic transmission of transmissible spongiform encephalopathy (TSE) or prion disease has bec

209 The viral and transmissible spongiform encephalopathy (TSE) safety of therapeutics o

210 eared to be dependent upon the transmissible spongiform encephalopathy (TSE) strain, allowing discrim

211 Different transmissible spongiform encephalopathy (TSE)-associated forms of prio

212 discriminatory testing of all transmissible spongiform encephalopathy (TSE)-positive small ruminant

213 are infected with prions from cattle (bovine spongiform encephalopathy [BSE]), both PrP variants occu

214 line CWD (fCWD) and feline BSE (i.e., feline spongiform encephalopathy [FSE]).

215 e (CWD) is a universally fatal transmissible spongiform encephalopathy affecting cervids, and natural

216 essing cells appear to support transmissible spongiform encephalopathy agent replication.

217 The process by which transmissible spongiform encephalopathy agents, or prions, infect cell

218 degenerative diseases, such as transmissible spongiform encephalopathy and Alzheimer disease.

219 roinvasion in many prion diseases, in bovine spongiform encephalopathy and atypical cases of sheep sc

220 al host systems, including strains of bovine spongiform encephalopathy and chronic wasting disease.

221 nfluence the susceptibility to transmissible spongiform encephalopathy and determine the characterist

222 T treatment also inhibits the development of spongiform encephalopathy and gliosis in the central ner

223 ldt-Jakob disease (CJD) in humans and bovine spongiform encephalopathy and scrapie in animals.

224 ecific, and early diagnosis of transmissible spongiform encephalopathy and to further understand the

225 wild-type mice and was also found in bovine spongiform encephalopathy cattle brain, indicating that

226 Human transmission of bovine spongiform encephalopathy causes the fatal neurodegenera

227 n to replicate many aspects of transmissible spongiform encephalopathy disease to investigate the cel

228 Prion diseases or transmissible spongiform encephalopathy diseases are typically charact

229 kob disease in humans and scrapie and bovine spongiform encephalopathy in animals.

230 sease in humans, scrapie in sheep and bovine spongiform encephalopathy in cattle.

231 n, we show that prions causing transmissible spongiform encephalopathy in wild-type hamsters can be g

232 als in feedstuffs in order to prevent Bovine Spongiform Encephalopathy infection and diffusion, howev

233 significant removal of rodent transmissible spongiform encephalopathy infections by filtration of re

234 sarily be a reliable marker of transmissible spongiform encephalopathy infectivity.

235 hypothesis that human infection with bovine spongiform encephalopathy occurred in Saudi Arabia.

236 ronic wasting disease (CWD), a transmissible spongiform encephalopathy of cervids, was first document

237 ronic wasting disease (CWD), a transmissible spongiform encephalopathy of cervids, was first document

238 ronic wasting disease (CWD), a transmissible spongiform encephalopathy of deer, elk, and moose, is th

239 d factor for susceptibility to transmissible spongiform encephalopathy or prion diseases.

240 ry response may play a role in transmissible spongiform encephalopathy pathogenesis.

241 Just as spread of bovine spongiform encephalopathy prion variant is less impaired

242 We demonstrate that bovine spongiform encephalopathy prions maintain their transspe

243 ion strain resulting from exposure to bovine spongiform encephalopathy prions to which the Fore were

244 in those with primary infection with bovine spongiform encephalopathy prions.

245 sive to infection with natural transmissible spongiform encephalopathy strains.

246 ged into at least two distinct transmissible spongiform encephalopathy strains.

247 Chronic wasting disease (CWD) is a fatal spongiform encephalopathy that is efficiently transmitte

248 imental challenge and the outbreak of bovine spongiform encephalopathy that occurred in the late 1980

249 l as the interspecies transmission of bovine spongiform encephalopathy to humans in the form of varia

250 linical signs, neuropathology (transmissible spongiform encephalopathy vacuolation and prion protein

251 ronic wasting disease of cervids, and bovine spongiform encephalopathy) all seem to be laterally tran

252 on with a single strain of the agent (bovine spongiform encephalopathy).

253 raperitoneal, or oral); all groups developed spongiform encephalopathy, although the oral route requi

254 g PrP-101L with neurological disease, severe spongiform encephalopathy, and formation of proteinase K

255 were fed brain of (eleven) cows with bovine spongiform encephalopathy, and some were euthanized befo

256 Some animal prion diseases, such as bovine spongiform encephalopathy, can infect humans; however, h

257 21 overlap with QTLs associated with Bovine spongiform encephalopathy, clinical mastitis or somatic

258 risks posed by prion zoonoses such as bovine spongiform encephalopathy, has focused much attention on

259 Transmissible spongiform encephalopathy-associated forms from mouse an

260 an form of a prion disease of cattle, bovine spongiform encephalopathy-have been reported from 12 cou

261 ritical goal of discriminating transmissible spongiform encephalopathy-infected from healthy uninfect

262 stant core identical to that found in bovine spongiform encephalopathy-specific scrapie-associated pr

263 evalence in the United Kingdom with a bovine spongiform encephalopathy-unexposed population.

264 shown to develop a spontaneous transmissible spongiform encephalopathy.

265 chronic wasting disease, scrapie, and bovine spongiform encephalopathy.

266 disease, a naturally occurring transmissible spongiform encephalopathy.

267 st system to study this cervid transmissible spongiform encephalopathy.

268 nts including Alzheimer's disease and bovine spongiform encephalopathy.

269 cluding Creutzfeldt-Jakob disease and bovine spongiform encephalopathy.

270 otes PrP amyloidogenesis in the absence of a spongiform encephalopathy.

271 transgenic mice (Tg PrP101LL), resulting in spongiform encephalopathy.

272 om sheep with scrapie and cattle with bovine spongiform encephalopathy.

273 mum global risk for human exposure to bovine spongiform encephalopathy.

274 degenerative diseases known as transmissible spongiform encephalopathy.

275 evention of human dietary exposure to bovine spongiform encephalopathy.

276 nisms and/or at the onset of a transmissible spongiform encephalopathy.

277 herited prion disease; sheep scrapie; bovine spongiform encephalopathy; and chronic wasting disease.

278 disorder originating from exposure to bovine-spongiform-encephalopathy-like prions.

279 ibility and phenotype of human transmissible spongiform encyphalopathies, but the molecular mechanism

280 of PrP(Sc) deposits within the brain and the spongiform lesions they induce.

281 on of the Nrf2 gene in mice caused vacuolar (spongiform) leukoencephalopathy with widespread astrogli

282 s) are capable of inducing fatal progressive spongiform motor neuron disease in mice that is largely

283 murine leukemia virus (MLV) can cause acute spongiform neurodegeneration analogous to that induced b

284 ll defined even though a loss of neurons and spongiform neurodegeneration has been reported to accomp

285 sE and Moloney MLV-ts1 cause noninflammatory spongiform neurodegeneration in mice, manifested clinica

286 ons of FIG4 result in juvenile lethality and spongiform neurodegeneration in the mouse, and are respo

287 MLVs) can induce progressive noninflammatory spongiform neurodegeneration similar to that caused by p

288 y ataxia and paralysis and the appearance of spongiform neurodegeneration throughout the brain stem a

289 E3 ubiquitin-protein ligase Mahogunin causes spongiform neurodegeneration, a recessively transmitted

290 These pathological changes include spongiform neurodegeneration, astrogliosis, thymic atrop

291 nfection and before any marked appearance of spongiform neurodegeneration, we detected vessel leakage

292 cytosolic ubiquitin ligase whose loss causes spongiform neurodegeneration.

293 n dysregulation of endosomal trafficking and spongiform neurodegeneration.

294 Some murine retroviruses cause a spongiform neurodegenerative disease exhibiting patholog

295 oup of ecotropic murine retroviruses cause a spongiform neurodegenerative disease manifested by tremo

296 strong support for the hypothesis that this spongiform neurodegenerative disease represents a virus-

297 , no malignancies were detected in cystic or spongiform nodules (both, n = 11, 2.8%; 95% CI: 1.4%, 5.

298 logical function accompany early hippocampal spongiform pathology.

299 blocks neuronal cell loss and reverses early spongiform pathology.

300 spartic acid, elevates brain NAA and causes "spongiform" vacuolation of superficial brain white matte