ライフサイエンスコーパス: amyloid deposit

1 the brain or become part of an extracellular amyloid deposit.

2 ed the mutant peptide in the proband's renal amyloid deposits.

3 d relative beta-cell number, and presence of amyloid deposits.

4 s present in plasma, basement membranes, and amyloid deposits.

5 mutant peptide in the proband's renal and GI amyloid deposits.

6 ns are routinely found associated with these amyloid deposits.

7 y tau-laden neurofibrillary tangles and beta-amyloid deposits.

8 in levels of Abeta40 and Abeta42 and reduced amyloid deposits.

9 safely promotes the clearance of established amyloid deposits.

10 -SAP antibodies to reach residual SAP in the amyloid deposits.

11 nd markedly eliminate thioflavine-S positive amyloid deposits.

12 APP are precursors to the formation of these amyloid deposits.

13 cosaminoglycans are strongly associated with amyloid deposits.

14 globulin (beta2-m) can form dialysis-related amyloid deposits.

15 thioflavine-S- and apolipoprotein E-positive amyloid deposits.

16 mass spectrometric analysis of TTR from the amyloid deposits.

17 e of diffuse Abeta deposits but not vascular amyloid deposits.

18 promote clearance of parenchymal or vascular amyloid deposits.

19 minish deposition of parenchymal or vascular amyloid deposits.

20 aled protein components that are shared with amyloid deposits.

21 uced peptide ultimately forms more extensive amyloid deposits.

22 e resulted in the clearance of intraneuronal amyloid deposits.

23 ve as a source for some of the extracellular amyloid deposits.

24 ng fibrillogenesis or destabilizing existing amyloid deposits.

25 te abundant cerebral microvascular fibrillar amyloid deposits.

26 minated by a specific interaction with Abeta amyloid deposits.

27 s a possible means for the solubilization of amyloid deposits.

28 the severity of organ dysfunction induced by amyloid deposits.

29 ia had a markedly reduced ability to envelop amyloid deposits.

30 n and protein fragments is common in ex vivo amyloid deposits.

31 g, found even in brains that did not contain amyloid deposits.

32 id diseases is the presence of extracellular amyloid deposits.

33 of transgenic mice that exhibit hippocampal amyloid deposits.

34 rphosphorylation and axonal dystrophy around amyloid deposits.

35 d at autopsy, which has been associated with amyloid deposits.

36 s the main component of the highly insoluble amyloid deposits.

37 was in smooth muscle cells in arteries with amyloid deposits.

38 cytokines and complement factors surrounding amyloid deposits.

39 of the exocrine lesion and in the absence of amyloid deposits.

40 n function by accelerating the resorption of amyloid deposits.

41 nt, but never develops parenchymal fibrillar amyloid deposits.

42 ocardiography and the histological extent of amyloid deposits.

43 t is associated with aging and not with beta-amyloid deposits.

44 terstitial fluid Abeta levels and attenuated amyloid deposits.

45 reside within swollen axons that contact the amyloid deposits.

46 binds specifically to myocardial AL and ATTR amyloid deposits.

47 and identify spatially and temporally unique amyloid deposits.

48 table finding of lipid deposition within the amyloid deposits.

49 ore quantitative imaging of expansive tissue amyloid deposits.

50 n association with low levels of parenchymal amyloid deposits.

51 prevalence (percentage of islets containing amyloid deposits; 34 +/- 8, 45 +/- 8, and 58 +/- 10%, P

52 on of pathological markers such as fibrillar amyloid deposits (49-62%) and activated glia (42-68%) in

53 like AD, the mice develop memory deficits as amyloid deposits accumulate.

54 g of these antibodies to the residual SAP in amyloid deposits activates complement and triggers the r

55 was a reduction in both diffuse and compact amyloid deposits after 2 months of treatment.

56 The role of microglia in the removal of amyloid deposits after systemically administered anti-Ab

57 of Abeta42 led to the formation of diffused amyloid deposits, age-dependent learning defects, and ex

58 dditional elderly patients with Apo-CII-rich amyloid deposits, all of whom had kidney involvement and

59 nes encoding non-fibrillar components of TTR amyloid deposits and a molecule metabolically interactin

60 Brain parenchymal and cerebrovascular beta-amyloid deposits and Abeta abundance were markedly (up t

61 lated muscle fibers containing intracellular amyloid deposits and accumulations of "Alzheimer-charact

62 It is based on histologic evidence of amyloid deposits and characterization of the amyloidogen

63 te abundant cerebral microvascular fibrillar amyloid deposits and exhibit robust neuroinflammation.

64 or amylin) transgenic mice developing islet amyloid deposits and hyperglycemia to suggest that the p

65 Shown to lower amyloid deposits and improve cognition in APP transgenic

66 nsgenic 5XFAD/Tg197 AD/TNF mice that develop amyloid deposits and inflammatory arthritis induced by h

67 In Alzheimer disease both extracellular amyloid deposits and intracellular amyloid beta protein

68 m infrared (FTIR) microscopy, to co-localize amyloid deposits and lipid peroxidation in tissue slides

69 Significantly fewer vascular amyloid deposits and microhemorrhages were observed in m

70 Based on the known association of amyloid deposits and relative hyperproinsulinemia, it is

71 tion of Abeta without affecting pre-existing amyloid deposits and restored cognitive performance to t

72 events are evident 6 months before the first amyloid deposits and significantly precede the appearanc

73 the accumulation of amyloid beta (Abeta) in amyloid deposits and toxic oligomeric species.

74 with PET/CT using (11)C-PIB to study cardiac amyloid deposits and with (11)C-acetate to measure myoca

75 onent (SAP) binds to fibrils in all types of amyloid deposits, and contributes to the pathogenesis of

76 idespread microglial activation, age-related amyloid deposits, and dystrophic neurites.

77 3 d, is responsible for clearance of compact amyloid deposits, and is associated with microglial acti

78 ntigraphy tracers can localize to myocardial amyloid deposits, and use of this imaging modality for t

79 Amyloid deposits are a characteristic feature of advance

80 Islet amyloid deposits are a characteristic pathological hallm

81 nd brain degeneration in the absence of beta-amyloid deposits are also hallmarks of neurodegenerative

82 rt the concept that parenchymal and vascular amyloid deposits are associated with a different array o

83 Although IAPP amyloid deposits are associated with areas of pancreatic

84 Naturally occurring amyloid deposits are associated with sulfated proteoglyc

85 In vivo, amyloid deposits are found in the extracellular space an

86 Beta(2)-microglobulin (beta(2)m) amyloid deposits are linked to dialysis-related amyloido

87 Wild-type (wt) TTR amyloid deposits are linked to senile systemic amyloidos

88 t pathway projection to the hippocampus, and amyloid deposits are often found in the molecular layer

89 hemical analysis confirmed the nature of the amyloid deposits as an AA type derived from amyloidogeni

90 so observed the co-localization of NETs with amyloid deposits as well as with oligomers, which are pr

91 ursor (APP) to hinder the formation of toxic amyloid deposits associated with AD.

92 oligomerize, including cystatin C that forms amyloid deposits associated with cerebral amyloid angiop

93 is the major protein component of the islet amyloid deposits associated with type 2 diabetes.

94 Conversely, their association with vascular amyloid deposits, blood-brain barrier disruption, and he

95 ts that begin the pathogenic cascade are not amyloid deposits but damaged blood vessels caused by inf

96 ed with conversion of a soluble protein into amyloid deposits, but how this is connected to toxicity

97 of the United States, and subtyping hepatic amyloid deposits by an accurate analytic method such as

98 The amyloid deposit can be facilitated by disease-associated

99 is present in demented PD and, on occasion, amyloid deposits can be detected.

100 S-extractable pool, suggesting that cerebral amyloid deposits can rapidly sequester soluble Abeta fro

101 our results suggest that extracellular beta-amyloid deposits cause a local impairment in the retrogr

102 rillary tangles and parenchymal and vascular amyloid deposits co-localizing with markers of glial act

103 usion-body myositis, vacuolar formation with amyloid deposits coexists with the immunological feature

104 nced reductions in cerebral Abeta levels and amyloid deposits, compared to animals raised under "stan

105 Cardiac tissues containing amyloid deposits composed of either transthyretin (TTR)

106 ed with the formation of extracellular islet amyloid deposits composed of islet amyloid polypeptide (

107 Observation of amyloid deposits composed of mature SP-C in lung tissue

108 Pancreatic amyloid deposits, composed primarily of the 37-residue i

109 Congo red staining revealed brilliant red amyloid deposits confirmed by apple-green birefringence

110 val biopsy under optical microscopy revealed amyloid deposit, confirmed by Congo red staining.

111 However, all amyloid deposits contain the normal, non-fibrillar plasm

112 on of anti-human-SAP antibodies to mice with amyloid deposits containing human SAP triggers a potent,

113 umber of microglial cells does not result in amyloid deposit degradation.

114 pite the presence of high amounts of APP and amyloid deposits, deleting the alpha7nAChR subunit in th

115 cell endoplasmic reticulum stress, and islet amyloid deposits derived from islet amyloid polypeptide

116 type 2 diabetes, including the formation of amyloid deposits derived from islet amyloid polypeptide

117 rized by loss of beta cells and formation of amyloid deposits derived from islet amyloid polypeptide

118 eased beta-cell apoptosis, and extracellular amyloid deposits derived from islet amyloid polypeptide

119 analysis of Congo red-positive renal and GI amyloid deposits detected abundant lysozyme C protein.

120 These LC form both toxic oligomers and amyloid deposits disrupting vital organ function.

121 PP tg and hAPP tg/RAP-/- mice, the amount of amyloid deposited doubled in the hAPP tg/RAP-/- backgrou

122 , pyroGlu-3 Abeta is a major species of beta-amyloid deposited early in diffuse and focal plaques and

123 ansgenic mice consistently had minor cardiac amyloid deposits, enabling us to extend to the heart the

124 the antibody primarily to fibrillar vascular amyloid deposits even in the presence of a large excess

125 f CatB in aged hAPP mice reduced preexisting amyloid deposits, even thioflavin S-positive plaques.

126 of SAA3 as a cause of amyloidosis and of AA amyloid deposited exclusively in the uterus.

127 ated amyloid fibrils are stable in vitro, AA amyloid deposits exist in a state of dynamic turnover, a

128 There is no therapy that directly targets amyloid deposits for enhanced clearance.

129 In localized amyloidosis, amyloid deposits form at the site of precursor protein s

130 Applied to amyloid deposits formed in a cell culture model of syste

131 olypeptide (amylin) is the main component in amyloid deposits formed in type II diabetes.

132 polypeptide (IAPP) is the major component of amyloid deposits found in pancreatic islets of patients

133 r amylin) is a causative agent in pancreatic amyloid deposits found in patients with type 2 diabetes.

134 the glycosaminoglycan chains associated with amyloid deposits found in type 2 diabetes.

135 (IAPP) is the major protein component of the amyloid deposits found in type-II diabetes.

136 ctrometry (MS)-based proteomics, we subtyped amyloid deposits from 130 cases of hepatic amyloidosis.

137 -derived elastase and histones were found in amyloid deposits from patients with different systemic a

138 xarotene treatment clearing preexisting beta-amyloid deposits from the brains of APP/PS1DeltaE9 mice

139 i-SAP antibody safely triggered clearance of amyloid deposits from the liver and some other tissues.

140 insight, but structural analyses of TTR from amyloid deposits have been hindered thus far by the lack

141 estigation, focusing on reducing or removing amyloid deposits, have failed to produce any meaningful

142 hibitors, and immunotherapeutic targeting of amyloid deposits holds promise to transform outcomes in

143 al flanking region of proIAPP is detected in amyloid deposits; however, the C-terminal flanking regio

144 hat the beta-amyloid peptide (Abeta) or beta-amyloid deposits impact many processes that can contribu

145 The optical orientation in amyloid deposited in blood vessels from subjects having

146 amyloid fibrils in vitro but is absent from amyloid deposited in vivo.

147 With the determination of how fast amyloid deposits in a given region relative to the whole

148 te amyloidogenic peptides that accumulate as amyloid deposits in a tissue-specific manner.

149 is up-regulated on myeloid cells surrounding amyloid deposits in AD mouse models and human AD tissue.

150 within dystrophic neurites surrounding beta-amyloid deposits in AD mouse models but the pathological

151 mulates in dystrophic neurites near cerebral amyloid deposits in AD.

152 ion cortex known to contain large amounts of amyloid deposits in AD.

153 Histological examination revealed amyloid deposits in all cases and all carried the p.Trp8

154 oidogenic peptide, Abeta, the constituent of amyloid deposits in Alzheimer disease.

155 ory protein, is an integral component of the amyloid deposits in Alzheimer's disease (AD) and has bee

156 In this way, we show that the amyloid deposits in Alzheimer's disease plaques contain

157 a-peptide, which forms neuronal and vascular amyloid deposits in Alzheimer's disease, is derived from

158 rea positively correlated with cerebral beta-amyloid deposits in B6Tg2576 mice on both atherogenic an

159 5 and 3d6 led to clearance of 50% of diffuse amyloid deposits in both animal models within 3 d.

160 -binding peptides recognize murine and human amyloid deposits in both in vivo and ex vivo tissues and

161 Compact core and diffuse amyloid deposits in both vaccinated individuals were foc

162 Congo red staining detects amyloid deposits in brain tissue of amyloid precursor pr

163 arately quantifying vascular and parenchymal amyloid deposits in brain tissue sections.

164 ntly discriminate between different types of amyloid deposits in brain.

165 iant form of cystatin C (L68Q) readily forms amyloid deposits in cerebral arteries in affected indivi

166 sidue peptide that is the major component of amyloid deposits in familial British dementia.

167 ABri was found to be the main component of amyloid deposits in FBD brains.

168 hat prion infectivity can also be present as amyloid deposits in heart tissue.

169 sozyme variant that has not been detected in amyloid deposits in human patients.

170 found in association with all extracellular amyloid deposits in humans, are known to accelerate the

171 nsulin and is the major constituent of islet amyloid deposits in individuals with type 2 diabetes or

172 l analysis, we demonstrate the occurrence of amyloid deposits in islets transplanted into the liver i

173 eta-induced protein (TGFBIp) responsible for amyloid deposits in lattice corneal dystrophy (LCD) have

174 PIB, can provide quantitative information on amyloid deposits in living subjects.

175 s (GAGs) are routinely found associated with amyloid deposits in most amyloidosis diseases, and there

176 p = 0.0005), and difficult identification of amyloid deposits in nerve and muscle biopsies.

177 The data indicate that myocardial amyloid deposits in patients diagnosed with systemic amy

178 ument objectively the location and extent of amyloid deposits in patients with systemic forms of amyl

179 The polypeptide hormone amylin forms amyloid deposits in patients with type 2 diabetes mellit

180 ers for the noninvasive molecular imaging of amyloid deposits in situ.

181 convincingly demonstrate toxicity of native amyloid deposits in the aged and Alzheimer brains.

182 Thus, the presence of amyloid deposits in the axonal terminal zone of patholog

183 ease is characterized by the accumulation of amyloid deposits in the brain and the progressive loss o

184 and specifically binds to extracellular beta-amyloid deposits in the brain parenchyma (Abeta plaques)

185 icroglial activation and recruitment to beta-amyloid deposits in the brain.

186 er-Scheinker-like disease with extensive PrP amyloid deposits in the brain.

187 onditions, transgenic mice do not develop AA amyloid deposits in the brain; however, induction of a s

188 peptide is the major component found in the amyloid deposits in the brains of Alzheimer's disease pa

189 ta(1-42) IgG exhibited enhanced affinity for amyloid deposits in the cerebrovasculature.

190 hy (PET) studies, could specifically bind to amyloid deposits in the complex milieu of human brain or

191 actoferrin has previously been identified in amyloid deposits in the cornea, seminal vesicles, and br

192 educed numbers of microglia surrounding beta-amyloid deposits in the CX3CR1-deficient APPPS1 animals.

193 ed a moderate, but significant, reduction in amyloid deposits in the forebrain of mice expressing S-p

194 y the presence of large numbers of fibrillar amyloid deposits in the form of senile plaques in the br

195 (18)F-labeled tracer for PET imaging of beta-amyloid deposits in the human brain.

196 lin suggests their presence in intracellular amyloid deposits in the increasingly stressed beta cells

197 diabetes includes the presence of cytotoxic amyloid deposits in the islets of Langerhans.

198 lization of all ApoE proteins with fibrillar amyloid deposits in the mice.

199 ulin (beta2m) self-associates into fibrillar amyloid deposits in the musculoskeletal system of patien

200 PGs) are ubiquitous components of pathologic amyloid deposits in the organs of patients with disorder

201 n forms both intracellular and extracellular amyloid deposits in the pancreas of most type II diabeti

202 (IAPP, also known as amylin) forms cytotoxic amyloid deposits in the pancreas, and these are believed

203 yloid polypeptide/hIAPP) is found in vivo as amyloid deposits in the pancreatic islets of sufferers o

204 velop neurologic dysfunction and Congophilic amyloid deposits in the stomach.

205 evelopment of lattice corneal dystrophy with amyloid deposits in the superficial and deep stroma, cla

206 drug action potently removes SAP from human amyloid deposits in the tissues and may provide a new th

207 Systemic amyloidosis, with amyloid deposits in the viscera, blood vessel walls, and

208 By contrast, the addition of amyloid deposits in this area leads to disruption of the

209 ble to detect mouse IgG bound to congophilic amyloid deposits in those mice treated with the anti-Abe

210 transthyretin amyloidosis (ATTR), and Abeta amyloid deposits in tissue sections.

211 The distribution of beta-amyloid deposits in tissue was based on measurement of E

212 coincided with the extracellular myocardial amyloid deposits in tissues from patients with familial

213 essed in reactive astrocytes in regions with amyloid deposits in transgenic mice.

214 tes in the islet extracellular space to form amyloid deposits in up to 95% of patients with the disea

215 diolabeled, putrescine-modified Abeta labels amyloid deposits in vivo in a transgenic mouse model of

216 er, these results indicate that clearance of amyloid deposits in vivo may involve, in addition to Fc-

217 Numerous polypeptides and proteins form amyloid deposits in vivo or in vitro.

218 al plasma cells, but only in AL do they form amyloid deposits in vivo We investigated the amyloid for

219 hat Abeta42 is critical for the formation of amyloid deposits in vivo.

220 Methoxy-X04 was used to visualize amyloid deposits in vivo.

221 models of amyloid deposition, the amount of amyloid deposits increase with mouse age.

222 The formation of amyloid deposits is a common feature of a broad range of

223 Accumulation of Abeta protein in beta-amyloid deposits is a hallmark event in Alzheimer's dise

224 ein tau (MAPT, tau) into toxic oligomers and amyloid deposits is a primary pathology in tauopathies,

225 their soluble native states into intractable amyloid deposits is associated with a wide range of huma

226 ding of proteins leading to the formation of amyloid deposits is associated with more than 40 types o

227 systemic amyloidoses, unequivocal typing of amyloid deposits is now essential.

228 chanism underlying the targeting of systemic amyloid deposits is unclear.

229 hy (CAA), characterised by cortical vascular amyloid deposits, is associated with cortical tissue los

230 the major protein component of the fibrillar amyloid deposits isolated from patients diagnosed with d

231 Amyloid-deposited light chain (AL) amyloidosis is correl

232 y is able to enter the brain and bind to the amyloid deposits, likely opsonizing the Abeta and result

233 on in that it prevented the formation of new amyloid deposits, limited their growth, and was associat

234 s still be found associated with a subset of amyloid deposits many months after the final injection.

235 an amylin, a major constituent of pancreatic amyloid deposits, may be a pathogenetic factor for nonin

236 The number of amyloid deposits measured by Congo Red birefringence was

237 role of these cells in the encapsulation of amyloid deposits ("microglia barrier").

238 ally processed forms of proIAPP are found in amyloid deposits; most notable is a 48-residue intermedi

239 /PS1dE9) produced 20% more A beta but formed amyloid deposits no faster and to no greater extent than

240 with neurodegeneration and the formation of amyloid deposits of alpha-synuclein (alphaSyn), which co

241 Amyloid deposits of amylin in the pancreas are an import

242 An illustrative example shows that amyloid deposits of lysozyme are only the tip of an iceb

243 TTR is found in amyloid deposits of patients with senile systemic amyloi

244 sma pool of Abeta and thus indirectly to the amyloid deposits of the brain parenchyma and cerebral bl

245 Amyloid deposits often develop rapidly in transplanted k

246 test whether glial cells are linked only to amyloid deposits or also to tangle deposition, thus inte

247 defects but did not lead to the formation of amyloid deposits or neurodegeneration.

248 Some amyloid deposits originate within morphologically abnorm

249 main causative factors for the formation of amyloid deposits outside the brain.

250 As expected, amyloid deposits persisted after new APP/Abeta productio

251 n were also found as fibrillar components of amyloid deposits predominantly in the blood vessels of s

252 Amyloid deposits regressed in 25 of 42 patients whose me

253 5 peptide was posited to bind effectively to amyloid deposits, relative to similarly charged polybasi

254 till release vasoactive substances, vascular amyloid deposits render blood vessels rigid and reduce t

255 d by deficient microglia polarization toward amyloid deposits, resulting in ineffective plaque encaps

256 pectrometry for their original constituents, amyloid deposits reveal a unique signature of chaperones

257 We found that vascular amyloid deposits separated astrocyte end-feet from the e

258 of this novel combined therapy to eliminate amyloid deposits should be applicable to all forms of sy

259 myloid-beta (Abeta), particularly those with amyloid deposits, showed weaker memory for the platform

260 Amyloid deposits slowly regressed with restoration of no

261 ulfate proteoglycan (HSPG) perlecan in islet amyloid deposits, suggesting a role for HSPGs in mediati

262 eptibility and response to the disruption of amyloid deposits suggests that Tg-SwDI mice provide an e

263 Analysis of beta-amyloid deposits, tau phosphorylation, and inflammatory

264 ice had significantly fewer fibrillar Abeta (amyloid) deposits than PDAPP mice expressing clusterin.

265 ses is the capability to distinguish between amyloid deposits that are associated with related, but d

266 e such pathology and features TTR-containing amyloid deposits that are found primarily in the heart.

267 s SAP from the plasma but leaves some SAP in amyloid deposits that can be specifically targeted by th

268 se transgenic mice contained PrPres-positive amyloid deposits that led to myocardial stiffness and ca

269 familial Danish dementia (FDD) are caused by amyloid deposits that trigger tauopathy, neurodegenerati

270 Subclinical amyloid deposits that were present in his spleen and hea

271 In the amyloid deposits, the ABri peptide adopts aggregated bet

272 In contrast to the extracellular amyloid deposits, the alpha-synuclein deposits in Lewy b

273 under conditions leading to the formation of amyloid deposits, the domain-swapped dimer of chicken cy

274 function coupled with regression of visceral amyloid deposits, the results of OLT are influenced by m

275 f cholesterol may induce targeted binding of amyloid deposits to biomembranes.

276 u gene transfer to the hippocampal region of amyloid-depositing transgenic mice produced pretangles a

277 For characterization of the amyloid deposited TTR, we investigated cardiac tissue sa

278 Although amyloid A (AA) amyloid deposits typically consist of an N-terminal frag

279 dendrites passing through or near fibrillar amyloid deposits undergo spine loss and shaft atrophy, a

280 In transgenic mice containing amyloid deposits, uptake was dramatically increased and

281 suggest that although immunization disrupted amyloid deposits, vascular capture prevented large-scale

282 fying the mechanistic links between vascular amyloid deposits, vascular dysfunction, and CAA-related

283 The removal of preexisting amyloid deposits was associated with the appearance of a

284 The association of CLU with cardiac amyloid deposits was confirmed by immunogold electron mi

285 Second, testing for neurodegeneration and amyloid deposits, we investigated retromer-deficient fli

286 centration was measured monthly and visceral amyloid deposits were assessed annually by serum amyloid

287 The larger parenchymal amyloid deposits were associated with a higher loss of c

288 SAA3 transcripts, suggests that the uterine amyloid deposits were due to locally produced SAA3.

289 His outcome was followed clinically and his amyloid deposits were monitored with serum amyloid P com

290 ssociated with Abeta oligomers, as fibrillar amyloid deposits were not detected in oligomer-injected

291 AL amyloid deposits were usually distributed in a reticular

292 r this occurs prior to the emergence of beta amyloid deposits, when only soluble beta amyloid (Abeta)

293 the constituent peptide of pancreatic islet amyloid deposits which form in islets of Type 2 diabetic

294 s, including soluble oligomers and fibrillar amyloid deposits, which are linked with neurodegeneratio

295 All of the peptides bound amyloid deposits within 1 h post-injection, but the exte

296 PIB entered the brain quickly and labeled amyloid deposits within minutes.

297 ese findings indicate that polymorphic Abeta-amyloid deposits within the brain cluster as clouds of c

298 muscle blood vessel amyloid and congophilic amyloid deposits within vacuolated muscle fibers.

299 The JNK activation was localized to amyloid deposits, within neurites containing phosphoryla

300 action that swiftly removes massive visceral amyloid deposits without adverse effects.