ライフサイエンスコーパス: amyloid deposit

1 table finding of lipid deposition within the amyloid deposits.

2 ore quantitative imaging of expansive tissue amyloid deposits.

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

4 ns are routinely found associated with these amyloid deposits.

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

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

7 safely promotes the clearance of established amyloid deposits.

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

9 nd markedly eliminate thioflavine-S positive amyloid deposits.

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

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

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

13 mass spectrometric analysis of TTR from the amyloid deposits.

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

15 promote clearance of parenchymal or vascular amyloid deposits.

16 minish deposition of parenchymal or vascular amyloid deposits.

17 aled protein components that are shared with amyloid deposits.

18 biomarkers and their relationship with skin amyloid deposits.

19 uced peptide ultimately forms more extensive amyloid deposits.

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

21 ng fibrillogenesis or destabilizing existing amyloid deposits.

22 te abundant cerebral microvascular fibrillar amyloid deposits.

23 minated by a specific interaction with Abeta amyloid deposits.

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

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

26 the severity of organ dysfunction induced by amyloid deposits.

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

28 e resulted in the clearance of intraneuronal amyloid deposits.

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

30 id diseases is the presence of extracellular amyloid deposits.

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

32 of transgenic mice that exhibit hippocampal amyloid deposits.

33 n association with low levels of parenchymal amyloid deposits.

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

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

36 cosaminoglycans are strongly associated with amyloid deposits.

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

38 rphosphorylation and axonal dystrophy around amyloid deposits.

39 n function by accelerating the resorption of amyloid deposits.

40 nt, but never develops parenchymal fibrillar amyloid deposits.

41 ocardiography and the histological extent of amyloid deposits.

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

43 terstitial fluid Abeta levels and attenuated amyloid deposits.

44 ia as the only myeloid cells present at beta-amyloid deposits.

45 reside within swollen axons that contact the amyloid deposits.

46 ant increase of 6E10 and thioflavin-positive amyloid deposits.

47 binds specifically to myocardial AL and ATTR amyloid deposits.

48 and identify spatially and temporally unique amyloid deposits.

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

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

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

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

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

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

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

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

57 In Alzheimer's disease, amyloid deposits along the brain vasculature lead to a c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

72 by diastolic heart failure, the presence of amyloid deposits, and electrophysiological changes, comp

73 3 d, is responsible for clearance of compact amyloid deposits, and is associated with microglial acti

74 n inflammatory manifestations, regression of amyloid deposits, and normalization of proinflammatory a

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

76 Amyloid deposits are a characteristic feature of advance

77 Islet amyloid deposits are a characteristic pathological hallm

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

79 Although IAPP amyloid deposits are associated with areas of pancreatic

80 Naturally occurring amyloid deposits are associated with sulfated proteoglyc

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

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

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

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

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

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

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

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

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

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

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

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

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

94 The amyloid deposit can be facilitated by disease-associated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

113 in type 2 diabetes (T2D) is characterized by amyloid deposits derived from islet amyloid polypeptide

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

148 ar amyloid, although to a lesser degree than amyloid deposits in ADAD.

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

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

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

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

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

154 5 and 3d6 led to clearance of 50% of diffuse amyloid deposits in both animal models within 3 d.

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

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

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

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

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

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

161 ent state, rationalizing the localization of amyloid deposits in DRA.

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

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

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

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

166 The formation of amyloid deposits in human tissues is a defining feature

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

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

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

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

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

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

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

174 The role of amyloid deposits in patients with AF without valvular he

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

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

177 lvement, (18)F-florbetapir PET/CT identified amyloid deposits in substantially higher percentages of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

195 an beta(2)-microglobulin (beta(2)m) found in amyloid deposits in the joints of patients with dialysis

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

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

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

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

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

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

202 lammatory infiltrates in various organs, and amyloid deposits in the spleen, liver, and kidneys.

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

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

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

206 In most instances, amyloid deposits in the various organs were not associat

207 eased risk for atrial fibrillation(AF) while amyloid deposits in the ventricles is increasingly being

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

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

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

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

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

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

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

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

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 peptides have been previously identified in amyloid deposits in vivo, supporting the idea that HtrA1

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

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

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

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

224 and characterization of [Formula: see text]-amyloid deposits is a fundamental task in pre-clinical s

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

226 gregation of the peptide hormone amylin into amyloid deposits is a pathological hallmark of type-2 di

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

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

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

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

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

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

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

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

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

236 After intraportal injection in patients, amyloid deposits <15 um diameter were identified in 5%-1

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

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

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

240 of this protein suppresses the formation of amyloid deposits, neuroinflammation and cognitive defici

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

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

243 Amyloid deposits of amylin in the pancreas are an import

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

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

246 tive diseases characterized by intracellular amyloid deposits of tau protein.

247 Amyloid deposits often develop rapidly in transplanted k

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

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

250 Some amyloid deposits originate within morphologically abnorm

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

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

253 It accumulates within amyloid deposits, physically interacts with amyloid-beta

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

255 5 peptide was posited to bind effectively to amyloid deposits, relative to similarly charged polybasi

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

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

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

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

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

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

262 Amyloid deposits slowly regressed with restoration of no

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

264 istration of anti-amyloid antibodies reduced amyloid deposits, suggesting that immunotherapies may be

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

291 Extensive organ amyloid deposits were observed in active AL as well as i

292 AL amyloid deposits were usually distributed in a reticular

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

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 Abeta42 is the principal component of amyloid deposits within the brain parenchyma, and an inc

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.