ライフサイエンスコーパス: TTR

1 TTR also inhibited amyloid-dependent biofilm formation i

2 TTR amyloidoses are of particular interest regarding the

3 TTR binds Abeta, alters its aggregation, and inhibits it

4 TTR concentration was also induced in the serum, broncho

5 TTR demonstrated a great influence on a wide spectrum of

6 TTR for bronchoalveolar lavage (BAL) and endotracheal as

7 TTR is a tetrameric carrier of thyroxine in blood and ce

8 TTR possesses cytokine functions to stimulate myeloid ce

9 TTR stability was assessed by changes in serum TTR, and

10 TTR stabilization was more complete and less variable at

11 TTR tetramer dissociation precedes pathological TTR aggr

12 TTR V122I was associated with higher rates of heart fail

13 TTR-treated endothelial cells suppressed T cell prolifer

14 Both AL amyloidosis and 2 of 10 TTR-noPN subjects were Congo red-positive.

15 failure (cross-sectional cohort: n = 51/116 TTR V122I carriers [44%], n = 1070/3608 noncarriers [30%

16 There were 116 TTR V122I carriers (3.1%); 1121 participants (30%) had h

17 myloidotic polyneuropathy (FAP; n = 20), (2) TTR mutation carriers without peripheral neuropathy (TTR

18 We present 2D terahertz-terahertz-Raman (2D TTR) spectroscopy, the first technique, to our knowledge

19 comparison of experimental and simulated 2D TTR spectra of bromoform (CHBr3), carbon tetrachloride (

20 There were 70 TTR-mutant subjects (22 carriers and 48 patients), and 6

21 Ten of 92 TTR V122I carriers with heart failure (11%) were diagnos

22 A TTR/Abeta(1-42) (1:1) complex with a dissociation consta

23 cking and peptide screening, we identified a TTR segment that is capable of altering Abeta aggregatio

24 TTR tends to form linear oligomers, while a TTR variant (G53A) prefers forming annular oligomers wit

25 rating effects of AD symptoms observed in AD/TTR(+/-) animal models after IDIF treatment and eventual

26 Adding TTR to ORBIT, ATRIA and HEMORR2HAGES led to improved pre

27 eding risk scores and investigated if adding TTR would improve their predictive value and clinical us

28 ccur in cardiomyocytes exposed to aggregated TTR, and provide clues as to the molecular and physiolog

29 ecreasing circulating TTR levels or altering TTR-RBP4 binding could be a potential therapeutic approa

30 The rate of diagnosis with hATTR-CM among TTR V122I carriers with heart failure was measured.

31 mation of binary and ternary complexes among TTR, Abeta(1-42) peptide, and TTR stabilizers using isot

32 Amyloid TTR cytotoxicity results in mitochondrial potential modi

33 hen compared to patients with CV > 44.2% and TTR > 40% (high intra-patient variability and optimal ti

34 en compared with patients with CV >44.2% and TTR >=40% (high intrapatient variability and optimal TTR

35 Patients with CV > 44.2% and TTR < 40% (high intra-patient variability and low time i

36 Patients with CV >44.2% and TTR <40% (high intrapatient variability and low TTR) had

37 es (SMD=-1.27), CGI-S scores (SMD=-1.57) and TTR (SMD=-1.22).

38 lecular interactions between the ligands and TTR were further characterized using molecular dynamics

39 omplexes among TTR, Abeta(1-42) peptide, and TTR stabilizers using isothermal titration calorimetry (

40 identification of bispecific RBP4 antagonist-TTR tetramer kinetic stabilizers.

41 Sections were stained with anti-PGP9.5, anti-TTR, and Congo red.

42 We conclude that antibody-TTR fusions may provide a powerful platform for multimer

43 sylmethionine, and the computer-designed ATP-TTR-3 aptamer with and without AMP.

44 R stabilizes the homotetramer and attenuates TTR amyloidosis.

45 ructural features of the interaction between TTR and the Abeta(12-28) peptide (3), the essential reco

46 o better understand the interactions between TTR and THDCs, we determined the crystallographic struct

47 is bound with similar high affinity in both TTR binding sites without the usual negative cooperativi

48 hesis, we have examined the effects of brain TTR on food intake and body weight and have further dete

49 al nerves, and transthyretin cardiomyopathy (TTR-CM), which primarily affects the heart.

50 eviously unknown anorectic action of central TTR in the control of energy balance, providing a potent

51 cise-induced anorexia, implying that central TTR may also play a functional role in modulating food i

52 These data show that decreasing circulating TTR levels or altering TTR-RBP4 binding could be a poten

53 indicating the presence of a ternary complex TTR/IDIF/Abeta(1-42).

54 The conatumumab-TTR fusions displayed substantially enhanced potency in

55 Under the amyloid-forming conditions, TTR initially forms a dimer through interactions between

56 3 heterodimerization substitutions to create TTR-mediated conatumumab tetramers.

57 ce of RBP4, we determined whether decreasing TTR levels with antisense oligonucleotides (ASOs) improv

58 signaling impairs secretion of destabilized TTR during thapsigargin (Tg)-induced ER stress by increa

59 , but adding the 'labile INR' criteria (i.e. TTR <65%) to ATRIA, ORBIT and HEMORR2HAGES increased the

60 inol-binding protein 4 (RBP4), an endogenous TTR ligand, could be used as a diagnostic test for ATTR

61 Assays of affinity for TTR and inhibition of its tendency to form fibrils were

62 at the French National Reference Center for TTR-FAP from June 1, 2013, to June 30, 2014.

63 d for their in vitro capacity to compete for TTR-binding with a fluorescent FITC-T4 probe.

64 ly, no effective pharmacological therapy for TTR amyloidoses is available, mostly due to a substantia

65 ls found in humans and how displacement from TTR in vitro relates to in vivo T4-TTR binding is unknow

66 een in the proportions of patients free from TTR events between the accelerated and standard epirubic

67 een in the proportions of patients free from TTR events between the CMF and capecitabine groups (HR 0

68 eiving accelerated epirubicin were free from TTR events.

69 To demonstrate this utility, we fused TTR to the C terminus of conatumumab, an antibody that t

70 ation using ASOs targeting SRB-1, A1AT, FXI, TTR, and ApoC III mRNAs.

71 A novel mutation in the transthyretin gene (TTR) in Indian patients with familial amyloid polyneurop

72 n, transthyretin (TTR), and over 120 genetic TTR variants are amyloidogenic and cause, respectively,

73 Pharmacologic or genetic TTR stabilization partially restores secretion of native

74 st 1 gene associated with an HCM mimic (GLA, TTR, PRKAG2, LAMP2, PTPN11, RAF1, and DES).

75 les such as iododiflunisal (IDIF, 4), a good TTR stabilizer.

76 credible in health care systems with higher TTRs.

77 The homotetrameric TTR contains two identical thyroxine binding pockets, oc

78 ned the crystallographic structures of human TTR in complex with perfluorooctanesulfonic acid (PFOS),

79 ICV TTR decreased neuropeptide Y (NPY) levels in the DMH and

80 This effect was not due to sickness as icv TTR did not cause a conditioned taste aversion.

81 ssociated with cardiomyopathy is identified, TTR genotyping.

82 of normal repeats at ATXN2 may modify AO in TTR-FAP Val30Met and may function as a risk factor.

83 r implications for therapeutic approaches in TTR amyloidosis.

84 as a biomarker to detect treatment effect in TTR-FAP drug trials.

85 es and frequency of ocular manifestations in TTR amyloidosis is presented.

86 Mutations in TTR and postoperative visual acuity.

87 ficantly associated with an earlier onset in TTR-FAP Val30Met, decreasing mean AO by 6 years (95% con

88 Wild-type TTR staining was less prominent in TTR-FAP patients.

89 and PMNFD were all significantly reduced in TTR-FAP patients versus healthy controls, whereas TTR-no

90 l molecules to the thyroxin-binding sites in TTR stabilizes the homotetramer and attenuates TTR amylo

91 by ligands that occupy both binding sites in TTR.

92 r is widely accepted as the critical step in TTR amyloid fibrillogenesis.

93 (now classified as Val50Met) substitution in TTR.

94 logic therapies shown to improve survival in TTR-CM.

95 complications in association with individual TTR (iTTR), INR variability, and aspirin use and identif

96 ime, and hospital teaching status influenced TTR.

97 ion of which by specific ligands can inhibit TTR amyloidogenesis in vitro.

98 ones, Tafamidis((R)) and diflunisal, inhibit TTR misfolding by stabilizing native tetrameric TTR; how

99 h reconstituted serum mixture, its inhibitor-TTR dissociation constant (Ki) was used to estimate inhi

100 amer in vivo in mice and humans and inhibits TTR cytotoxicity.

101 n RNA interference therapeutic that inhibits TTR production, in patients with hereditary transthyreti

102 Adding 'labile INR' (TTR < 65%) to ORBIT, ATRIA and HEMORR2HAGES significantl

103 tructures of unlabeled and deuterium-labeled TTR are essentially identical, subunit exchange kinetics

104 e of our previously reported bivalent ligand TTR 'superstabiliser' family, is notably more potent tha

105 oronic acid-substituted stilbenes that limit TTR amyloidosis in vitro.

106 <40% (high intrapatient variability and low TTR) had a high risk of dnDSA (adjusted OR = 4.93, 95% c

107 Since lowering TTR levels increases renal clearance of RBP4, we determi

108 ts engineered nontetramer-forming monomer (M-TTR, F87M/L110M) inhibit CsgA amyloid formation in vitro

109 ot significantly compromise the ability of M-TTR to inhibit CsgA amyloidogenesis.

110 ibit CsgA amyloid formation in vitro, with M-TTR being the more efficient inhibitor.

111 as available in only 18.7% of patients (mean TTR: 49.5% +/- 22.3%).

112 Median TTR for major respiratory pathogens by organism ranged f

113 ng Abeta aggregation and toxicity, mimicking TTR cellular protection.

114 misTTR inhibits fibrillogenesis of misfolded TTR under micromolar concentrations.

115 ation partially restores secretion of native TTR tetramers.

116 sordered regions (~60%) than those of native TTR.

117 tion carriers without peripheral neuropathy (TTR-noPN; n = 10), (3) healthy controls (n = 20), (4) di

118 with X-ray crystallographic analysis of nine TTR.ligand complexes.

119 an efficient tool for the discovery of novel TTR-binders from the Tox21 inventory.

120 e mutation in the 33rd position of exon 2 of TTR in 1 patient of 1 pedigree, confirming the diagnosis

121 id was detected in 70% of TTR-FAP and 20% of TTR-noPN subjects.

122 ON: Cutaneous amyloid was detected in 70% of TTR-FAP and 20% of TTR-noPN subjects.

123 stigate whether the amyloidogenic ability of TTR and its antiamyloid inhibitory effect are associated

124 racerebroventricular (icv) administration of TTR in normal growing rats decreased food intake and bod

125 While the in vivo analysis of TTR in mammalian models is complex, time- and resource-c

126 agnosed disease caused by destabilization of TTR due to pathogenic mutations or aging.

127 o TTR, crystal structures were determined of TTR in complex with four of the identified compounds inc

128 udies have documented a protective effect of TTR against cellular toxicity of pathogenic Abeta, a pro

129 gest that mimicking the inhibitory effect of TTR with peptide-based therapeutics represents an additi

130 The destabilizing effects of TTR deuteration are rather similar in character to those

131 and familial amyloid cardiomyopathy forms of TTR amyloidoses.

132 eeds in favour of the amyloidogenic forms of TTR.

133 The natural history of TTR-CM is poorly characterized, which presents difficult

134 Chronic icv infusion of TTR in Otsuka Long-Evans Tokushima Fatty rats reversed h

135 rature and ionic strength on the kinetics of TTR complex formation.

136 ledge about both the molecular mechanisms of TTR aggregation in tissue and the ensuing functional and

137 Many mutations of TTR have been identified; most of these are pathogenic,

138 o those observed for aggressive mutations of TTR such as L55P (associated with familial amyloid polyn

139 onal analysis of carriers and noncarriers of TTR V122I of African ancestry aged 50 years or older enr

140 This review provides a brief overview of TTR-CM and the challenges of identifying clinically mean

141 dentified a new mechano-enzymatic pathway of TTR fibrillogenesis in vitro, catalysed by selective pro

142 and efficacy with respect to progression of TTR amyloid cardiomyopathy.

143 tion relationships due to oxidative PTPMs of TTR should contribute to the understanding of pathophysi

144 mutations in this region enhance the rate of TTR fibrillation.

145 However, the release of TTR by selective RBP4 antagonists may be associated with

146 creases the ER stress-dependent secretion of TTR in non-native conformations that accumulate extracel

147 creases the ER stress-dependent secretion of TTR in non-native conformations under these conditions,

148 ligands within the thyroxine binding site of TTR can stabilize the tetrameric integrity and is a pote

149 dings suggest that the Abeta-binding site of TTR may be hidden in its tetrameric form.

150 n-label trial evaluated the stabilization of TTR tetramers using 20 mg of tafamidis daily at week 6 (

151 demonstrated near-complete stabilization of TTR.

152 ligand, which is a more potent stabilizer of TTR in vitro that occupies both thyroxine pockets and th

153 o TTR stabilises non-amyloidogenic states of TTR in a manner similar to that occurring for the protec

154 by assembly of dimers in the early steps of TTR disassembly.

155 Isotope labeling is used for the study of TTR by NMR, neutron diffraction, and mass spectrometry (

156 and safety of tafamidis for the treatment of TTR-CM.

157 % (high intrapatient variability and optimal TTR), while the latter patients had similar risk to pati

158 AG10 is a selective, oral TTR stabilizer under development for transthyretin amylo

159 tetramer dissociation precedes pathological TTR aggregation.

160 ansthyretin familial amyloid polyneuropathy (TTR-FAP).

161 By immune-targeting sparsely populated TTR misfolding intermediates (i.e. monomers), we achieve

162 possible modifier effect in AO in Portuguese TTR-FAP Val30Met families.

163 olecule for Parkinson's disease, as a potent TTR aggregation inhibitor.

164 R tetramer destabilization and, potentially, TTR amyloid formation.

165 owers mouse plasma RBP4 levels, and prevents TTR aggregation in a gel-based assay.

166 As promising TTR therapies are in development, increased awareness an

167 omyopathy (ATTR-CM) that mimics a protective TTR mutation.

168 nship between time in the therapeutic range (TTR) and clinical outcomes in heart failure patients in

169 ility and low TAC time in therapeutic range (TTR) have been associated with risk of de novo donor-spe

170 ility and low TAC time in therapeutic range (TTR) have been associated with risk of de novo donor-spe

171 ved incorporating time in therapeutic range (TTR) in warfarin-treated patients.

172 Time in Therapeutic Range (TTR) was available in only 18.7% of patients (mean TTR:

173 nts, reflected by time in therapeutic range (TTR).

174 rfarin arms with times in therapeutic range (TTRs) of 55.2% to 64.9%, making the results less credibl

175 Median (interquartile range) TTR were 37.0 h (21.8 to 51.7 h) and 60.5 h (46.6 to 72.

176 Circulating RBP4, TTR, B-type natriuretic peptide (BNP), and troponin I (T

177 nical prediction algorithm composed of RBP4, TTR, left ventricular ejection fraction, interventricula

178 antagonists that dissociate circulating RBP4-TTR-retinol complexes, reduce serum RBP4 levels, and inh

179 Recombinant TTR stimulated lung tumor cell proliferation and growth,

180 inversely correlated with time to recovery (TTR) (r = -0.272, P = .02).

181 cin would improve time to tumour recurrence (TTR); and whether use of oral capecitabine instead of cy

182 dies, and transcription termination regions (TTRs) showed strong positive correlation with gene expre

183 reading of H3S10ph at RT transition regions (TTRs) is accompanied by aberrant transcription initiatio

184 on-Severity Scale (CGI-S), time to response (TTR), discontinuation rate and individual adverse effect

185 w studies have examined the time to results (TTR) for this critical specimen, and such data can be va

186 was assessed by estimating time to results (TTR), prioritising/assigning putative therapeutic target

187 Average serum TTR increased by 36 +/- 21% and 51 +/- 38% at 400 and 80

188 Baseline serum TTR in treated subjects was below normal in 80% of mutan

189 R stability was assessed by changes in serum TTR, and 2 established ex vivo assays (fluorescent probe

190 AG10 treatment restored serum TTR to the normal range in all subjects.

191 ychotics (SGAs) were associated with shorter TTR (SMD=-0.27) and a lower incidence of extrapyramidal

192 ides and the positive effect exerted by some TTR stabilizers for modulating the TTR-Abeta interaction

193 Pan-specific TTR antibodies do not possess such fibril inhibiting pro

194 spectively, sporadic and hereditary systemic TTR amyloidosis.

195 was used to estimate inhibition levels of T4-TTR binding in human blood.

196 um was extrapolated to 1.3% inhibition of T4-TTR binding in maternal and 1.5% in infant blood.

197 g potency to in vivo inhibition levels of T4-TTR binding in maternal and infant serum.

198 thesize, however, that 1.3% inhibition of T4-TTR binding may ultimately be decisive for reaching a st

199 ment from TTR in vitro relates to in vivo T4-TTR binding is unknown.

200 t loss by non-dosed-corrected TAC CV and TAC TTR during the first posttransplant year in a cohort of

201 t loss by non dosed corrected TAC CV and TAC TTR during the first posttransplant year in a cohort of

202 ent of variation (CV) is a result of low TAC TTR rather than the variability itself.

203 ts and their metabolites for THDCs targeting TTR, we developed a quantitative structure-activity rela

204 developed an antibody (misTTR) that targets TTR residues 89-97, an epitope buried in the tetramer bu

205 misfolding by stabilizing native tetrameric TTR; however, their minimal effective concentration is i

206 ere, we report that both human WT tetrameric TTR (WT-TTR) and its engineered nontetramer-forming mono

207 We hypothesized that TTR might have broad antiamyloid activity because the bi

208 Here we show that TTR fibrillogenesis by the mechano-enzymatic pathway is

209 Further analyses showed that TTR treatment enhanced the reactive oxygen species produ

210 These discoveries suggest that TTR is an effective antibiofilm agent that could potenti

211 The TTR variant oligomers are also less structured than WT o

212 The TTR-binding potency of the mixtures was well predicted b

213 academic medical center-based biobanks, the TTR V122I genetic variant was significantly associated w

214 Our aims were to determine the TTR-binding potency for contaminant mixtures as found in

215 ls, have provided a structural model for the TTR-Abeta interaction, as well as for the ternary comple

216 The compounds were found to bind in the TTR hormone binding sites as predicted.

217 long-distance conformational changes in the TTR that have not previously been detected by X-ray crys

218 d variant show that it docks better into the TTR T4 pocket than tafamidis, so far the only drug on th

219 ssociation (SID) are used to investigate the TTR disassembly mechanism(s) and the effects of temperat

220 d by some TTR stabilizers for modulating the TTR-Abeta interaction have been previously studied.

221 Molecular aspects related to the role of the TTR stabilizer iododiflunisal (IDIF, 5) on the TTR-Abeta

222 ssays, we found that the dissociation of the TTR tetramer, required for its amyloid pathogenesis, is

223 R stabilizer iododiflunisal (IDIF, 5) on the TTR-Abeta complex have been also examined.

224 gregation and cytotoxicity revealed that the TTR segment inhibits Abeta oligomer formation and also p

225 amyloid cardiomyopathy (hATTR-CM) due to the TTR V122I variant is an autosomal-dominant disorder that

226 erum, and infant serum; to study whether the TTR-binding potency of the mixtures follows the principl

227 tional interactions of its linker within the TTR central channel.

228 s suggested that unfolding events within the TTR monomer originate at the C-D loop of the protein, an

229 12 representatives were selected, and their TTR binding affinities were studied with isothermal titr

230 y different fibrillation behaviours of these TTR mutants is poorly understood.

231 Three TTR mutations, Glu89Lys, Gly47Arg, and homozygous Gly6Se

232 idate structural details in their binding to TTR, crystal structures were determined of TTR in comple

233 that the binding of small molecule drugs to TTR stabilises non-amyloidogenic states of TTR in a mann

234 lain why no relationship between exposure to TTR-binding compounds and circulating T4 levels in human

235 Tolcapone binds specifically to TTR in human plasma, stabilizes the native tetramer in v

236 Transthyretin (TTR) amyloidoses are familial or sporadic degenerative c

237 Transthyretin (TTR) amyloidosis is an underdiagnosed disease caused by

238 Transthyretin (TTR) is a blood and cerebrospinal fluid transporter of t

239 Transthyretin (TTR) is a homotetrameric protein.

240 Transthyretin (TTR) is a plasma homotetrameric protein implicated in fa

241 Transthyretin (TTR) is an abundant homotetrameric serum protein and was

242 Transthyretin (TTR) modulates the deposition, processing, and toxicity

243 Transthyretin (TTR)-related familial amyloid polyneuropathy (FAP) is an

244 of patients were studied: (1) transthyretin (TTR) familial amyloidotic polyneuropathy (FAP; n = 20),

245 ndividuals with amyloidogenic transthyretin (TTR) mutations.

246 ntermediates populated during transthyretin (TTR) aggregation process.

247 amyloid polyneuropathy (FAP), transthyretin (TTR) displays this role primarily affecting the peripher

248 Hereditary transthyretin (TTR) amyloid cardiomyopathy (hATTR-CM) due to the TTR V1

249 Human transthyretin (TTR) is implicated in several fatal forms of amyloidosis

250 srupting chemicals (THDCs) is transthyretin (TTR), a thyroid hormone transporter in vertebrates.

251 rdial deposition of misfolded transthyretin (TTR) or pre-albumin.

252 jugate duplex targeting mouse transthyretin (TTR) indicated that GNA is well tolerated in the seed re

253 Wild-type and mutant transthyretin (TTR) can misfold and deposit in the heart, peripheral ne

254 Dissociation of the native transthyretin (TTR) tetramer is widely accepted as the critical step in

255 dation of the nonglycosylated transthyretin (TTR) D18G misfolded client.

256 blished that the formation of transthyretin (TTR) amyloid fibrils is linked to the destabilization an

257 hanism of fibril formation of transthyretin (TTR) involves self-assembly of partially unfolded monome

258 The protective effect of transthyretin (TTR) on cellular toxicity of beta-amyloid (Abeta) has be

259 The ability of transthyretin (TTR) to bind Abeta-peptides and the positive effect exer

260 The visceral protein transthyretin (TTR) is frequently affected by oxidative post-translatio

261 mic amyloid precursor protein transthyretin (TTR) is known to inhibit amyloid-beta (Abeta) aggregatio

262 The plasma protein transthyretin (TTR) is linked to human amyloidosis.

263 ecreted amyloidogenic protein transthyretin (TTR).

264 The wild type protein, transthyretin (TTR), and over 120 genetic TTR variants are amyloidogeni

265 inol binding protein 4 (RBP4)-transthyretin (TTR)-retinol complex.

266 Among them, the transthyretin (TTR) concentration was highly increased in human serum o

267 soleucine at codon 122 of the transthyretin (TTR) gene (V122I), present in 3.43% of African American

268 se caused by mutations in the transthyretin (TTR) gene.

269 amyloidosis, mutation in the transthyretin (TTR) protein is the most common type.

270 thyroxine (T4) for binding to transthyretin (TTR).

271 oid polyneuropathy (FAP) with transthyretin (TTR) mutations.

272 so far the only drug on the market to treat TTR amyloidoses.

273 ate stabilizers are promising drugs to treat TTR amyloidoses.

274 famidis, a small-molecule drug used to treat TTR-related amyloidosis in the clinic.

275 inhibits fibril formation by both wild-type TTR and a common disease-related variant, V30M TTR, as e

276 l structures of tolcapone bound to wild-type TTR and to the V122I cardiomyopathy-associated variant s

277 nongenetic disease associated with wild-type TTR misfolding.

278 to amyloid oligomers or fibrils of wild-type TTR or to its T4-stabilized form, which resists tetramer

279 Wild-type TTR staining was less prominent in TTR-FAP patients.

280 hs of time to variously aggregated wild-type TTR, a condition that characterizes senile systemic amyl

281 R and a common disease-related variant, V30M TTR, as effectively as does tafamidis, a small-molecule

282 on addition; and to extrapolate the in vitro TTR-binding potency to in vivo inhibition levels of T4-T

283 The primary endpoint was TTR, defined as time from randomisation to first invasiv

284 carriers and 48 patients), and 66 cases were TTR-A97S.

285 AP patients versus healthy controls, whereas TTR-noPN subjects had intermediate reductions.

286 ling studies, we propose a mechanism whereby TTR can form amyloid fibrils via a parallel equilibrium

287 tive RBP4 antagonists may be associated with TTR tetramer destabilization and, potentially, TTR amylo

288 e patients who presented to Mayo Clinic with TTR amyloidosis between January 1, 1970, and November 1,

289 ed by x-ray analysis of their complexes with TTR.

290 o develop PTM, and inversely correlates with TTR.

291 Patients with TTR amyloidosis have been noted to have ocular, especial

292 In this large cohort of patients with TTR amyloidosis, female sex and decreased VA were associ

293 Of 108 examined eyes in 54 patients with TTR amyloidosis, there were 26 eyes (24%) in 13 patients

294 tion alterations often seen in patients with TTR amyloidosis.

295 Fifteen patients with TTR-FAP underwent a complete neurologic examination, inc

296 In these 15 patients with TTR-FAP, IVCM measurement permitted rapid, noninvasive e

297 he place of IVCM in monitoring patients with TTR-FAP.

298 Notably, wild-type (WT) TTR tends to form linear oligomers, while a TTR variant

299 Preincubation of WT-TTR with small molecules that occupy the T4 binding site

300 report that both human WT tetrameric TTR (WT-TTR) and its engineered nontetramer-forming monomer (M-T