ライフサイエンスコーパス: tau protein

1 g., amyloid-beta40, total and phosphorylated tau protein).

2 and intracellular neurofibrillary tangles of tau protein.

3 en decorated with the secondary antibody for tau protein.

4 loping PET tracers that bind specifically to tau protein.

5 model independent of expression of a mutant tau protein.

6 ociated with the pathological aggregation of tau protein.

7 ated substrate, the intrinsically disordered Tau protein.

8 lular tangles containing hyperphosphorylated Tau protein.

9 viously reported fiber formed by VQIVYK from Tau protein.

10 igh molecular weight to low molecular weight Tau protein.

11 ation and posttranslational modifications of Tau protein.

12 ines associated with hyperphosphorylation of tau protein.

13 ct is translated into a full-length chimeric tau protein.

14 tangles, constituted by hyperphosphorylated tau protein.

15 vo, and here we investigate its influence on tau protein.

16 regates of amyloid-beta (Abeta) peptides and tau protein.

17 mprised of aggregates of hyperphosphorylated tau protein.

18 s composed of abnormally hyperphosphorylated tau protein.

19 etal ions and the neurofibrillary tangles of Tau protein.

20 illary tangles (NFTs) comprising filamentous tau protein.

21 ntly reduced, as was the amount of insoluble tau protein.

22 whether this concept can also be applied to Tau protein.

23 ng from alpha-syn seeds to over 50% of total tau protein.

24 tment of AD by preserving the O-GlcNAcylated tau protein.

25 eptides, and neuronal inclusions formed from tau protein.

26 fibrillary tangles are primarily composed of tau protein.

27 s a posttranslational modification of normal tau protein.

28 the accumulation of amyloid beta (Abeta) and Tau protein.

29 rative disease associated with dysfunctional tau protein.

30 terized by intracellular amyloid deposits of tau protein.

31 ation on beta-amyloid, little is known about Tau protein.

32 gation of abnormally and hyperphosphorylated tau proteins.

33 omarkers such as aggregated beta-amyloid and tau proteins.

34 ending on the combined activities of EBs and tau proteins.

35 on and clearance of amyloid beta (Abeta) and tau proteins.

36 ion of both ubiquitinated proteins and APP/p-Tau proteins.

37 rebrospinal fluid levels of beta-amyloid and tau proteins.

38 rranged in staggered arrays, cross-linked by tau proteins.

39 lation of Abeta oligomers and phosphorylated tau proteins.

40 lary tangles composed of hyperphosphorylated tau proteins.

41 d by the accumulation of aberrantly modified tau proteins.

42 elated with accumulation of amyloid beta and tau proteins.

43 produces and releases cytotoxic amyloid and tau proteins.

44 sensitive strategy for the determination of tau protein, a hallmark of Alzheimer's disease (AD), inv

45 We assessed CSF tau protein abnormalities in AD, a tauopathy with promin

46 Because PSP is associated with tau protein abnormalities, there is growing interest in

47 Furthermore, endogenous TAU protein abundance in human neuroblastoma SH-SY5Y cel

48 In some neurodegenerative disorders, tau protein accumulates in astrocytes and/or oligodendro

49 Aberrant tau protein accumulation drives neurofibrillary tangle (

50 diseases characterized by aberrant forms of tau protein accumulation leading to neuronal death in fo

51 es were observed in total and phosphorylated tau proteins across conditions.

52 Intrinsically disordered proteins, such as tau protein, adopt a variety of conformations in solutio

53 ENT The stereotypical spread of pathological tau protein aggregates have recently been attributed to

54 The tau protein aggregates in aging and Alzheimer disease an

55 sleep deprivation accelerates the spread of tau protein aggregates in neural networks.

56 aracterized by the formation of pathological tau protein aggregates in the brain and progressive neur

57 The deposition of tau protein aggregates in the brain is a pathological ha

58 In Alzheimer's disease and tauopathies, tau protein aggregates into neurofibrillary tangles that

59 The formation and deposition of tau protein aggregates is proposed to contribute to cogn

60 treatment of neurodegenerative diseases with tau protein aggregates known as tauopathies.

61 7 is a PET radiotracer developed for imaging tau protein aggregates, which are implicated in neurolog

62 geous for the insight into the properties of tau protein aggregates.

63 bilities to act as an antioxidant, to reduce tau protein aggregation and to improve energy metabolism

64 ium moiety, acts as a selective inhibitor of tau protein aggregation both in vitro and in transgenic

65 ed the hypothesis that neuroinflammation and tau protein aggregation colocalize macroscopically, and

66 Tau protein aggregations are a hallmark of amyloid-assoc

67 quence of the nonuniform distribution of MAP tau proteins along the bundle length.

68 sulin signaling modulates phosphorylation of tau protein, an early component in the development of Al

69 raneuronal inclusions of hyperphosphorylated tau protein and abnormal expression of brain-derived neu

70 and pseudo MS(n) were performed on oxidized Tau protein and acetylated bovine serum albumin to ident

71 caused by the dysfunction and aggregation of tau protein and an impairment of cellular protein degrad

72 01S tau transgenic mice express mutant human tau protein and develop progressive tau pathology.

73 peptide production, hyperphosphorylation of tau protein and endosomal abnormalities.

74 se, which is characterized by changes in the tau protein and in the cleaved fragments of the amyloid

75 ments over a large temperature range for the tau protein and its hydration water, indicating intimate

76 leading to new research in both the role of tau protein and its interaction with amyloid-beta.

77 lly disordered proteins, the K18 domain from Tau protein and N(TAIL) from measles virus nucleoprotein

78 the presence of intracellular aggregates of tau protein and neuronal loss leading to cognitive and m

79 uron-specific enolase, beta-amyloid protein, tau protein and phospho-tau were determined in CSF.

80 iated by insoluble tangles of phosphorylated tau protein and plaques of amyloid peptides.

81 between cerebrospinal fluid (CSF) levels of tau proteins and alpha-synuclein, but not beta-amyloid 1

82 el to test the possible interactions between tau proteins and amyloid-beta and study the resulting co

83 aggregation of the beta-amyloid (Abeta) and tau proteins and atrophy of medial temporal lobe (MTL) s

84 rs or amyloid-beta trimers, and pathological tau proteins and postsynaptic proteins correlated with A

85 associated with CSF levels of amyloid beta, tau protein, and F2-isoprostanes in elderly individuals

86 40 and their ratio (Abeta(1-42/1-40)), total tau protein, and neurofilament light chain (NFL); tau ph

87 ent of cerebrospinal fluid levels of orexin, tau proteins, and beta-amyloid 1-42 and polysomnographic

88 Levels of orexin, tau proteins, and beta-amyloid 1-42; macrostructural var

89 luble amyloid beta, total and phosphorylated tau proteins, and isoprostanes.

90 tests for prion diseases such as 14-3-3 and tau proteins, and together with PRNP gene sequencing the

91 omposed of hyperphosphorylated and misfolded tau protein are a pathological hallmark of Alzheimer's d

92 usions of hyperphosphorylated and aggregated tau protein are a pathological hallmark of several neuro

93 Filaments made up of different isoforms of tau protein are associated with a variety of neurodegene

94 t effective therapies directly targeting the tau protein are currently lacking.

95 ("hyperphosphorylation") and aggregation of Tau protein are hallmarks of Alzheimer disease and other

96 Lesions containing abnormal aggregated tau protein are one of the diagnostic hallmarks of Alzhe

97 Amyloid-beta and tau protein are the two most prominent factors in the pa

98 Intriguingly, Tau proteins are able to alleviate the effect of the Pri

99 brillary tangles made of hyperphosphorylated tau proteins are closely associated with Alzheimer disea

100 Amyloid beta42, and tau proteins are established core cerebrospinal biomarke

101 Aggregated Tau proteins are hallmarks of Alzheimer disease and othe

102 c forms of amyloid-beta peptide (oAbeta) and tau proteins are likely to play a major role in Alzheime

103 rofibrillary deposits of hyperphosphorylated tau proteins are the diagnostic lesions of AD, but their

104 es, formed of misfolded, hyperphosphorylated tau protein, are a pathological hallmark of several neur

105 ofibrillary tangles (NFTs) of phosphorylated tau proteins, are a group of neurodegenerative diseases,

106 et al. identify a putative novel function of tau protein as a regulator of insulin signaling in the b

107 Several independent studies have implicated tau protein as central to Alzheimer's disease progressio

108 formation of the bonds between the connected tau proteins as they respond to mechanical stretch.

109 Tau protein assembles into paired helical filaments (PHF

110 cid inhibitor of the fibril formation of the tau protein associated with Alzheimer's disease, and a n

111 e generated four singly pseudophosphorylated Tau proteins (at Thr(231), Ser(262), Ser(396), and Ser(4

112 ary tangles (composed of hyperphosphorylated tau proteins) based on the progression model defined by

113 g30 murine tauopathy model expresses a human tau protein bearing two frontotemporal dementia with Par

114 gate their likelihood of fitting into VQIVYK tau protein binding channel model.

115 Normal tau protein binds and stabilizes the microtubules in neu

116 tal cortices; in contrast with amyloid-beta, tau protein burden had a broad effect on the epigenome,

117 s can form not only by the full-length human Tau protein, but also by the three repeated (K19) or fou

118 re composed of insoluble hyperphosphorylated Tau protein, but the mechanisms underlying the conversio

119 still unclear which specific domains in the tau protein can interact with Abeta oligomers and what c

120 Tau protein can transfer between neurons transneuronally

121 In the model, inverted pairs of tau proteins can dynamically cross-link parallel MTs via

122 SK-3beta) by attacking both beta-amyloid and tau protein cascades has been identified as a promising

123 uced the levels of the mutant huntingtin and tau proteins, cell death, and the resulting morphologica

124 that a sequence of progressive misfolding of tau proteins, circuit-based transfer to new cell populat

125 ked impaired glymphatic CSF-ISF exchange and tau protein clearance using the novel AQP4 inhibitor, TG

126 sect the molecular characteristics of native tau protein conformers from TgP301S tau mice and show th

127 Tau protein consists of an N-terminal projection domain,

128 eta-amyloid protein containing "plaques" and tau protein containing "tangles" that contribute to acce

129 To summarize, features in the Tau protein critical for disease intervention at differe

130 We show that LLPS-HS promotes tau protein dehydration, undergoes maturation and direct

131 nical diagnosis and correlated with cortical tau protein deposition measured by (18)F-flortaucipir PE

132 etitive brain trauma and hyperphosphorylated tau protein deposition promote the accumulation of other

133 of molecular probes capable of detection of tau protein deposits in vitro.

134 aggregated beta-amyloid peptides (Abeta) and tau protein derived intracellular tangles.

135 Pathological tau proteins derived from human AD brains (AD-tau) act a

136 heet peptide inhibits the aggregation of the tau-protein-derived peptide Ac-VQIVYK-NH2 (AcPHF6).

137 peptides 1 that inhibit the aggregation of a tau-protein-derived peptide.

138 As a consequence, Tau protein detaches from microtubules and eventually ag

139 sed biosensor that detects the net charge of tau protein directly under physiological conditions.

140 ), which are composed of hyperphosphorylated Tau protein dissociating from microtubules, is one of th

141 fruit fly Drosophila melanogaster expresses Tau proteins (dTau) that are homologous to hTau, we aime

142 All four singly pseudophosphorylated Tau proteins exhibited loss-of-function effects.

143 al distribution of mRNA expression and total tau protein expression levels were largely in agreement,

144 ing and reformation of the bonds between the tau proteins facilitate the extension of axons up to app

145 MAP tau proteins fail in clusters of 10-100 elements located

146 They further indicate that, in the case of tau protein, fibril annealing and fragmentation along wi

147 er's disease (AD) and other tauopathies, the tau protein forms fibrils, which are believed to be neur

148 tauopathy-a class of disorders in which the tau protein forms insoluble inclusions in the brain-that

149 Immunodepleting amyloid or tau proteins from the PA103 supernatant with the A11 or

150 ly induced seizure models, mice with reduced tau protein had less severe seizures than control mice.

151 aged Tg mice of both sexes expressing human tau proteins harboring a pathogenic P301L MAPT mutation

152 In Alzheimer disease and other tauopathies, Tau protein has a reduced affinity toward microtubules.

153 SIGNIFICANCE STATEMENT: The tau protein has a relevant role in the transport of carg

154 Although abnormally folded tau protein has been found to self-propagate from neuron

155 Liquid-liquid phase separation of tau protein has been implicated in normal biological fun

156 olecules that inhibit the aggregation of the tau protein have been identified, little is known about

157 rivatives as imaging probes for pathological tau protein have great potential, but have not been well

158 re composed of misfolded hyperphosphorylated tau proteins; however, the link between tau abnormalitie

159 Tau protein in cerebrospinal fluid (CSF) is a central an

160 osphorylation state at multiple sites of the tau protein in cerebrospinal fluid markers across four d

161 etic variability linked to altered levels of tau protein in cerebrospinal fluid.

162 f serum neurofilament light chain (NF-L) and tau protein in comparison to CSF markers (NF-L and phosp

163 el and substantial alterations of endogenous tau protein in glaucoma, including abnormal subcellular

164 eta plaques and intracellular aggregation of tau protein in neurofibrillary tangles (NFTs) (1, 2).

165 or imaging aggregates of hyperphosphorylated tau protein in neurofibrillary tangles, a process that o

166 es pathologically defined by accumulation of tau protein in neurons and glia cells.

167 re characterized by abnormal accumulation of tau protein in neurons and glia.

168 fined by an abundance of hyperphosphorylated tau protein in neurons, astrocytes and cell processes ar

169 intracellular lesions of hyperphosphorylated Tau protein in P301S Tau transgenic mice.

170 haracterized by aggregates of phosphorylated tau protein in the brain [2, 3].

171 Aggregation of tau protein in the brain is associated with a class of n

172 ses associated with accumulation of abnormal tau protein in the brain.

173 myloid-beta peptides and hyperphosphorylated tau protein in the brain.

174 3) show increased accumulation of oligomeric tau protein in the CNS and enhanced loss of motor neuron

175 Increased concentrations of tau protein in the CSF and an increase in brain atrophy

176 d reduced levels of total and phosphorylated tau protein in the CSF of treated AD patients.

177 elicits accumulation of detergent insoluble tau protein in the mouse brain and inhibits synaptic pla

178 au aggregates from one cell directly contact Tau protein in the recipient cell to trigger further agg

179 ning the molecular mechanism of the neuronal Tau protein in the tubulin heterodimer assembly has been

180 ar membrane and aggregates of GFP-conjugated Tau protein in three dimensions.

181 Tau protein in vitro can undergo liquid-liquid phase sep

182 perties of the P301L mutation confers to the tau protein in vivo have remained elusive, perhaps contr

183 gregates of the Alzheimer disease-associated Tau protein in vivo is vital for the development of ther

184 her demonstrated that ERalpha interacts with tau protein in vivo.

185 dies to detect oligomeric and phosphorylated Tau proteins in a non-transgenic rodent model of parasag

186 tification of Myelin Basic Protein (MBP) and Tau proteins in cerebrospinal fluid (CSF) and serum, obt

187 ques and accumulation of hyperphosphorylated tau proteins in neurofibrillary tangles.

188 ABEL) trap to prolong measurements of single tau proteins in solution.

189 it elevated levels of neurotoxic amyloid and tau proteins in the cerebrospinal fluid (CSF).

190 Pathological changes to the tau protein, including conformational changes and aggreg

191 Serum levels of tau protein increased 24 hours after surgery (p = 0.0015

192 Based on the stiffness and viscosity of tau proteins inferred from single-molecule force spectro

193 ation of PP2A/Balpha and deregulation of Fyn-Tau protein interactions have been linked to enhanced ta

194 ese findings provide novel information about tau-protein interactions in human brains, and they descr

195 self-assembly of the microtubule associated tau protein into fibrillar cell inclusions is linked to

196 degenerative disorders is the aggregation of tau protein into fibrillar structures.

197 associated with the conversion of monomeric tau protein into filamentous aggregates.

198 aggregation of the intrinsically disordered tau protein into highly ordered beta-sheet-rich fibrils

199 The aggregation of the tau protein into neurofibrillary tangles is believed to

200 Assembly of tau protein into paired helical filaments and straight f

201 Our data integrate Tau protein into the class of amyloidogenic proteins and

202 accumulation of aggregated beta-amyloid and tau proteins into plaques and tangles is a central featu

203 Misfolding of tau proteins into prions and their propagation along neu

204 beta) production and hyperphosphorylation of Tau protein involved in these diseases.

205 t of quantification for the full-length 2N4R tau protein is 0.03pM, a value unaltered when the assay

206 Abnormal hyperphosphorylation of tau protein is a characteristic feature of a class of ne

207 Intracellular deposition of tau protein is a hallmark lesion of Alzheimer's disease.

208 osition of aggregates of hyperphosphorylated tau protein is a hallmark of tauopathies like Alzheimer

209 Accumulation of pathological tau protein is a major hallmark of Alzheimer's disease.

210 The aberrant accumulation of tau protein is a pathological hallmark of a class of neu

211 Aggregated tau protein is associated with over 20 neurological diso

212 perphosphorylated, insoluble and filamentous tau protein is at the centre of many human neurodegenera

213 Abnormal metabolism of the tau protein is central to the pathogenesis of a number o

214 n of anisotropy values obtained from trapped tau protein is conspicuously bimodal while those obtaine

215 Interest on Tau protein is fast increasing in Alzheimer's disease (A

216 Tau protein is found to be aggregated and hyperphosphory

217 Intracellular accumulation of tau protein is hallmark of sporadic Alzheimer's disease

218 Amyloid aggregation of tau protein is implicated in neurodegenerative diseases,

219 Tau protein is subjected to proteolytic processing into

220 The Tau protein is the major component of intracellular fila

221 The tau protein is thus widely felt to play a key role in pr

222 Here, we show that the Tau protein is toxic due to its aggregation propensity,

223 Abnormal folding of tau protein leads to the generation of paired helical fi

224 ilure of large groups of interconnecting MAP tau proteins leads to detachment of MT filaments from th

225 at the viscoelastic behavior specifically of tau proteins leads to mechanical breaking of microtubule

226 levels were positively correlated with total tau protein levels (r = 0.32; P = .03) and strictly rela

227 Total tau protein levels and seizure severity were highly corr

228 s highly interconnected with tau, preserving tau protein levels and synergizing with it to assemble M

229 e findings suggest that other regions of the tau protein may be crucial in regulating normal function

230 lysis reveals ways in which amyloid-beta and tau proteins may conspire with each other to enhance the

231 Thus, propagation of Tau protein misfolding among cells can be mediated by re

232 iously overlooked role in the propagation of tau protein misfolding and AD pathogenesis, providing a

233 the Abeta peptide (amyloid plaques) and the tau protein (neurofibrillary tangles) in the brains of a

234 d in vitro system that uses unmodified human tau protein now suggests electrostatic interactions prov

235 he pulmonary endothelium-derived amyloid and tau proteins on brain function have not been elucidated.

236 ectrochemical biosensor for the detection of tau protein - one of the possible markers for the predic

237 date, the presence of the hypophosphorylated tau protein (P-tau) in plasma from patients with acute T

238 oE genotypes display distinct phosphorylated tau protein (p-tau) staining patterns.

239 regional accumulation of hyperphosphorylated tau protein (p-tau).

240 ich include tauopathy made of phosphorylated tau protein (P-tau).

241 ibrils (the main component of "plaques") and tau protein paired helical filaments/fibrils (the main c

242 ssing both human Abeta1-42 peptide and human tau protein pan-neuronally.

243 In addition, our findings suggest that tau protein pathology in these areas may contribute to t

244 kinase 3beta, cyclin-dependent kinase 5, and tau protein phosphatase 2A.

245 he hypothesis that synaptic distributions of tau protein phosphorylated at serine 214 (pS214-tau) are

246 concentrations of amyloid-beta1-42 peptide, tau protein phosphorylated at threonine 181, total tau,

247 pathology, including beta-amyloid 42, total tau protein, phosphorylated tau 181, and soluble amyloid

248 ve demonstrated that hyperphosphorylation of tau protein plays a role in neuronal toxicities of alpha

249 s including tauopathies, where the misfolded tau protein propagates pathology through connected brain

250 sive accumulation of phosphorylated or total tau proteins, reactive oxygen species, and higher acetyl

251 rly, we elucidated the importance of certain Tau protein regions and unique residues, including the r

252 Amyloid deposition and tau protein-related neuronal injury in early Alzheimer's

253 On the other hand, the tau protein repeats with the characteristic U-turn shape

254 insight into the regulatory mechanism of the tau protein's microtubule binding activity.

255 Microtubule bundles cross-linked by tau protein serve a variety of neurological functions in

256 P301L tau protein showed the greatest oligomer formation follo

257 re, we examined the cellular distribution of tau protein species in human tau overexpressing line 66

258 Tau protein spreads from the entorhinal cortex to the hi

259 Human tau protein spreads to these regions and coaggregates wi

260 Abnormal changes of neuronal Tau protein, such as phosphorylation and aggregation, ar

261 nt models for the intracellular transport of Tau protein suggest motor protein-dependent co-transport

262 preformed Abeta fibrils (1-42 and 1-40) and tau protein tangles/filaments.

263 (phosphorylated tau) and non-specific (total tau) protein targets.

264 HtrA1 has also been reported to cleave the tau protein (Tau) and the amyloid protein precursor (APP

265 f hyperphosphorylated microtubule-associated tau protein (tau, gene MAPT) are typical of AD.

266 characterized by intracellular aggregates of tau proteins, termed tauopathies, include Alzheimer's di

267 nd Tau release is modified by changes in the Tau protein that are associated with tauopathies.

268 lusions containing abnormally phosphorylated tau protein that co-localized in some instances with mut

269 s lithium attenuates iron efflux by lowering tau protein that traffics amyloid precursor protein to f

270 R2-fragment ((273)GKVQIINKKLDL(284)) of the Tau protein, that TMAO can counteract the denaturing eff

271 rainstem nuclei in our model expressed human tau protein, the development of neurofibrillary tangles,

272 Here, we report that tau protein, the primary constituent of Alzheimer neurof

273 ve tauopathy characterized by aggregation of Tau protein through the repeat domain to form intraneuro

274 mice), which overexpresses a mutant form of tau protein, to examine the effects of tauopathy on hipp

275 0 mice) which overexpresses a mutant form of tau protein, to examine the effects of tauopathy on hipp

276 , which overexpresses a mutant form of human tau protein, to investigate the effects of tau pathology

277 isease, the density and spread of aggregated tau protein track well with neurodegeneration and cognit

278 Further, tau protein transference via the extracellular space, th

279 study was to investigate the serum levels of tau protein, ubiquitin carboxyl-terminal hydrolase L1 (U

280 ate the interaction between microtubules and tau proteins under mechanical loading.

281 We identified hyperphosphorylated tau protein using AT8 immunohistochemistry and compared

282 r(404)) and four doubly pseudophosphorylated Tau proteins using the same sites.

283 ay vary if the properties of the propagating tau proteins vary across individuals.

284 ce receiving endothelium-derived amyloid and tau proteins via intracerebroventricular injection exhib

285 We found that the exogenous mutant tau protein was restricted in MEC without spreading to o

286 groups of the 3D-Au-PAMAM-p-ABA-SPCE, where tau protein was sandwiched with a secondary antibody lab

287 athways protecting neurons from pathological tau protein, we employed a transgenic Caenorhabditis ele

288 Despite being charged and soluble, the tau proteins were also highly surface active and favorab

289 Oligomeric and phosphorylated Tau proteins were detected 4 and 24 h and 2 weeks post-T

290 albumin (HSA), beta-casein, and recombinant Tau proteins were submitted to in source decay in the MA

291 tion limits of 0.30nM for MBP and 0.15nM for Tau proteins which were sufficient for the levels to be

292 rotofilaments comprising residues 306-378 of tau protein, which adopt a combined cross-beta/beta-heli

293 Tau protein, which contains two naturally occurring cyst

294 scenario has recently been observed for the tau protein, which has four repeats.

295 ell-known IDPs is the microtubule-associated tau protein, which regulates microtubule growth in the n

296 We review evidence that the -amyloid and tau proteins, which aggregate to form senile plaques and

297 ion sites from in vivo phosphorylated tau (p-tau) protein, which is associated with Alzheimer's disea

298 liquid-liquid phase separation (LLPS) of the tau protein, whose pathological aggregation is implicate

299 brillary tangles made of hyperphosphorylated tau protein with neuronal loss.

300 by insoluble deposits of hyperphosphorylated tau protein within brain neurons.

301 educed levels of ~55 and 50 kDa forms of the tau protein without significant alterations of total tau