ライフサイエンスコーパス: tau

1 of hyperphosphorylated, aggregated forms of tau.

2 proteins, including beta-amyloid and phospho-Tau.

3 e normal microtubule-stabilizing function of tau.

4 ed of both T40PL-GFP and WT endogenous mouse tau.

5 ically reduced the accumulation of insoluble tau.

6 cellular accumulation of hyperphosphorylated tau.

7 en cells and seed the aggregation of soluble tau.

8 ci, and biochemical oxygen demand (Kendall's tau = 0.348 to 0.605, p < 0.05), a result supporting the

9 -beta ((11) C-PiB or (18) F-florbetapir) and tau ((18) F-flortaucipir).

10 n the population of a relatively long-lived (tau = 19 ns) Ru(dpi) --> qdpq(pi*) (3)MLCT excited state

11 tion of molecules (characteristic dwell time tau = 192 +/- 15 s and tau = 98 +/- 15 s for the more an

12 ssignments of non-seeded three-repeat-domain Tau(3RD) with an inherent heterogeneity.

13 ower mean (SD) cerebrospinal fluid levels of tau (59.2 [32.8] vs 111.3 [56.4]).

14 acteristic dwell time tau = 192 +/- 15 s and tau = 98 +/- 15 s for the more and less stable GQ, respe

15 d cognitive deficits by triggering Abeta and Tau accumulation through increases in oxidative damage a

16 duced phosphorylated and detergent-insoluble tau accumulation, and reduced tau-mediated neuron loss.

17 d oligomeric tau species in a mouse model of tau accumulation, preserving neuronal health and cogniti

18 ransgenic mice is associated with increasing tau accumulation.

19 ies a potential "two-hit" mechanism in which tau acetylation disengages tau from MTs and also promote

20 Tau acetylation has recently emerged as a dominant post-

21 aggregation, revealing a potential role for tau acetylation in the propagation of tau pathology.

22 eported tau aggregation inhibitor, modulates tau acetylation, a novel mechanism of action for this cl

23 To investigate the potential impact of these Tau activities on MT stabilization, we incorporated them

24 fer from early synaptic dysfunction prior to Tau aggregate formation, but the underlying mechanism is

25 ver, differences in cell-type specificity of tau aggregate transmission were observed between tau str

26 643, and RO6924963-that bind specifically to tau aggregates and have the potential to become PET trac

27 This heterogeneity could be due to tau aggregates forming distinct structural conformations

28 in vivo selective and reliable detection of tau aggregates in these non-Alzheimer tauopathies.

29 ays that allow the formation of pathological tau aggregates to be measured in situ within 24 h in the

30 r (also called (18)F-AV-1451) PET, targeting tau aggregates, detects these differences, and we compar

31 ion, and enhances the formation of fibrillar tau aggregates, highlighting both loss and gain of tau f

32 these mice did not develop de novo insoluble tau aggregates, which are characteristic of human AD and

33 thermore, 6C5 slowed down the progression of tau aggregation even after uptake had begun.

34 ntial for acetylation-mediated inhibition of tau aggregation in vitro and a molecular tactic for prev

35 demonstrate that methylene blue, a reported tau aggregation inhibitor, modulates tau acetylation, a

36 iffraction explain its dominant influence on tau aggregation.

37 on disengages tau from MTs and also promotes tau aggregation.

38 including the role of Pro(301) in inhibiting Tau aggregation.

39 rly, other proteins, including amyloid-beta, tau, alpha-synuclein, and serum amyloid A, misfold into

40 Pronounced tau and Abeta pathologies were primarily detected in the

41 transgenic mice with this inhibitor reduces tau and APP cleavage, ameliorates synapse loss and augme

42 erved between tau strains such that only PSP-tau and CBD-tau strains induce astroglial and oligodendr

43 sought to map all HDAC6-responsive sites in tau and determine how acetylation in a site-specific man

44 generation reduced levels of phosphorylated tau and increased expression of synaptophysin.

45 endent mediator of the toxicity of wild-type tau and of all the FTDP-17 mutants tested.

46 The expression levels of tau and TDP-43 were inverse in the frontal cortex and th

47 mutations tested increase phosphorylation of tau and trigger a cascade of neurotoxicity critically im

48 ew role for caspase-3 in the neurobiology of tau, and suggest that therapeutic strategies aimed at in

49 Thus, tau- and amyloid protein precursor-knockout mice were pr

50 Finally, CBD-tau- and PSP-tau-injected mice showed spatiotemporal tra

51 cross-linked by two disulfide bridges named tau-AnmTX Ms 9a-1 (short name Ms 9a-1) according to a st

52 nt (40E8 and p396) and C-terminal half (4E4) tau antibodies also reduced tau uptake despite removing

53 een established by immobilization of MBP and Tau antibodies.

54 LFP in aqueous solution (lambdamax = 410 nm, tau approximately 90 mus).

55 s indicate that several acetylation sites in tau are responsive to HDAC6 and that acetylation on Lys-

56 Intrinsically disordered proteins, like tau, are enriched with proline residues that regulate bo

57 ontrast, the population of aggregation-prone tau as induced by the complexation with heparin is accom

58 However, precisely how tau becomes toxic is unclear.

59 The Logan plot provided the best estimate of tau binding using arterial input functions.

60 ta+ group, increasing levels of flortaucipir tau binding were associated with increased cognitive imp

61 08-.40; P = .005), but not inferior temporal tau burden (beta = 0.10; 95% CI, -0.08 to 0.28; P = .27)

62 sociated with increasing entorhinal cortical tau burden (beta = 0.35; 95% CI, 0.19-.52; P < .001) and

63 of tau pathology, suggesting that increased tau burden cannot fully account for the effects of LC de

64 vels are positively associated with cerebral tau burden in FTLD.

65 taging and robust measurements of changes in tau burden over time for the evaluation of putative ther

66 Tau burden, amyloid burden, and cortical thickness.

67 Further, trazodone reduced p-tau burden.

68 duced tau uptake despite removing less total tau by immunodepletion, suggesting specific interactions

69 ll and animal models revealed that misfolded tau can propagate from cell to cell and from region to r

70 Assembled tau can transfer between cells and seed the aggregation

71 rea and was accompanied by increased local p-tau, changes in dendritic spine density and morphology,

72 rin is accompanied by large changes in local tau conformations and irreversible aggregation.

73 created a series of truncated and scrambled tau constructs and characterized the size and heterogene

74 ypical tauopathy characterized by grain-like tau-containing neurites in gray and white matter with he

75 lanks the core microtubule-binding domain of tau, contributes largely to the formation of large, hete

76 (75, 30-min sessions) or treatment as usual (TAU) control over 25 wk.

77 e also found that the increase with depth of tau cr is very gradual in the uppermost several metres o

78 n CDA and the microtubule-associated protein Tau deficiencies, and report that Tau depletion affects

79 deaminase and microtubule-associated protein Tau deficiencies.

80 h neurofibrillary tangles and is involved in tau degradation.

81 They find that tau deletion impairs hippocampal response to insulin thr

82 We found that tau deletion leads to an impaired hippocampal response t

83 ed protein Tau deficiencies, and report that Tau depletion affects rRNA synthesis, ribonucleotide poo

84 INTERPRETATION: Biomarkers of fibrillar tau deposition can be included with those of beta-amyloi

85 al PiB uptake suggest an atypical pattern of tau deposition in DLB.

86 ically by neuronal cell loss due to abnormal tau deposits.

87 Studies using Tau-derived peptides enabled the design of mutants that

88 Up to now, SPR has been poorly exploited for tau detection by immunosensing, due to sensitivity limit

89 Under pathological conditions, Tau dissociates from axonal microtubules and missorts to

90 jecting nontransgenic mice with pathological tau enriched from human tauopathy brains.

91 phosphorylation, the alternative splicing of tau exon 10, and cognitive performance.

92 regulates alternative splicing of exogenous tau exon 10.

93 tively correlated to tau phosphorylation, 3R-tau expression and tau pathology, and negatively correla

94 ied with cytoplasmic accumulation of TDP-43, tau expression was elevated in TDP-43M337V transgenic mo

95 Alzheimer's disease, and hyperphosphorylated tau facilitates Abeta toxicity.

96 se data demonstrate that Aha1 contributes to tau fibril formation and neurotoxicity through Hsp90.

97 ein likely reflects an intrinsic property of Tau fibrils.

98 endosomes/lysosomes ruptured by endocytosed tau fibrils.

99 ns induces the ordered assembly of monomeric Tau, followed by its spreading to distant brain regions.

100 in young 3xTg mice strongly promotes APP and tau fragmentation and facilitates amyloid plaque deposit

101 echanism in which tau acetylation disengages tau from MTs and also promotes tau aggregation.

102 role of membrane interactions in regulating Tau function, aggregation and toxicity.

103 gregates, highlighting both loss and gain of tau function.

104 rtance of heterogeneous complex formation in tau function.

105 result in the loss of specific physiological tau functions, which are largely unknown but could contr

106 ere were no differences between the iCST and TAU groups in the outcomes of cognition (mean difference

107 The link between Abeta and tau, however, remains controversial.

108 physiological and pathogenic roles of human Tau (hTau) is crucial to further understand the mechanis

109 ge of Akt may prove beneficial in preventing tau hyperphosphorylation and subsequent neuropathology i

110 related to the Abeta accumulation including tau hyperphosphorylation, neurodegeneration, neuroinflam

111 ding protein (TDP) inclusions in 40.5%, FTLD-tau in 40.5%, and Alzheimer disease (AD) pathology in 19

112 5 also blocked neuron-to-neuron spreading of tau in a unique three-chamber microfluidic device.

113 u pathology, and negatively correlated to 4R-tau in AD brains.

114 a (VTA), supporting an important function of tau in maintaining the survival of midbrain dopaminergic

115 These results suggest an important role for tau in regulating cytoskeletal organization and dynamics

116 onship of the pathological role of Abeta and tau in synapse dysfunction, several questions remain as

117 protein aggregates; amyloid-beta (Abeta) and tau in the brain during AD, and islet amyloid polypeptid

118 tomically connected brain regions, and these tau inclusions consisted of both T40PL-GFP and WT endoge

119 In mice, the intracerebral injection of Tau inclusions induces the ordered assembly of monomeric

120 rains induce astroglial and oligodendroglial tau inclusions, recapitulating the diversity of neuropat

121 Loss of the DDC bas-1 reduced tau-induced toxicity in a C. elegans model of tauopathy,

122 d serotonin synthesis pathways did not alter tau-induced toxicity; however, their function is require

123 Here the authors show that cis P-tau induction is a feature of several different forms of

124 Finally, CBD-tau- and PSP-tau-injected mice showed spatiotemporal transmission of

125 s enabled the design of mutants that disrupt Tau interactions with phospholipids without interfering

126 several questions remain as to how Abeta and tau interdependently cause impairments in synaptic funct

127 e microtubule associating protein tau (MAPT, tau) into toxic oligomers and amyloid deposits is a prim

128 On the basis of previous observations that tau is a direct substrate of histone deacetylase 6 (HDAC

129 Tau is a microtubule-associated protein that functions i

130 Tau is a microtubule-associated protein that is highly s

131 Tau is a multifaceted neuronal protein that stabilizes m

132 The neuronal MAP tau is also not sensitive to tubulin acetylation, but en

133 consistent with the hypothesis that cortical tau is associated with cognitive impairment.

134 The microtubule-associated protein tau is implicated in various neurodegenerative diseases

135 ar tools to study the link between 3R and 4R-Tau isoform expression, mitotic progression in neuronal

136 at overexpression of wild type and mutant 4R-Tau isoform in neuroblastoma SH-SY5Y cell lines is suffi

137 restingly, the relative expression levels of Tau isoforms containing either 3 (3R-Tau) or 4 repeats (

138 erties and distributions of human and rodent Tau isoforms in primary forebrain rodent neurons.

139 seeding between three-repeat and four-repeat Tau isoforms.

140 on, characterized by accumulation of all six tau isoforms.

141 Importantly, we found that tau knockdown reduced axon outgrowth and growth cone tur

142 Homozygous tau knockout (Mapt(-/-)) mice develop age-dependent dopa

143 of B-meson decays involving the higher-mass tau lepton have resulted in observations that challenge

144 The P-tau level and P-tau-T-tau ratio outperformed the T-tau l

145 The P-tau level and P-tau-T-tau ratio were higher in individua

146 of the Abeta42:Abeta40 ratio and T-tau or P-tau level did not improve the accuracy compared with the

147 vel and P-tau-T-tau ratio outperformed the T-tau level in distinguishing cranial computed tomography-

148 Compared with T-tau levels alone, P-tau levels and P-tau-T-tau ratios sh

149 Acute P-tau levels and P-tau-T-tau ratio weakly distinguished pa

150 Compared with T-tau levels alone, P-tau levels and P-tau-T-tau ratios show more robust and s

151 INTERPRETATION: CSF phosphorylated-tau levels are positively associated with cerebral tau b

152 Meanwhile, both RanBP9 and tau levels are simultaneously reduced by Hsp90 or Hsc70

153 that P301S/E4 mice have significantly higher tau levels in the brain and a greater extent of somatode

154 CSF tau levels were compared between groups and correlated w

155 on tested the association of ante mortem CSF tau levels with postmortem tau pathology adjusting for d

156 down of RanBP9 directly enhances and reduces tau levels, respectively, in vitro and in vivo.

157 for phosphorylated tau staining or insoluble tau levels.

158 n with hTau inserted into the endogenous fly tau locus and expressed under the control of the endogen

159 t of brain insulin signaling might occur via tau loss of function.

160 encoding the microtubule-associated protein TAU (MAPT).

161 ation of the microtubule associating protein tau (MAPT, tau) into toxic oligomers and amyloid deposit

162 n specifically at residues K280/K281 impairs tau-mediated MT stabilization, and enhances the formatio

163 ilizing agents have proven effective against tau-mediated neurodegeneration in animal models, and bec

164 gent-insoluble tau accumulation, and reduced tau-mediated neuron loss.

165 TMs are driving factors for the induction of tau-mediated neuronal damage.

166 ves both amyloid precursor protein (APP) and tau, mediating the amyloid-beta and tau pathology in Alz

167 Tg mouse line) exhibited hyperphosphorylated tau mislocalized to the somatodentritic domain of neuron

168 Pathological Tau mutants lacking the vesicle binding domain still loc

169 ring the biochemical activities of different tau mutations with their in vivo toxicity in a well cont

170 The newly developed GO/pPG/anti-MBP/anti-Tau nanoimmunosensor has been established by immobilizat

171 (AD) is associated with the accumulation of tau neurofibrillary tangles, which may spread throughout

172 ifferent types and cellular distributions of tau neuropathology in our model that recapitulate the he

173 n in vivo (18) F-flortaucipir and postmortem tau neuropathology.

174 ive inhibitor inhibited c-Abl activation and tau oligomer accumulation.

175 hway was responsible for the accumulation of tau oligomers after TBI, as post-TBI injection of a calp

176 sing TIA1 also inhibited the accumulation of tau oligomers at the expense of increasing neurofibrilla

177 mbination of the Abeta42:Abeta40 ratio and T-tau or P-tau level did not improve the accuracy compared

178 vels of Tau isoforms containing either 3 (3R-Tau) or 4 repeats (4R-Tau) play an important role both d

179 ive disorders, such as amyloid-beta (Abeta), tau, or alpha-synuclein (alphaSyn) might be the major de

180 The mechanisms by which tau organizes microtubule networks remain poorly underst

181 Chronic treatment of tau P301S and 5XFAD transgenic mice with this inhibitor

182 in RanBP9 not only ameliorates tauopathy in Tau-P301S mice but also rescues the deficits in synaptic

183 These distinct tau pathologies have different temporal onsets and funct

184 f ante mortem CSF tau levels with postmortem tau pathology adjusting for demographics.

185 s have revealed a tight relationship between tau pathology and cognitive impairment across the Alzhei

186 igated the effect of synaptic stimulation on Tau pathology and synapses in in vivo and in vitro model

187 digital histology measurement of postmortem tau pathology averaged from three cerebral regions (angu

188 se neurodegenerative diseases, but also that tau pathology can manifest in healthy neural tissue tran

189 hological tau resulted in the propagation of tau pathology from the injection site to neuroanatomical

190 -regulation of TDP-43 may be involved in the tau pathology in AD and related neurodegenerative disord

191 PET imaging of tau pathology in Alzheimer disease may benefit from the

192 g affinity for paired helical filament (PHF)-tau pathology in Alzheimer's brains.

193 APP) and tau, mediating the amyloid-beta and tau pathology in Alzheimer's disease (AD).

194 For example, the tau pathology in corticobasal degeneration is distinct f

195 osis of corticobasal degeneration had severe tau pathology in PSP-related brain structures with good

196 Overt tau pathology in the aged mice was accompanied by spatia

197 Notably, the pathological features of tau pathology in these diseases can be very distinct.

198 ing not only adds to the recent reports that tau pathology is a feature of these neurodegenerative di

199 Together, these results show that tau pathology is related in a region-specific manner to

200 However, tau pathology may also result in the loss of specific ph

201 studies and further suggest that entorhinal tau pathology underlies memory decline in old age even w

202 o tau phosphorylation, 3R-tau expression and tau pathology, and negatively correlated to 4R-tau in AD

203 showed spatiotemporal transmission of glial tau pathology, suggesting glial tau transmission contrib

204 re accompanied by only a mild aggravation of tau pathology, suggesting that increased tau burden cann

205 le for tau acetylation in the propagation of tau pathology.

206 likely to contain TDP-43 and not significant tau pathology.

207 ions for future therapeutic trials targeting tau pathology.

208 Tau PET and neurodegeneration biomarkers were discordant

209 ers a first look at the relationship between Tau-PET imaging with F(18)-AV1451 and functional connect

210 sequential phases: (1) a treatment as usual (TAU) phase from August 2010 to December 2011, (2) a univ

211 rements of two key fibril-forming regions of tau, PHF6 and PHF6*, in transient as aggregation happens

212 ermining the functional relationship between Tau phosphorylation and aggregation has proven a challen

213 No significant changes were observed in tau phosphorylation and neuroinflammation.

214 of CK1epsilon were positively correlated to tau phosphorylation, 3R-tau expression and tau pathology

215 CK1epsilon is involved in the regulation of tau phosphorylation, the alternative splicing of tau exo

216 ontaining either 3 (3R-Tau) or 4 repeats (4R-Tau) play an important role both during brain developmen

217 Lys-321/Ser-324 that coordinately regulates tau polymerization and function.

218 of RanBP9 significantly diminishes the anti-tau potency of Hsp90/Hsc70 inhibitors as well as Hsc70 v

219 Alternative splicing of exon 10 in the tau primary transcript gives rise to protein isoforms wi

220 ssed under the control of the endogenous fly tau promoter, thus avoiding potential toxicity due to ge

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

222 7 is a PET radiotracer developed for imaging tau protein aggregates, which are implicated in neurolog

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

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

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

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

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

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

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

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

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

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

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

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

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

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

237 suggests the microtubule-stabilizing protein Tau/PTL-1 potentially inhibits RPM-1.

238 beta (-0.34; P=0.051) or relaxation constant tau (r=-0.33; P=0.06).

239 The P-tau level and P-tau-T-tau ratio outperformed the T-tau level in distinguishing

240 Acute P-tau levels and P-tau-T-tau ratio weakly distinguished patients with TBI who had

241 The P-tau level and P-tau-T-tau ratio were higher in individuals with more severe TB

242 (UPSIT) scores, CSF amyloid - (Abeta42) to t-tau ratio, and APOE status were associated with change i

243 T-tau levels alone, P-tau levels and P-tau-T-tau ratios show more robust and sustained elevations amo

244 rain and a greater extent of somatodendritic tau redistribution by three months of age compared with

245 d whether the microtubule-associated protein tau regulates the differentiation and survival of mDANs

246 Accumulation of amyloid beta (Abeta) and tau represent the two major pathological hallmarks of Al

247 These injections of pathological tau resulted in the propagation of tau pathology from th

248 regulated phosphorylation event, we examined tau's ability to promote microtubule assembly and found

249 cetylation in a site-specific manner affects tau's biophysical properties in vitro Our findings indic

250 We propose that Tau's GDP preference allows the cell to independently re

251 Here, we sought to determine how assembled tau seeds gain access to the cytosol and whether this ac

252 After binding, TRIM21 neutralizes tau seeds through the activity of the proteasome and the

253 the presence of picomolar concentrations of tau seeds.

254 horylation sites and their clustering in the Tau sequence.

255 r M344 reduces beta-amyloid (Abeta), reduces tau Ser(396) phosphorylation, and decreases both beta-se

256 Full-length acetylation-mimic tau showed increased propensity to undergo seed-dependen

257 0 ameliorated silver-positive and oligomeric tau species in a mouse model of tau accumulation, preser

258 antibodies successfully prevented uptake of tau species, whereas the distal C-terminal-specific anti

259 stem affects the accumulation of these toxic tau species, which can be modulated with Hsp90 inhibitor

260 o evaluate the in vivo kinetics of the novel tau-specific PET radioligand (18)F-AV-1451 in cognitivel

261 differences were observed for phosphorylated tau staining or insoluble tau levels.

262 of a sporadic tauopathy model to study human tau strains by intracerebrally injecting nontransgenic m

263 n tau strains such that only PSP-tau and CBD-tau strains induce astroglial and oligodendroglial tau i

264 We show human tau strains seed different types and cellular distributi

265 aggregate transmission were observed between tau strains such that only PSP-tau and CBD-tau strains i

266 The P-tau level and P-tau-T-tau ratio outperformed the T-tau level in distingu

267 Acute P-tau levels and P-tau-T-tau ratio weakly distinguished patients with TBI w

268 The P-tau level and P-tau-T-tau ratio were higher in individuals with more sev

269 with T-tau levels alone, P-tau levels and P-tau-T-tau ratios show more robust and sustained elevatio

270 udy, we first assessed the patterns of brain tau tangle accumulation (measured with the positron emis

271 ge even without Abeta.SIGNIFICANCE STATEMENT Tau tangles and beta-amyloid (Abeta) plaques are key les

272 ative disease characterized by deposition of tau tangles in the brain are highly susceptible to devel

273 in humans, and that administration of cis P-tau targeting antibody to rodents reduces or delays path

274 Already at steady-state conditions, tau-tg mice exhibit peripheral immune activation that is

275 n this article, we show that tau-transgenic (tau-tg) mice that develop neurodegenerative disease char

276 vely unfolded microtubule-associated protein Tau to a highly structured amyloid fibril underlies huma

277 al design relied on the assumptions that the tau torsion of the meta-amino-substituted BDI systems le

278 e ortho or para position could slow down the tau torsion.

279 ing morning for measurement of amyloid-beta, tau, total protein, YKL-40, and hypocretin.

280 function is required for the suppression of tau toxicity by bas-1.

281 D2-family dopamine receptors can ameliorate tau toxicity, we screened a collection of C. elegans mut

282 pread throughout the cortex by interneuronal tau transfer.

283 pamine-related genes (n = 45) for changes in tau transgene-induced behavioral defects.

284 Moreover, a reduction in progranulin in tau transgenic mice is associated with increasing tau ac

285 By generating P301S tau transgenic mice on either a human ApoE knock-in (KI)

286 as-1, ameliorated the behavioral deficits of tau transgenic worms, reduced phosphorylated and deterge

287 In this article, we show that tau-transgenic (tau-tg) mice that develop neurodegenerat

288 ion of glial tau pathology, suggesting glial tau transmission contributes to the progression of tauop

289 ely to the formation of large, heterogeneous tau tubulin complexes; additional independent tubulin bi

290 We propose that tau-tubulin can be described as a "fuzzy" complex, and o

291 racterized the size and heterogeneity of the tau-tubulin complexes formed under nonpolymerizing condi

292 lf-propagation of misfolded conformations of tau underlies neurodegenerative diseases, including Alzh

293 minal half (4E4) tau antibodies also reduced tau uptake despite removing less total tau by immunodepl

294 The antibodies reduced tau uptake in an epitope-dependent manner: N-terminal (T

295 cally recognizes phosphothreonine-231) and T-tau using ultra-high sensitivity laser-based immunoassay

296 Plasma samples were assayed for P-tau (using an antibody that specifically recognizes phos

297 Higher MTL tau was related to higher age in the subjects without ev

298 brafish models expressing wild-type or A152T-tau, where A152T caused neurodegeneration and proteasome

299 t, surprisingly, the pseudo-repeat region of tau, which flanks the core microtubule-binding domain of

300 t and is less characterized than its homolog Tau, which has various roles in neurodegeneration.