ライフサイエンスコーパス: neurofibrillary

1 idlife BMI was associated with greater Braak neurofibrillary but not CERAD (Consortium to Establish a

2 The first neurofibrillary cortical lesions in Alzheimer's disease

3 y mechanism that may become perturbed during neurofibrillary degeneration and suggest that this regul

4 ing effect on Alzheimer's pathology, because neurofibrillary degeneration in a small number of neuron

5 ent abnormal hyperphosphorylation of tau and neurofibrillary degeneration in AD.

6 al-dominant genetic mutation associated with neurofibrillary degeneration in part owing to reduced ta

7 and high vulnerability to the tauopathy and neurofibrillary degeneration of Alzheimer's disease.

8 proteins that cause tau phosphorylation and neurofibrillary degeneration, insulin administration enh

9 had an extensive topographic distribution of neurofibrillary degeneration.

10 se plaque density score, and Braak stage for neurofibrillary degeneration.

11 at rapidly and robustly recapitulates mature neurofibrillary inclusion and Lewy body formation found

12 Tau neurofibrillary inclusions were found in only one dog.

13 sease is defined by the presence of abundant neurofibrillary lesions and neuritic plaques in the cere

14 Neurofibrillary lesions comprise paired helical and stra

15 dentified with antibodies used to detect tau neurofibrillary lesions in the human brain.

16 Although tau hyperphosphorylation and neurofibrillary-like pathology have been observed in the

17 by neurodegeneration and amyloid plaque and neurofibrillary pathologies.

18 on after TBI and promoted the development of neurofibrillary pathology and neurodegeneration in the p

19 gly, we found that ERalpha co-localized with neurofibrillary pathology in AD brain and further demons

20 Although the spread of neurofibrillary pathology in the hippocampus throughout

21 Neurofibrillary pathology of abnormally hyperphosphoryla

22 shown utility in detection and monitoring of neurofibrillary pathology over time.

23 tex pyramidal cells were not associated with neurofibrillary pathology suggesting there is a vascular

24 Neurofibrillary pathology was also detected with Gallyas

25 Males tended to predominate, the neurofibrillary pathology was more intense in the langua

26 (CERAD) (neuritic plaque burden), and Braak (neurofibrillary pathology) scores.

27 characteristic spatiotemporal progression of neurofibrillary pathology.

28 au at the depth of sulci to later widespread neurofibrillary pathology.

29 Aberrant tau protein accumulation drives neurofibrillary tangle (NFT) formation in several neurod

30 an trigger increased tau phosphorylation and neurofibrillary tangle (NFT) formation in vivo, the mole

31 and facilitates amyloid plaque deposits and neurofibrillary tangle (NFT) formation, resulting in cog

32 gnaling and its relation to Abeta plaque and neurofibrillary tangle (NFT) pathology during disease on

33 rk (DMN) displays amyloid and tau-containing neurofibrillary tangle (NFT) pathology during the onset

34 The study used Braak neurofibrillary tangle (NFT) stage, frequency of neuriti

35 is independently associated with lower Braak neurofibrillary tangle (NFT) stages and possibly fewer n

36 y associated with age, presence of infarcts, neurofibrillary tangle and neuritic plaque scores, APOE

37 Alzheimer's disease (AD) is characterized by neurofibrillary tangle and neuropil thread deposition, w

38 uclear palsy, corticobasal degeneration, and neurofibrillary tangle Braak stage regions of interest,

39 of these "Abeta-negative" subjects have low neurofibrillary tangle Braak stages.

40 dance of these UFAs with neuritic plaque and neurofibrillary tangle burden as well as domain-specific

41 t to model the possibility that knowledge of neurofibrillary tangle burden in the presence of moderat

42 ic vesicles, hyperphosphorylated tau (pTau), neurofibrillary tangle conformational-epitope (cNFT), am

43 Flortaucipir correlated with neurofibrillary tangle counts in entorhinal cortex, but

44 predominant, and typical AD--on the basis of neurofibrillary tangle counts in hippocampus and cortex

45 Neurofibrillary tangle counts were performed using thiof

46 Braak staging, Abeta plaque and neurofibrillary tangle counts, and semiquantitative tau

47 enuated the effect of the epsilon4 allele on neurofibrillary tangle density (interaction estimate, -0

48 er dementia (AD) (p value = 5.42 x 10(-13)), neurofibrillary tangle density (p value = 1.89 x 10(-6))

49 In addition to amyloid-beta plaque and tau neurofibrillary tangle deposition, neuroinflammation is

50 's disease via its presence in intraneuronal neurofibrillary tangle deposits, where it takes the form

51 n, on both SUVR images and W-score maps, and neurofibrillary tangle distribution in patients with pri

52 f Alzheimer's Disease (AD) in regard to both neurofibrillary tangle formation and neuronal network hy

53 rtantly, oligomer injections induced AD-type neurofibrillary tangle formation in the macaque brain.

54 cellular deposition of amyloid-beta (Abeta), neurofibrillary tangle formation, and a microglial-drive

55 in tau cause familial neurodegeneration and neurofibrillary tangle formation.

56 logical hallmark of Alzheimer's disease; the neurofibrillary tangle load correlates strongly with cli

57 TDP-43 and Braak neurofibrillary tangle pathological staging schemes were

58 s12570088 were significantly associated with neurofibrillary tangle pathology (P = .01352 and .03151,

59 lysis can reliably track the distribution of neurofibrillary tangle pathology and can predict patholo

60 dentate gyrus of patients with AD and severe neurofibrillary tangle pathology and were accompanied by

61 ammatory signaling may promote or accelerate neurofibrillary tangle pathology, we explored the effect

62 s of Alzheimer's disease, including distinct neurofibrillary tangle pathology.

63 E genotype on incident AD and development of neurofibrillary tangle pathology.

64 nic AD mice exacerbates hallmark amyloid and neurofibrillary tangle pathology.

65 ies and may not detect early Braak stages of neurofibrillary tangle pathology.

66 didate variants included neuritic plaque and neurofibrillary tangle pathology; longitudinal Alzheimer

67 Each individual was also assigned a neurofibrillary tangle stage (B1-B3), relating to the li

68 ow likelihood of having Alzheimer's disease (neurofibrillary tangle stage B1; n=37).

69 te likelihood of having Alzheimer's disease (neurofibrillary tangle stage B2; n=56), those with hippo

70 gh likelihood of having Alzheimer's disease (neurofibrillary tangle stage B3; n=205), those with hipp

71 We found that knowledge of neurofibrillary tangle stage, modeled as the sort of inf

72 acceleration was associated with high Braak neurofibrillary tangle stage.

73 were decreased in association with the Braak neurofibrillary tangle stage.

74 bal 11C-PiB in regions associated with Braak neurofibrillary tangle stages I-VI.

75 psy data to evaluate the effect of different neurofibrillary tangle stages on the rates of progressio

76 nt-insoluble tau, neuronal loss and reverses neurofibrillary tangle-associated brain dysfunction.

77 measures for certain non-amyloid-plaque, non-neurofibrillary-tangle neuropathologies.

78 -1.34 to -0.04]), less severe and widespread neurofibrillary tangles (beta = -0.77 score units [95% C

79 brain volume ratio, and hippocampal volume), neurofibrillary tangles (cerebrospinal fluid phosphoryla

80 hases, the extent of involvement (spread) by neurofibrillary tangles (composed of hyperphosphorylated

81 k amyloid-beta (Abeta) plaques or tau-filled neurofibrillary tangles (NFT), is considered the most pr

82 are amyloid beta protein (Abeta) plaques and neurofibrillary tangles (NFT).

83 intracellular aggregation of tau protein in neurofibrillary tangles (NFTs) (1, 2).

84 osis is based on density and distribution of neurofibrillary tangles (NFTs) and amyloid-rich neuritic

85 amyloid beta (Abeta) peptide in propagating neurofibrillary tangles (NFTs) and eventual cognitive im

86 surrounding Abeta plaques (NP tau), AD-like neurofibrillary tangles (NFTs) and neuropil threads (NTs

87 Neurofibrillary tangles (NFTs) are a pathological hallma

88 Neurofibrillary tangles (NFTs) are the pathological hall

89 lzheimer's disease (AD) is very distinctive: neurofibrillary tangles (NFTs) composed of hyperphosphor

90 Neurofibrillary tangles (NFTs) composed of hyperphosphor

91 neurodegenerative diseases characterized by neurofibrillary tangles (NFTs) comprising filamentous ta

92 n (CBF) nucleus basalis (NB) neurons display neurofibrillary tangles (NFTs) during Alzheimer's diseas

93 e accumulation of hyperphosphorylated tau in neurofibrillary tangles (NFTs) is a neuropathological ha

94 on of tau and subsequent aggregation to form neurofibrillary tangles (NFTs) is closely related to pro

95 Tauopathies, characterized by neurofibrillary tangles (NFTs) of phosphorylated tau pro

96 zed by cognitive decline and the presence of neurofibrillary tangles (NFTs) of the protein tau in pat

97 Neurofibrillary tangles (NFTs) were counted in four brai

98 ion of the density and neocortical spread of neurofibrillary tangles (NFTs) with clinical AD disease

99 Neurofibrillary tangles (NFTs), a marker of neuronal alt

100 europathological burden of neuritic plaques, neurofibrillary tangles (NFTs), and vascular brain injur

101 uggest that tau oligomers, which form before neurofibrillary tangles (NFTs), are the true neurotoxic

102 Neurofibrillary tangles (NFTs), composed of truncated an

103 Neurofibrillary tangles (NFTs), hippocampal sclerosis, l

104 he hallmark pathology of amyloid plaques and neurofibrillary tangles (NFTs), it has been reported tha

105 functional brain protein that accumulates in neurofibrillary tangles (NFTs), most commonly in Alzheim

106 The formation of neurofibrillary tangles (NFTs), oxidative stress and neu

107 neurodegenerative diseases characterized by neurofibrillary tangles (NFTs), the predominant tau path

108 n tissue over co-existing tau aggregates and neurofibrillary tangles (NFTs), which are associated in

109 CMV antibody levels were associated with neurofibrillary tangles (NFTs).

110 subnanomolar-affinity PET tracer for imaging neurofibrillary tangles (NFTs).

111 ons, are defined by a pathological hallmark: neurofibrillary tangles (NFTs).

112 aggregation of hyperphosphorylated tau into neurofibrillary tangles (NFTs).

113 eta level, plays a critical role in inducing neurofibrillary tangles (NTFs) in human neurons.

114 s showed a lower frequency of Alzheimer-type neurofibrillary tangles (p < 0.05).

115 (p = 4.9 x 10(-4) ), an increased burden of neurofibrillary tangles (p = 9.1 x 10(-3) ), and an incr

116 1204) showed a sex-specific association with neurofibrillary tangles among males (P = 2.5 x 10-8) but

117 Early observations of the patterns of neurofibrillary tangles and amyloid plaques in Alzheimer

118 ligomer formation precedes the appearance of neurofibrillary tangles and contributes to neuronal loss

119 oid precursor protein (APP), and presence of neurofibrillary tangles and dystrophic neurites containi

120 AD, p62 immunoreactivity is associated with neurofibrillary tangles and is involved in tau degradati

121 nantly associated with thioflavin-S-positive neurofibrillary tangles and less reactive in neuropil th

122 ology was quantified by a summary measure of neurofibrillary tangles and neuritic and diffuse plaques

123 Tau immune-reactive neurofibrillary tangles and neuritic threads were presen

124 tau P301S mutation and exhibit age-dependent neurofibrillary tangles and neurodegeneration, overexpre

125 s, aggregation of hyperphosphorylated tau in neurofibrillary tangles and neuroinflammation, together

126 uorescent staining) pathological inclusions, neurofibrillary tangles and neuropil threads but only in

127 chemical stainings] pathological inclusions, neurofibrillary tangles and neuropil threads.

128 l pathological Tau inclusions in the form of neurofibrillary tangles and Pick bodies and in some case

129 responses and the resulting sera recognized neurofibrillary tangles and plaque-associated dystrophic

130 athology in the form of neuropil threads and neurofibrillary tangles and pre-tangles.

131 ce of other hallmarks of the disease such as neurofibrillary tangles and widespread neuronal losses.

132 Neurofibrillary tangles are a pathological hallmark of A

133 We show that neurofibrillary tangles are neither sufficient nor requi

134 sed of misfolded alpha-synuclein (aSyn), and neurofibrillary tangles are primarily composed of tau pr

135 en shown to produce hyperphosphorylated tau, neurofibrillary tangles as well as aberrant amyloid prec

136 Cerebral neurofibrillary tangles burden, in addition to alpha-syn

137 e model that co-develops amyloid plaques and neurofibrillary tangles but also because it enabled us t

138 Amyloid plaques and neurofibrillary tangles co-occur in Alzheimer disease, b

139 Alzheimer disease (AD) include intraneuronal neurofibrillary tangles composed of abnormally hyperphos

140 ccumulation of amyloid-beta peptide leads to neurofibrillary tangles composed of aggregated hyperphos

141 plaques containing amyloid-beta (Abeta) and neurofibrillary tangles composed of aggregated, hyperpho

142 nset Alzheimer-like dementia associated with neurofibrillary tangles composed of hyperphosphorylated

143 d beta peptide (Abeta) in brain is linked to neurofibrillary tangles composed of hyperphosphorylated

144 evident as senile plaques and intracellular neurofibrillary tangles composed of hyperphosphorylated

145 the post-traumatic brain frequently exhibits neurofibrillary tangles comprised of aggregates of the p

146 n of insoluble protein aggregates, including neurofibrillary tangles comprised of tau in Alzheimer's

147 thologically by abundant amyloid plaques and neurofibrillary tangles concurrent with synaptic and neu

148 ther, the development of amyloid plaques and neurofibrillary tangles contributes to neuronal loss.

149 s in Alzheimer's disease, demonstrating that neurofibrillary tangles develop downstream of amyloid-be

150 ampal insoluble pathological tau species and neurofibrillary tangles following a single dose of AAV-v

151 in the neocortex precedes the spread of tau neurofibrillary tangles from the limbic areas to the cor

152 Prion-like seeding of amyloid fibrils and neurofibrillary tangles has been invoked to explain the

153 sitron emission tomography tracers targeting neurofibrillary tangles has enabled the distribution of

154 Recently, PET tracers for tau neurofibrillary tangles have become available and have s

155 egates, known as Lewy bodies (LB) in PD, and neurofibrillary tangles in AD.

156 comes hyper-phosphorylated and deposits into neurofibrillary tangles in AD.

157 associated protein Tau, a major component of neurofibrillary tangles in Alzheimer disease and other t

158 merly (18) F-AV1451 or (18) F-T807) binds to neurofibrillary tangles in Alzheimer disease, but tissue

159 pathology including dystrophic neuritis and neurofibrillary tangles in Alzheimer's disease (AD) brai

160 ncluding Lewy bodies in Parkinson's disease, neurofibrillary tangles in Alzheimer's disease, polyQ in

161 to reduce the risk of AD and development of neurofibrillary tangles in APOE epsilon4+ individuals.

162 well as plaques (diffuse and neuritic), and neurofibrillary tangles in autopsy specimens from age-ma

163 ominant-negatives markedly reduces tau-laden neurofibrillary tangles in FTLD mice in vivo.

164 omise as a sensitive biomarker for detecting neurofibrillary tangles in preclinical Alzheimer's disea

165 nd forms insoluble inclusion bodies known as neurofibrillary tangles in the brain tissue of patients

166 position of amyloid-beta (Abeta) plaques and neurofibrillary tangles in the brain, accompanied by syn

167 tion of amyloid-beta (Abeta) plaques and tau neurofibrillary tangles in the brain.

168 presence of amyloid beta (Abeta) plaques and neurofibrillary tangles in the brain.

169 ta) plaques and intracellular tau-containing neurofibrillary tangles in the brain.

170 gically characterized by amyloid plaques and neurofibrillary tangles in the brain.

171 rized by accumulation of amyloid plaques and neurofibrillary tangles in the brain.

172 typical AD, hippocampal-sparing AD has more neurofibrillary tangles in the cortex and fewer in the h

173 verity from focal perivascular epicentres of neurofibrillary tangles in the frontal neocortex to seve

174 ence of amyloid-beta (Abeta) plaques and tau neurofibrillary tangles in the neocortex is linked to ne

175 ometry confirmed that 75 proteins present in neurofibrillary tangles interacted with PHF1-immunoreact

176 and (or) association with senile plaques and neurofibrillary tangles is a major feature of several ne

177 The aggregation of the tau protein into neurofibrillary tangles is believed to correlate with co

178 Neurofibrillary tangles likely cause neurodegeneration i

179 stmortem studies have long demonstrated that neurofibrillary tangles made of hyperphosphorylated tau

180 ved from amyloid precursor protein (APP) and neurofibrillary tangles made of hyperphosphorylated Tau.

181 gyrus in THY-Tau22 mice, the development of neurofibrillary tangles made of mutant human tau was not

182 (i) quantitative proteomics was performed on neurofibrillary tangles microdissected from patients wit

183 bodies associated with Parkinson disease and neurofibrillary tangles observed in Alzheimer disease.

184 helical filaments (PHFs) that constitute the neurofibrillary tangles observed in neuronal cell bodies

185 th protein misfolding and aggregation as the neurofibrillary tangles of Alzheimer's disease, whereas

186 In contrast, neurofibrillary tangles of CTE contain both 3R and 4R ta

187 loid deposition as plaques and intracellular neurofibrillary tangles of tau protein.

188 high levels of transition metal ions and the neurofibrillary tangles of Tau protein.

189 rized by plaques of amyloid beta (Abeta) and neurofibrillary tangles of tau.

190 There was no difference in Braak stage for neurofibrillary tangles or consortium to establish a reg

191 During the development of AD, neurofibrillary tangles progress in a fixed pattern, sta

192 r accumulation of hyperphosphorylated tau as neurofibrillary tangles remains the primary neuropatholo

193 endent negative associations of cerebral tau neurofibrillary tangles score with the interval between

194 re Sarkosyl-insoluble and associate with Tau neurofibrillary tangles selectively in Alzheimer disease

195 tion of many proteins known to be present in neurofibrillary tangles such as tau, ubiquitin, neurofil

196 and tauopathies, tau protein aggregates into neurofibrillary tangles that progressively spread to syn

197 Further, the march of neurofibrillary tangles through brain circuits appears t

198 relative contribution of amyloid plaques and neurofibrillary tangles to brain dysfunction in Alzheime

199 pants who died, and beta-amyloid (Abeta) and neurofibrillary tangles were identified by immunohistoch

200 in brains of Alzheimer's disease and diffuse neurofibrillary tangles with calcification, characterize

201 myloid plaques with amyloid beta (Abeta) and neurofibrillary tangles with tau accumulation.

202 The spread of tau aggregates (neurofibrillary tangles) across the cerebral cortex para

203 al cortex (reflecting incidental age-related neurofibrillary tangles) and neuromelanin-containing neu

204 Alzheimer's pathology (neuritic plaques and neurofibrillary tangles) and the interval between time o

205 efore overt histopathological lesions (i.e., neurofibrillary tangles) are apparent.

206 k neuropathology of Alzheimer's disease (AD; neurofibrillary tangles) had its first foothold in speci

207 hological markers of AD (amyloid plaques and neurofibrillary tangles) in aged chimpanzee brains provi

208 ptide (amyloid plaques) and the tau protein (neurofibrillary tangles) in the brains of affected indiv

209 Along with aggregated tau in the form of neurofibrillary tangles, (18)F-flortaucipir has been rep

210 phorylation of Tau leads to the formation of neurofibrillary tangles, a hallmark of Alzheimer disease

211 egates of hyperphosphorylated tau protein in neurofibrillary tangles, a process that occurs late in t

212 clusters can simultaneously account for tau neurofibrillary tangles, alpha-synuclein inclusions, neu

213 ology, with the co-occurrence of both LB and neurofibrillary tangles, among other protein inclusions.

214 Alzheimer's disease (AD) is characterized by neurofibrillary tangles, amyloid plaques, and neurodegen

215 ium (never vs ever) and pathologic burden of neurofibrillary tangles, amyloid plaques, vascular lesio

216 isease, such as altered Tau phosphorylation, neurofibrillary tangles, and accumulation of insoluble p

217 d estimates of the densities of Lewy bodies, neurofibrillary tangles, and aminergic neurons in the lo

218 nscripts and an increase in amyloid plaques, neurofibrillary tangles, and cognitive decline.

219 including beta-amyloid (Abeta) plaques, tau neurofibrillary tangles, and cognitive deficits, suggest

220 t, clinical progression, amyloid deposition, neurofibrillary tangles, and composite neuropathological

221 decline, white matter damage, brain atrophy, neurofibrillary tangles, and dementia.

222 , including beta-amyloid senile plaques, tau neurofibrillary tangles, and fused in sarcoma (FUS) and

223 normalities, brain accumulation of Abeta and neurofibrillary tangles, and influence of apolipoprotein

224 abolites/pathways and cognitive performance, neurofibrillary tangles, and neuritic plaque burden.

225 of amyloid-beta (Abeta)-containing plaques, neurofibrillary tangles, and neuronal loss in the brain.

226 e (AD) include amyloid-beta (Abeta) plaques, neurofibrillary tangles, and reactive gliosis.

227 sease (AD) is hallmarked by amyloid plaques, neurofibrillary tangles, and widespread cortical neurona

228 res of TDP-43 pathology, density of neuronal neurofibrillary tangles, area occupied by amyloid-beta p

229 racellular amyloid plaques and intraneuronal neurofibrillary tangles, both of which comprise highly i

230 rotein, the primary constituent of Alzheimer neurofibrillary tangles, can form liquid droplets and th

231 Neurofibrillary tangles, composed of hyperphosphorylated

232 yloid (Abeta) core and a neuritic component; neurofibrillary tangles, composed predominantly of hyper

233 eta) extracellular plaques and intracellular neurofibrillary tangles, constituted by hyperphosphoryla

234 Activated PSK is associated with neurofibrillary tangles, dystrophic neurites surrounding

235 gional post-mortem amyloid load and neuronal neurofibrillary tangles, even after accounting for APOE,

236 (18)F]RO6958948)) with high affinity for tau neurofibrillary tangles, excellent selectivity against A

237 iated with deposition of amyloid plaques and neurofibrillary tangles, formed by amyloid beta (Abeta)

238 Neurofibrillary tangles, formed of misfolded, hyperphosp

239 se is characterized by amyloid-beta plaques, neurofibrillary tangles, gliosis, and neuronal loss.

240 rgence of PET probes for amyloid plaques and neurofibrillary tangles, hallmarks of Alzheimer disease

241 ques and markers to assess the burden of tau neurofibrillary tangles, neuritic plaques, alpha-synucle

242 hippocampal) and time interaction terms for neurofibrillary tangles, neuritic plaques, gross infarct

243 Neuropathologic outcomes included neurofibrillary tangles, neuritic plaques, microinfarcts

244 At this age point these mice exhibit neurofibrillary tangles, neurodegeneration and cognitive

245 ascade of events leading to the formation of neurofibrillary tangles, neurodegeneration, and the symp

246 ted with intracellular aggregation of tau as neurofibrillary tangles, neuronal and synaptic loss, and

247 aque burden, stereologically-based counts of neurofibrillary tangles, neurons and reactive glia, and

248 ressed human tau protein, the development of neurofibrillary tangles, neuropil threads and ghost tang

249 by influencing amyloid-beta (Abeta) and Tau (neurofibrillary tangles, NFTs) deposition in the brain.

250 Neurofibrillary tangles, one of the hallmarks of Alzheim

251 with neuropathology (NIA ADC, Braak stage of neurofibrillary tangles, p = 3.9 x 10-6, and Consortium

252 ults in tau phosphorylation and formation of neurofibrillary tangles, requires the recruitment of the

253 , which aggregate to form senile plaques and neurofibrillary tangles, respectively, are induced to mi

254 e tau pathway-leading to amyloid plaques and neurofibrillary tangles, respectively, which are histopa

255 nd semiquantitative scores for the burden of neurofibrillary tangles, senile plaques, Lewy bodies (LB

256 by accumulation of amyloid-beta plaques and neurofibrillary tangles, synaptic and neuronal loss, and

257 re the main components of senile plaques and neurofibrillary tangles, the two histopathological hallm

258 Despite the increase in neurofibrillary tangles, TIA1 reduction increased neuron

259 ) is associated with the accumulation of tau neurofibrillary tangles, which may spread throughout the

260 ed in transgenic Abeta rats that do not form neurofibrillary tangles, which support these findings as

261 beta-amyloid and tau aggregation, including neurofibrillary tangles, with age, making them a promisi

262 characterize the disease-senile plaques and neurofibrillary tangles-ramify systematically through th

263 by accumulation of amyloid beta (Abeta) and neurofibrillary tangles.

264 cular pathologies: amyloid abeta1-42 and Tau neurofibrillary tangles.

265 ized by beta-amyloid (Abeta) plaques and tau neurofibrillary tangles.

266 loid beta (Abeta) peptides and intracellular neurofibrillary tangles.

267 europathologic markers of senile plaques and neurofibrillary tangles.

268 neuropathologically by neuronal vacuoles and neurofibrillary tangles.

269 be associated with increased risk for AD and neurofibrillary tangles.

270 amyloid-beta plaques and tau-immunoreactive neurofibrillary tangles.

271 , but not dementia, AD, neuritic plaques, or neurofibrillary tangles.

272 of pathologic tau aggregates in the form of neurofibrillary tangles.

273 ion of tau, thus leading to the formation of neurofibrillary tangles.

274 We identified 542 proteins in neurofibrillary tangles.

275 ) peptide and the intracellular formation of neurofibrillary tangles.

276 ological hallmarks: amyloid-beta plaques and neurofibrillary tangles.

277 did not demonstrate amyloid-beta plaques or neurofibrillary tangles.

278 d around the blood vessels, and formation of neurofibrillary tangles.

279 are inversely proportional to the number of neurofibrillary tangles.

280 turb cellular interactions and accumulate in neurofibrillary tangles.

281 n the complete absence of amyloid plaques or neurofibrillary tangles.

282 rized by the formation of senile plaques and neurofibrillary tangles.

283 horylated and aggregates into characteristic neurofibrillary tangles.

284 d yeast prion proteins, and Tau, which forms neurofibrillary tangles.

285 ation of hyperphosphorylated tau proteins in neurofibrillary tangles.

286 erphosphorylation that leads to formation of neurofibrillary tangles.

287 rphosphorylation and subsequent formation of neurofibrillary tangles.

288 rment, neuronal dysfunction and formation of neurofibrillary tangles.

289 of the brain to amyloid-beta plaques and tau neurofibrillary tangles.

290 f tau oligomers at the expense of increasing neurofibrillary tangles.

291 aques, cerebral amyloid angiopathy (CAA) and neurofibrillary tangles.

292 onal amyloid-beta protein and tau associated neurofibrillary tangles; and (iv) four common non-Alzhei

293 ising PET radioligand for in vivo imaging of neurofibrillary tau aggregates in AD with minimal off-ta

294 servations establish that the astroglial and neurofibrillary tau pathologies of CTE are phenotypicall

295 (MTL) is the first brain area to succumb to neurofibrillary tau pathology in Alzheimer's disease (AD

296 tion corresponded well with Braak staging of neurofibrillary tau pathology.

297 binding and to compare binding patterns with neurofibrillary tau staging established in neuropatholog

298 gions were consistent with neuropathological neurofibrillary tau staging.

299 N THIS ARTICLE: Post-mortem Braak staging of neurofibrillary tau tangle topographical distribution is

300 lassic Braak staging from in vivo imaging of neurofibrillary tau tangles have not yet been explored.