ライフサイエンスコーパス: neurofibrillary tangle

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

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

3 europathologic markers of senile plaques and neurofibrillary tangles.

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

5 neuropathologically by neuronal vacuoles and neurofibrillary tangles.

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

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

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

9 ) peptide and the intracellular formation of neurofibrillary tangles.

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

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

12 We identified 542 proteins in neurofibrillary tangles.

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

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

15 are inversely proportional to the number of neurofibrillary tangles.

16 turb cellular interactions and accumulate in neurofibrillary tangles.

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

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

19 horylated and aggregates into characteristic neurofibrillary tangles.

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

21 ation of hyperphosphorylated tau proteins in neurofibrillary tangles.

22 erphosphorylation that leads to formation of neurofibrillary tangles.

23 e in the formation of Alzheimer's-associated neurofibrillary tangles.

24 es, loss of neurons, and the accumulation of neurofibrillary tangles.

25 undant neuronal tau inclusions that resemble neurofibrillary tangles.

26 o those formed by tau protein in Alzheimer's neurofibrillary tangles.

27 rphosphorylation and subsequent formation of neurofibrillary tangles.

28 rment, neuronal dysfunction and formation of neurofibrillary tangles.

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

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

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

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

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

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

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

36 ation of paired helical filaments (PHFs) and neurofibrillary tangles, a key neuropathological feature

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

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

39 Neurofibrillary tangles advance from layer II of the ent

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

41 1204) showed a sex-specific association with neurofibrillary tangles among males (P = 2.5 x 10-8) but

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

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

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

45 euritic plaque, paired helical filaments tau neurofibrillary tangle and cerebral amyloid angiopathy r

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

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

48 es, which are proposed to contribute to both neurofibrillary tangles and amyloid plaque formation.

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

50 is pathologically characterized by tau-laden neurofibrillary tangles and beta-amyloid deposits.

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

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

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

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

55 In Alzheimer disease (AD), deposition of neurofibrillary tangles and loss of synapses in the neoc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

70 ory, even after adjusting for Abeta plaques, neurofibrillary tangles, and APOE epsilon4.

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

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

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

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

75 mulation of phosphorylated tau, formation of neurofibrillary tangles, and eventual neurodegeneration.

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

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

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

79 ells and patient brains accumulate less tau, neurofibrillary tangles, and neuritic plaques, respectiv

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

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

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

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

84 Neurofibrillary tangles are a pathological hallmark of A

85 We show that neurofibrillary tangles are neither sufficient nor requi

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

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

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

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

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

91 ase domain-containing 6 expression ceases in neurofibrillary tangle-bearing pyramidal cells.

92 -1.34 to -0.04]), less severe and widespread neurofibrillary tangles (beta = -0.77 score units [95% C

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

108 ining the amyloid-beta (Abeta) peptides, and neurofibrillary tangles composed of hyperphosphorylated

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

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

111 Neurofibrillary tangles, composed of hyperphosphorylated

112 Neurofibrillary tangles, composed of insoluble aggregate

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

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

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

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

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

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

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

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

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

122 By comparison with typical AD, neurofibrillary tangle counts per 0.125 mm(2) in hippoca

123 Neurofibrillary tangle counts were performed using thiof

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

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

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

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

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

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

130 otective mechanisms, such as the presence of neurofibrillary tangles, disconnection, as well as compe

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

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

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

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

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

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

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

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

139 in tau cause familial neurodegeneration and neurofibrillary tangle formation.

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

141 Neurofibrillary tangles, formed of misfolded, hyperphosp

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

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

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

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

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

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

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

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

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

151 s with the neurotoxicity of Tau, which forms neurofibrillary tangles in AD.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

170 assessed the density and the distribution of neurofibrillary tangles in three cortical regions and tw

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

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

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

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

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

176 ntracellular tau to promote the formation of neurofibrillary tangle-like aggregates.

177 Neurofibrillary tangles likely cause neurodegeneration i

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

179 ar plaques of amyloid-beta and intraneuronal neurofibrillary tangles made from tau are the histopatho

180 eptide forming extracellular senile plaques, neurofibrillary tangles made of hyperphosphorylated tau

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

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

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

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

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

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

187 Neuropathologic outcomes included neurofibrillary tangles, neuritic plaques, microinfarcts

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

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

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

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

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

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

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

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

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

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

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

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

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

201 Neurofibrillary tangles (NFT), intracellular inclusions

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

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

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

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

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

207 cterized by brain pathology of intracellular neurofibrillary tangles (NFTs) and extracellular amyloid

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

209 Neurofibrillary tangles (NFTs) are a pathological hallma

210 Neurofibrillary tangles (NFTs) are the pathological hall

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

212 Neurofibrillary tangles (NFTs) composed of hyperphosphor

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

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

215 dicated the nApoE4CF Ab specifically labeled neurofibrillary tangles (NFTs) in AD frontal cortex sect

216 Neurofibrillary tangles (NFTs) in Alzheimer disease and

217 a microtubule-associated protein that forms neurofibrillary tangles (NFTs) in the selective vulnerab

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

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

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

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

222 Neurofibrillary tangles (NFTs) were counted in four brai

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

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

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

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

227 er's disease (AD), senile plaques (SPs), and neurofibrillary tangles (NFTs), but the specific contrib

228 Neurofibrillary tangles (NFTs), composed of truncated an

229 Neurofibrillary tangles (NFTs), hippocampal sclerosis, l

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

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

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

233 Aggregated tau is the major component of neurofibrillary tangles (NFTs), structures present in th

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

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

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

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

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

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

240 her brain weight (BW) and Alzheimer lesions (neurofibrillary tangles [NFTs] or neuritic plaques [NPs]

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

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

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

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

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

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

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

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

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

250 Neurofibrillary tangles, one of the hallmarks of Alzheim

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

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

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

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

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

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

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

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

259 Calignon et al. recreated an early stage of neurofibrillary tangle pathology to show that tau aggreg

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

275 Amyloid plaques and neurofibrillary tangles simultaneously accumulate in Alz

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

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

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

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

280 AD cases with a Braak neurofibrillary tangle stage of more than IV were identi

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

282 acceleration was associated with high Braak neurofibrillary tangle stage.

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

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

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

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

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

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

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

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

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

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

293 defined on the basis of the distribution of neurofibrillary tangles: typical AD, hippocampal-sparing

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

295 eimer's disease are amyloid-beta plaques and neurofibrillary tangles, which are primarily composed of

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

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

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

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

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