ライフサイエンスコーパス: neurofibrillary

1 cases also had significantly more Alzheimer neurofibrillary and amyloid-beta plaque pathology.

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

3 The first neurofibrillary cortical lesions in Alzheimer's disease

4 cidation of the etiopathogenic mechanisms of neurofibrillary degeneration and beta-amyloidosis, the t

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

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

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

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

9 which is known to play a crucial role in the neurofibrillary degeneration of Alzheimer's disease.

10 to abnormal hyperphosphorylation of tau and neurofibrillary degeneration via downregulation of tau O

11 of tau and neurofilaments and, consequently, neurofibrillary degeneration.

12 had an extensive topographic distribution of neurofibrillary degeneration.

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

14 plaques of amyloid beta-proteins (Abeta) and neurofibrillary deposits of hyperphosphorylated tau prot

15 interacts with tau in some way to accelerate neurofibrillary disease and induce neurodegeneration.

16 ding protein, tau, is the major component of neurofibrillary inclusions characteristic of Alzheimer's

17 Tau neurofibrillary inclusions were found in only one dog.

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

19 er brainstem, the degree and distribution of neurofibrillary lesions as well as the pattern of cholin

20 Neurofibrillary lesions comprise paired helical and stra

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

22 by neurodegeneration and amyloid plaque and neurofibrillary pathologies.

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

24 Neurofibrillary pathology has a stereotypical progressio

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

26 ut this was offset by an overall increase in neurofibrillary pathology in this age group.

27 ubjects tended to exhibit marginally greater neurofibrillary pathology including tauopathy and Lewy b

28 Neurofibrillary pathology of abnormally hyperphosphoryla

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

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

31 re was evidence that the threshold score for neurofibrillary pathology to cause dementia increased in

32 ed out Braak staging for Alzheimer's disease neurofibrillary pathology using tau protein immunohistoc

33 Neurofibrillary pathology was also detected with Gallyas

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

35 characteristic spatiotemporal progression of neurofibrillary pathology.

36 significantly lower than in neurons lacking neurofibrillary pathology.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

52 Neurofibrillary tangle counts were performed using thiof

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

54 hologically as increased neuritic plaque and neurofibrillary tangle density.

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

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

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

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

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

60 in tau cause familial neurodegeneration and neurofibrillary tangle formation.

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

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

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

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

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

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

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

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

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

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

71 Disease neuritic plaque score and the Braak neurofibrillary tangle score, remained significant predi

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

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

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

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

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

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

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

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

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

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

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

83 -1.34 to -0.04]), less severe and widespread neurofibrillary tangles (beta = -0.77 score units [95% C

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

85 hallmarks: neurotoxic amyloid-beta (Abeta), neurofibrillary tangles (NFT), and extensive cell death.

86 Neurofibrillary tangles (NFT), intracellular inclusions

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

88 e location of fibrillar tau deposits, called neurofibrillary tangles (NFT), matches closely with regi

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

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

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

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

93 by the production of amyloidogenic peptides, neurofibrillary tangles (NFTs) and neurodegeneration.

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

95 Neurofibrillary tangles (NFTs) are a pathological hallma

96 Neurofibrillary tangles (NFTs) are one of the pathologic

97 Neurofibrillary tangles (NFTs) are the pathological hall

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

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

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

101 formed by beta-amyloid peptides (Abeta) and neurofibrillary tangles (NFTs) formed by hyperphosphoryl

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

103 Neurofibrillary tangles (NFTs) in Alzheimer disease and

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

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

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

107 Neurofibrillary tangles (NFTs) were counted in four brai

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

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

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

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

112 Neurofibrillary tangles (NFTs), composed of truncated an

113 Neurofibrillary tangles (NFTs), hippocampal sclerosis, l

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

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

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

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

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

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

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

121 cal hallmarks of Alzheimer's disease (AD) is neurofibrillary tangles (NFTs), which are composed of ab

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

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

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

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

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

127 Neurofibrillary tangles advance from layer II of the ent

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

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

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

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

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

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

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

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

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

137 ody), an early precursor to the formation of neurofibrillary tangles and neurodegeneration of the kin

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

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

140 ntracellular aggregation and accumulation as neurofibrillary tangles and neuropil treads.

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

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

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

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

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

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

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

148 loidosis, familial Danish dementia, in which neurofibrillary tangles coexist with extensive pre-amylo

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

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

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

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

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

154 amyloid-beta (Abeta)-containing plaques and neurofibrillary tangles composed of hyperphosphorylated

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

156 many frontotemporal dementias (FTDs) contain neurofibrillary tangles comprised of hyperphosphorylated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 beta-amyloid (Abeta) protein deposits and/or neurofibrillary tangles in association with progressive

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

174 which can further condense into higher order neurofibrillary tangles in neurons.

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

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

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

178 cally by the abundance of senile plaques and neurofibrillary tangles in the brain.

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

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

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

182 reamyloid deposits, severe CAA, and abundant neurofibrillary tangles in the presence of remarkably fe

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

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

185 Accumulation of tau into neurofibrillary tangles is a pathological consequence of

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

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

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

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

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

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

192 amyloid beta plaques, neuritic plaques, and neurofibrillary tangles observed in cortical biopsies ob

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

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

195 ques and intracellular inclusions containing neurofibrillary tangles of phospho-Tau and intraneuronal

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

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

198 n Parkinson's disease (PD) and is present in neurofibrillary tangles or Lewy bodies.

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

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

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

202 Amyloid plaques and neurofibrillary tangles simultaneously accumulate in Alz

203 sclerosis can cause the neuritic plaques and neurofibrillary tangles that define Alzheimer neuropatho

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

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

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

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

208 opil threads and of neurofibrillary tangles: neurofibrillary tangles were sparse in brains that had n

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

230 and progressively develops amyloid plaques, neurofibrillary tangles, and synaptic dysfunction.

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

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

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

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

235 Neurofibrillary tangles, composed of hyperphosphorylated

236 Neurofibrillary tangles, composed of insoluble aggregate

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

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

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

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

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

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

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

244 Neuropathologic outcomes included neurofibrillary tangles, neuritic plaques, microinfarcts

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

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

247 dementia, characterized by amyloid plaques, neurofibrillary tangles, neuroinflammation, and neuronal

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

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

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 with AD, including measures of amyloid load, neurofibrillary tangles, reactive astrocytes, and activa

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

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

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

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

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

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

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

260 in vivo imaging of beta-amyloid plaques and neurofibrillary tangles, were obtained from 12 AD patien

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

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

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

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

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

266 ) peptide and the intracellular formation of neurofibrillary tangles.

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

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

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

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

271 are inversely proportional to the number of neurofibrillary tangles.

272 turb cellular interactions and accumulate in neurofibrillary tangles.

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

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

275 horylated and aggregates into characteristic neurofibrillary tangles.

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

277 ation of hyperphosphorylated tau proteins in neurofibrillary tangles.

278 erphosphorylation that leads to formation of neurofibrillary tangles.

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

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

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

282 undant neuronal tau inclusions that resemble neurofibrillary tangles.

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

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

285 erphosphorylated tau, the major component of neurofibrillary tangles.

286 f beta-amyloid (Abeta) plaques and tau-laden neurofibrillary tangles.

287 ulation of beta-amyloid (Abeta) peptides and neurofibrillary tangles.

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

289 associated pathology of amyloid plaques and neurofibrillary tangles.

290 europathologic markers of senile plaques and neurofibrillary tangles.

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

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

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

294 tween the numbers of neuropil threads and of neurofibrillary tangles: neurofibrillary tangles were sp

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

296 r disease (AD) and abnormally accumulates as neurofibrillary tangles; therefore, the pathways by whic

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

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

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.