ライフサイエンスコーパス: NFT

1 NFT accumulation is thought to be closely linked to cogn

2 NFT and AT8 (or Alz-50) immunostaining in cholinergic nu

3 NFT burden correlates with cognitive decline and neurode

4 NFT burden in the left orbitofrontal cortex across all 3

5 NFT deposition, vascular lesions, and high NPC scorewere

6 NFT-like inclusions were first detected in Tg mice at 18

7 NFTs contain aberrantly hyperphosphorylated Tau as paire

8 NFTs identical to those found in AD brains have also bee

9 NFTs in the substantia nigra are associated with gait im

10 NFTs result from the intracellular aggregation of abnorm

11 NFTs, such as JTH and GPT, may have utility for predicti

12 brain cortex homogenates containing abundant NFTs but bound poorly to amyloid plaque-rich, NFT-poor A

13 ificantly, the presence of Abeta accelerated NFT formation and enhanced tau amyloidosis; however, tau

14 ced tau inclusions more closely resembled AD NFTs because they were Thioflavin S positive, acetylated

15 Also, NFTs developed slower in the CBF compared with previousl

16 o acids (PALLREAENFTLFIKNS) that includes an NFT consensus sequence for N-linked glycosylation.

17 r RFS rate is 42% and 36% for the IP 32P and NFT groups, respectively; the difference is not statisti

18 tream signaling levels relative to Abeta and NFT pathology were evaluated using biochemistry and hist

19 relationship between caspase activation and NFT formation, double-labeling experiments with fodrin C

20 Aberrant motor behavior and NFT density in the left orbitofrontal cortex showed a si

21 e in regulating Tau hyperphosphorylation and NFT formation in vivo.

22 AD and may play a role in neuronal loss and NFT pathology.

23 2 inhibitor) blocked Tau phosphorylation and NFT formation in these WOX1 knock-down cells.

24 ly beneficial role of tau polymerization and NFT formation.

25 t that GSK-3alpha contributes to both SP and NFT pathogenesis while GSK-3beta only modulates NFT form

26 h agitation scores (r = 0.41, p < 0.015) and NFTs correlated significantly (r = 0.66, p = 0.004) with

27 nderlying the formation of tau filaments and NFTs in tauopathies remain unclear.

28 cognitive phenotype in mice with plaques and NFTs.

29 e models of SPs (PDAPP(+)/(-)), both SPs and NFTs (PDAPP(+)/(-);PS19(+)/(-)), or wild-type controls.

30 ermines the localization and load of SPs and NFTs in vivo in AD patients.

31 behavioral impairments linked to AD SPs and NFTs.

32 uestionnaires, nerve conduction studies, and NFTs, including the Jebsen Test of Hand Function (JTH) a

33 ation of Tau, GSK-3beta, and ERK, as well as NFT formation, was observed in the AD hippocampi.

34 ular system that robustly develops authentic NFT-like Tau aggregates, which provides mechanistic insi

35 pffs alone are capable of inducing authentic NFT-like tau aggregates and initiating spreading of tau

36 suggest that there is an association between NFT formation and the activation of apoptotic pathways i

37 ease (AD); however, the relationship between NFTs and disease progression remains controversial.

38 ecline, but the precise relationship between NFTs and neuronal death and downstream mechanisms of cel

39 ggesting high tracer selectivity for binding NFTs in vivo.

40 Braak NFT stage and the presence of neuritic plaques were not

41 Braak NFT stage, brain weight and presence of vascular patholo

42 d between rates of brain loss and age, Braak NFT stage, and change over time in cognitive measures.

43 LBD, and this effect is independent of Braak NFT stage or extent of neuritic plaque disease.

44 CAA, but has no independent effect on Braak NFT stage.

45 though this disease is also characterized by NFT formation and cell death.

46 ed a total of 155 proteins in laser captured NFT's, 72 of which were identified by multiple unique pe

47 , whereas apathy and left anterior cingulate NFTs showed a significant relationship only for the enti

48 Left anterior cingulate NFTs, although not within our hypotheses, also showed a

49 of the cells with active caspases contained NFTs.

50 Y279/216 was observed in neurons containing NFTs and granulovacuolar degeneration (GVD), but not in

51 olling for age, sex, education, and cortical NFTs, nigra NFTs were related to gait impairment (p < 0.

52 olling for age, sex, education, and cortical NFTs.

53 ant form of tau (P301L) and develop cortical NFTs by the age of 7-8 mo (10).

54 y and the optical disector was used to count NFTs.

55 features of neuronal system deafferentation, NFT progression and propagation, and neuronal loss.

56 sal hippocampus causes cognitive deficiency, NFTs-like pathological changes, and oxidative stress as

57 se with an antemortem diagnosis of dementia, NFTs had the strongest associations with BW and with CF,

58 c and nontransgenic mice that do not develop NFT pathology.

59 from P301L tau transgenic mice that develop NFTs to four-repeat wild-type (4RWT) tau transgenic and

60 e absence of mouse tau (htau mice) developed NFTs and extensive cell death.

61 rhinal cortex are among the first to display NFTs, indicating its compromise in early stages of AD.

62 d tau posttranslational modifications during NFT evolution within the CBF neurons of the nucleus basa

63 and biochemical features of oligomers during NFT development in AD brain.

64 nase 3beta (GSK-3beta) and ERK, and enhanced NFT formation.

65 A/AD group showed predominance of entorhinal NFT typical of the amnestic dementia of the Alzheimer ty

66 venting NFT formation or disrupting existing NFTs (7, 8).

67 As expected, NFTs and Abeta plaques were significantly increased in A

68 hesus monkeys, which do not natively express NFTs.

69 contrast, primary sensory cortices have few NFTs, even in late-stage disease.

70 o brain regions with a plausible pattern for NFT deposition in AD subjects.

71 perform a genome-wide association study for NFT pathologic burden and report the association of the

72 evaluate tracer affinity and selectivity for NFTs.

73 s within NB cholinergic neurons before frank NFT deposition.

74 itive; these resembled extracellular 'ghost' NFT.

75 ant motor behavior are correlates of greater NFT pathology in the orbitofrontal cortex in AD, whereas

76 reas increasing apathy may relate to greater NFT burden in the anterior cingulate.

77 loss-of-function toxicity in cells harboring NFTs.

78 More GSK3 immunoreactive NFTs were detected in TAPP than JNPL3 mice, especially i

79 ggest that the pY216 GSK3beta accumulates in NFT and GVD due to redistribution rather than increased

80 d concentration of phospho-tau at Ser-214 in NFTs.

81 and accumulation of fibrillar aggregates in NFTs mediates neurodegeneration underlies most current t

82 de direct evidence on the identity of NFs in NFTs by immunochemical and mass spectrometric analysis.

83 n debate that the identity of NF proteins in NFTs is due to the cross-reactivity of phosphorylated NF

84 al impairments, leading to tau truncation in NFTs.

85 s can cause neurodegeneration and can induce NFT-like inclusions in cultured neuronal cells and in tr

86 To recapitulate age-induced NFT formation in a mouse model, we examined 12- to 24-mo

87 cts with cytoskeletal components and induces NFT-like inclusions containing phosphorylated tau and ph

88 staining revealed that OA treatment induces NFTs-like conformational changes in both the cortex and

89 s post-translational modifications influence NFT formation, the molecular mechanisms responsible for

90 ZCWPW1 AD susceptibility variant influences NFT accumulation and that this effect is mediated by an

91 version of highly soluble Tau into insoluble NFTs remain elusive.

92 We have purified sarkosyl-insoluble NFTs and performed liquid chromatography/tandem mass spe

93 es, which provides mechanistic insights into NFT pathogenesis and a potential tool for identifying Ta

94 ons in primates, crossing the threshold into NFTs and degeneration in humans.

95 s and cultured neurons, induce intracellular NFT-like inclusions in neurons.

96 clinical diagnosis of AD and severe AD-like NFTs.

97 eta) plaques and neuronal and synaptic loss, NFTs constitute the primary pathological hallmarks of Al

98 pathogenesis while GSK-3beta only modulates NFT formation, suggesting common but also different targ

99 At 24 months, NFTs progress, tau inclusions propagate to the dentate g

100 on revealed extensive limbic and neocortical NFT formation and neuritic plaques consistent with a Bra

101 ubgroup examined quantitatively, neocortical NFTs were more numerous in the left hemisphere of PPA/AD

102 ge, sex, education, and cortical NFTs, nigra NFTs were related to gait impairment (p < 0.001), but no

103 ne parkinsonian signs as a function of nigra NFTs, controlling for age, sex, education, and cortical

104 Substantia nigra NFTs were present in 67 of 86 persons (77.9%).

105 FTD), furazolidone (FZD) and nitrofurantoin (NFT).

106 one (AHD), the metabolite of Nitrofurantoin (NFT).

107 is was significantly mediated by BW, and not NFTs or NPs.

108 This novel NFT staging scheme provides new insights into the mechan

109 With the novel technique of observing NFTs and caspase activation in the living brain, we demo

110 The inconsistent concordance of NFT distribution with the asymmetric atrophy and the non

111 tative analysis showed that as the extent of NFT formation increased, there was a significant corresp

112 regated tau species, before the formation of NFT, is associated with the development of functional de

113 g that cell death can occur independently of NFT formation.

114 nding repeats resulted in rapid induction of NFT-like inclusions that propagated from injected sites

115 hyperphosphorylated tau, while the level of NFT-related neuronal loss was low in AD.

116 Abeta plaque load, but not with measures of NFT.

117 NFTs, can be reversed in an animal model of NFT-associated toxicity, providing proof in principle th

118 eposition, and (2) the process or product of NFT formation in Tau mice is sufficient to deleteriously

119 Progression of NFT pathology is closely correlated with both increased

120 d chromatography/tandem mass spectrometry of NFT tryptic digests.

121 ase in the formation and/or stabilization of NFT and paired helical filaments and provide a model sys

122 Only a small subset of NFT were 6-CN-PiB positive; these resembled extracellula

123 The significance of the accumulation of NFTs for neuronal and cognitive function is still obscur

124 e to stage the emergence and accumulation of NFTs with advancing age.

125 ated tau species but not the accumulation of NFTs.

126 erphosphorylated tau, a primary component of NFTs.

127 as some of the neural system consequences of NFTs, can be reversed in an animal model of NFT-associat

128 The primary constituent of NFTs is a hyperphosphorylated form of the microtubule-bi

129 MAPT H1 associated with lower counts of NFTs in the middle frontal (p<0.001) and inferior pariet

130 Notably, the development of NFTs followed a spatiotemporal Braak-like pattern simila

131 ition is thought to precede the formation of NFTs in AD, the molecular steps connecting these two pat

132 uble aggregates, leading to the formation of NFTs in Alzheimer's disease and progressive supranuclear

133 We recently studied the formation of NFTs in the entorhinal cortex (EC) and their subsequent

134 Consistent with the formation of NFTs, immunoblots indicated an age-dependent transition

135 in rTg4510 mice results in the formation of NFTs, learning and memory impairment and massive neurona

136 tion of transglutaminase in the formation of NFTs, we compared the levels of cross-linked tau protein

137 e of tau oligomers in the natural history of NFTs, and they highlight the suitability of tau oligomer

138 Thus, PET imaging of NFTs not only holds promise as a diagnostic tool but als

139 ata are the first proteomic investigation of NFTs.

140 we find that the early pathological loci of NFTs in CTE brains are regions of high deformation durin

141 that GAPDH co-localized with the majority of NFTs as well as plaque-like structures in AD brain and w

142 sociates with both early and late markers of NFTs and is correlated with cognitive decline.

143 r protein) and tau and reduced the number of NFTs and extracellular deposits of Abeta associated with

144 ate that NF proteins are an integral part of NFTs in AD brains.

145 een shown immunohistologically to be part of NFTs, there has been debate that the identity of NF prot

146 The phosphoproteomics of NFTs clearly identified NF-M phosphopeptides SPVPKS*PVEE

147 The presence of NFTs in the forebrain is associated with impairments of

148 These data suggest that propagation of NFTs, as well as some of the neural system consequences

149 PET tracer for the in vivo quantification of NFTs in AD patients.

150 was followed by the formation and spread of NFTs and NTs, likely through secondary seeding events.

151 rvival rate of patients who underwent cRT or NFT was, respectively, 91% (95% CI, 84% to 99%) and 95%

152 sponding matched control preparations of PHF/NFTs, none of these phosphorylated neuronal cytoskeletal

153 tion of tau oligomers but not phosphorylated NFTs or monomeric tau.

154 yed decreased inflammation, amyloid plaques, NFTs, cell death, and an extended life by 2 mo.

155 ositive, TOC-1-positive, and Tau C3-positive NFT densities were unchanged, whereas only AT8-positive

156 ution of Gallyas-positive and Alz50-positive NFTs, and abrogation of progressive neuronal loss.

157 th tau hyperphosphorylation, and potentially NFTs formation.

158 t therapeutic strategies aimed at preventing NFT formation or disrupting existing NFTs (7, 8).

159 may prove beneficial not only in preventing NFT formation, but also in slowing cognitive decline.

160 tiotemporal mapping paradigm for progressive NFT accumulation is urgently needed to stage disease pro

161 methods such as SUVR can be used to quantify NFT binding.

162 au variant developed progressive age-related NFTs, neuronal loss, and behavioral impairments.

163 e Tau into filamentous inclusions resembling NFTs with unprecedented efficiency, suggesting a "seedin

164 ielschowsky silver method in order to reveal NFTs and 'ghost' tangles, ii) single-stained with anti-A

165 FTs but bound poorly to amyloid plaque-rich, NFT-poor AD brain homogenates.

166 cation of high affinity and highly selective NFT ligands, and recent progress in the clinical develop

167 ron numbers stabilized, but to our surprise, NFTs continued to accumulate.

168 ive determination of neurofibrillary tangle (NFT) density.

169 ropathology, but not neurofibrillary tangle (NFT) deposition.

170 have been linked to neurofibrillary tangle (NFT) formation in several neurodegenerative diseases kno

171 accumulation drives neurofibrillary tangle (NFT) formation in several neurodegenerative diseases.

172 phosphorylation and neurofibrillary tangle (NFT) formation in vivo, the molecular link associating A

173 plaque deposits and neurofibrillary tangle (NFT) formation, resulting in cognitive impairment.

174 ccur with respect to neurofibrillary tangle (NFT) formation.

175 to Abeta plaque and neurofibrillary tangle (NFT) pathology during disease onset is unknown.

176 d and tau-containing neurofibrillary tangle (NFT) pathology during the onset of Alzheimer's disease (

177 Neurofibrillary tangle (NFT) pathology was first observed in the neocortex and p

178 oprotein E genotype, neurofibrillary tangle (NFT) pathology, and vascular lesion burden were determin

179 amination (MMSE) and neurofibrillary tangle (NFT) scores across all 31 subjects regardless of diagnos

180 The study used Braak neurofibrillary tangle (NFT) stage, frequency of neuritic plaques, and LBD stage

181 ted with lower Braak neurofibrillary tangle (NFT) stages and possibly fewer neuritic plaques, but has

182 ks and the number of neurofibrillary tangle (NFT)-containing neurons in neocortex and hippocampus.

183 escence to identify neurofibrillary tangles (NFT) and two tau antibodies (AT8, Alz-50) to identify pr

184 Neurofibrillary tangles (NFT) containing tau are a hallmark of neurodegenerative

185 yloid-beta (Abeta), neurofibrillary tangles (NFT), and extensive cell death.

186 and tau-containing neurofibrillary tangles (NFT), has not been thoroughly investigated.

187 Neurofibrillary tangles (NFT), intracellular inclusions of abnormal fibrillar for

188 aques or tau-filled neurofibrillary tangles (NFT), is considered the most predictive pathological fea

189 au deposits, called neurofibrillary tangles (NFT), matches closely with regions of massive neuronal d

190 amyloid plaques and neurofibrillary tangles (NFT), the two hallmark lesions of Alzheimer's disease (A

191 (Abeta) plaques and neurofibrillary tangles (NFT).

192 n of tau protein in neurofibrillary tangles (NFTs) (1, 2).

193 and distribution of neurofibrillary tangles (NFTs) and amyloid-rich neuritic plaques.

194 r quantification of neurofibrillary tangles (NFTs) and diffuse and neuritic plaques.

195 tide in propagating neurofibrillary tangles (NFTs) and eventual cognitive impairment in AD.

196 gy of intracellular neurofibrillary tangles (NFTs) and extracellular amyloid plaques.

197 oidogenic peptides, neurofibrillary tangles (NFTs) and neurodegeneration.

198 dence suggests that neurofibrillary tangles (NFTs) and neuronal cell loss are prominent features of A

199 s (NP tau), AD-like neurofibrillary tangles (NFTs) and neuropil threads (NTs).

200 Neurofibrillary tangles (NFTs) are a characteristic neuropathological feature of

201 Neurofibrillary tangles (NFTs) are a pathological hallmark of Alzheimer's disease

202 Neurofibrillary tangles (NFTs) are a pathological hallmark of Alzheimer's disease

203 Neurofibrillary tangles (NFTs) are a pathological hallmark of many neurodegenerat

204 Neurofibrillary tangles (NFTs) are composed of abnormal aggregates of the cytoske

205 e plaques (SPs) and neurofibrillary tangles (NFTs) are hallmark pathologies accompanying the neurodeg

206 inclusions such as neurofibrillary tangles (NFTs) are neuropathological hallmarks of Alzheimer's dis

207 Neurofibrillary tangles (NFTs) are one of the pathological hallmarks of AD that h

208 at substantia nigra neurofibrillary tangles (NFTs) are related to parkinsonian signs in older persons

209 Neurofibrillary tangles (NFTs) are the most common intraneuronal inclusion in the

210 Neurofibrillary tangles (NFTs) are the pathological hallmark of neurodegenerative

211 Neurofibrillary tangles (NFTs) composed of hyperphosphorylated and misfolded tau

212 s very distinctive: neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau selectively af

213 es characterized by neurofibrillary tangles (NFTs) comprising filamentous tau protein.

214 cal neurons develop neurofibrillary tangles (NFTs) consisting of hyperphosphorylated tau.

215 amyloid (Abeta) and neurofibrillary tangles (NFTs) consisting of modified tau.

216 NB) neurons display neurofibrillary tangles (NFTs) during Alzheimer's disease (AD) progression, yet t

217 eptides (Abeta) and neurofibrillary tangles (NFTs) formed by hyperphosphorylated tau, a microtubule-a

218 amyloid plaques and neurofibrillary tangles (NFTs) in AD brains; however, its role in the pathogenesi

219 pecifically labeled neurofibrillary tangles (NFTs) in AD frontal cortex sections that colocalized wit

220 Neurofibrillary tangles (NFTs) in Alzheimer disease and related tauopathies are c

221 ajor constituent of neurofibrillary tangles (NFTs) in Alzheimer's brain, undergoes site-selective nit

222 amyloid plaques and neurofibrillary tangles (NFTs) in Alzheimer's disease (AD) brains, but its role i

223 Accumulation of neurofibrillary tangles (NFTs) in Alzheimer's disease correlates with neuronal lo

224 to the formation of neurofibrillary tangles (NFTs) in the neurons of Alzheimer's disease (AD).

225 protein that forms neurofibrillary tangles (NFTs) in the selective vulnerable long projection neuron

226 osphorylated tau in neurofibrillary tangles (NFTs) is a neuropathological hallmark of tauopathies, in

227 aggregation to form neurofibrillary tangles (NFTs) is closely related to progression of neurodegenera

228 oteomic analysis of neurofibrillary tangles (NFTs) obtained by laser capture microdissection from pyr

229 s, characterized by neurofibrillary tangles (NFTs) of phosphorylated tau proteins, are a group of neu

230 and the presence of neurofibrillary tangles (NFTs) of the protein tau in patients' brains.

231 Neurofibrillary tangles (NFTs) were counted in four brain regions, senile plaques

232 ocortical spread of neurofibrillary tangles (NFTs) with clinical AD disease progression offers an opp

233 Neurofibrillary tangles (NFTs), a marker of neuronal alterations in Alzheimer's d

234 ive neurons, PHFtau neurofibrillary tangles (NFTs), and Abeta plaque burden in the subiculum in AD an

235 f neuritic plaques, neurofibrillary tangles (NFTs), and vascular brain injury (VBI).

236 , which form before neurofibrillary tangles (NFTs), are the true neurotoxic tau entities in neurodege

237 plaques (SPs), and neurofibrillary tangles (NFTs), but the specific contributions of each of the GSK

238 Neurofibrillary tangles (NFTs), composed of truncated and hyperphosphorylated tau

239 Neurofibrillary tangles (NFTs), consisting of abnormally hyperphosphorylated tau,

240 Neurofibrillary tangles (NFTs), hippocampal sclerosis, lacunar infarcts, hyaline

241 e appearance of the neurofibrillary tangles (NFTs), intracellular fibrous aggregates of the microtubu

242 amyloid plaques and neurofibrillary tangles (NFTs), it has been reported that cyclin-dependent kinase

243 that accumulates in neurofibrillary tangles (NFTs), most commonly in Alzheimer's disease (AD) and pri

244 The formation of neurofibrillary tangles (NFTs), oxidative stress and neuroinflammation have emerg

245 major component of neurofibrillary tangles (NFTs), structures present in the brains of people affect

246 es characterized by neurofibrillary tangles (NFTs), the predominant tau pathology in Alzheimer diseas

247 tau aggregates and neurofibrillary tangles (NFTs), which are associated in AD and tauopathies.

248 r's disease (AD) is neurofibrillary tangles (NFTs), which are composed of abnormally hyperphosphoryla

249 is the presence of neurofibrillary tangles (NFTs), which are intracellular aggregates of conformatio

250 tracer for imaging neurofibrillary tangles (NFTs).

251 s and intracellular neurofibrillary tangles (NFTs).

252 amyloid plaques and neurofibrillary tangles (NFTs).

253 luble filaments and neurofibrillary tangles (NFTs).

254 hological hallmark: neurofibrillary tangles (NFTs).

255 sed in neurons with neurofibrillary tangles (NFTs).

256 ed tau protein into neurofibrillary tangles (NFTs).

257 s of silver-stained neurofibrillary tangles (NFTs).

258 phorylated tau into neurofibrillary tangles (NFTs).

259 ere associated with neurofibrillary tangles (NFTs).

260 Alzheimer lesions (neurofibrillary tangles [NFTs] or neuritic plaques [NPs]) mediate the association

261 ta (Abeta) and Tau (neurofibrillary tangles, NFTs) deposition in the brain.

262 AT8 stains pre-tangles, NFTs and extracellular 'ghost' tangles due to the recogn

263 l of tauopathy (rTg4510) have suggested that NFT formation can be dissociated from memory loss and ne

264 It is possible that NFTs disrupt synaptic transmission and plasticity, leadi

265 This suggests that NFTs are not the major neurotoxic tau species, at least

266 ase-3beta and subsequently recognized by the NFT antibody PHF-1.

267 he IP 32P group (65%) and 63 patients in the NFT group (64%) have developed tumor recurrence.

268 e cellular origin and the consequence of the NFT formation are poorly understood.

269 ribe the preclinical characterization of the NFT PET tracer (18)F-MK-6240.

270 transgene expression with doxycycline on the NFT-associated pathological features of neuronal system

271 field normalisation approaches, and show the NFT can yield an effective model of the laser radiation

272 As it enters each zone, the NFT concentration adapts to the local electric field in

273 The NFTs were immunopositive, with multiple tau antibodies,

274 mCi IP 32P (n = 104) or no further therapy (NFT; n = 98).

275 Thus, NFTs are not sufficient to cause cognitive decline or ne

276 he relative risk of death is 0.85 (IP 32P to NFT) (90% CI, 0.62 to 1.16).

277 lative risk of recurrence is 0.90 (IP 32P to NFT) (90% confidence interval [CI], 0.68 to 1.19).

278 r of various signaling pathways that lead to NFT formation and membrane dysfunction in a subgroup of

279 r an evaluation of genetic susceptibility to NFT, a common end point for multiple different pathologi

280 D (CatD), a marker of neurons vulnerable to NFT pathology.

281 le binding protein, not only co-localized to NFTs and immunoprecipitated with PHF-tau, but also is on

282 This nonfocusing tracer (NFT) migrates through multiple isotachophoresis zones.

283 nstrate how the Nonlinear Fourier transform (NFT) based on the Zakharov-Shabat spectral problem can b

284 ve cRT over the LNM or no further treatment (NFT).

285 s as a highly plausible mechanism underlying NFT formation in vivo.

286 Unexpectedly, NFT-bearing neurons in the visual cortex appeared to be

287 rkers developed an effective and widely used NFT staging paradigm for human AD brains.

288 in the aged nonhuman primate brain, whereas NFT are found almost exclusively in humans.

289 gation of tau and neurodegeneration, whether NFTs per se contribute to neuronal and network dysfuncti

290 observed in regions commonly associated with NFT deposition in AD subjects.

291 pproximately 2-4) in regions associated with NFT deposition, whereas in HE subjects, SUVR was approxi

292 multiple neuropathologies that coexist with NFT and found suggestive evidence that certain loci may

293 orization indices negatively correlated with NFT densities while no significant correlations were fou

294 s in the subiculum and the correlations with NFT densities respectively suggest that deafferentation

295 The association of PTPRD with NFT is not dependent on the accumulation of amyloid path

296 bjects and was significantly associated with NFTs.

297 , 63 had previously unknown association with NFTs; one of these was glyceraldehyde-3-phosphate dehydr

298 mino-terminal fragment that localizes within NFTs of the AD brain.

299 difference between animals with and without NFTs in the level of total, inactive, or Y216-phosphoryl

300 ely decreased in the neurons with or without NFTs in PSP cases.