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 and Pick-body-like neuronal lesions occurred in the

4 NFT burden correlates with cognitive decline and neurode

5 NFT burden in the left orbitofrontal cortex across all 3

6 NFT deposition, vascular lesions, and high NPC scorewere

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

8 NFTs contain aberrantly hyperphosphorylated Tau as paire

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

10 NFTs in the substantia nigra are associated with gait im

11 NFTs result from the intracellular aggregation of abnorm

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

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

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

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

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

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

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

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

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

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

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

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

24 n the activation of apoptotic mechanisms and NFT formation in AD was investigated using a caspase-cle

25 2 inhibitor) blocked Tau phosphorylation and NFT formation in these WOX1 knock-down cells.

26 ly beneficial role of tau polymerization and NFT formation.

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

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

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

30 cognitive phenotype in mice with plaques and NFTs.

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

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

33 behavioral impairments linked to AD SPs and NFTs.

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

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

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

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

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

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

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

41 a42 immunoreactivity appears to precede both NFT and Abeta plaque deposition.

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

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

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

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

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

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

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

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

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

51 of the cells with active caspases contained NFTs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

70 hesus monkeys, which do not natively express NFTs.

71 The brainstem in PSP has extensive NFT pathology, whereas the frontal cortex and cerebellum

72 ed microglia, dystrophic neurites, and a few NFTs.

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

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

75 evaluate tracer affinity and selectivity for NFTs.

76 s within NB cholinergic neurons before frank NFT deposition.

77 itive; these resembled extracellular 'ghost' NFT.

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

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

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

81 ative to normal CA1 neurons, those harboring NFTs in AD brains showed significant reductions in sever

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

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

84 ions in tau mRNA isoform expression occur in NFT-vulnerable regions in this disease.

85 Because cathepsin D mRNA was upregulated in NFT-bearing CA1 neurons in AD brains, we performed immun

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

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

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

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

90 al impairments, leading to tau truncation in NFTs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

106 Areas with the most NFT had reactive gliosis.

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

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

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

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

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

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

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

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

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

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

117 age- and gene-dose-dependent development of NFT.

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

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

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

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

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

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

124 redoxin, utrophin) may be novel mediators of NFT formation or degeneration in affected neurons.

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

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

127 Progression of NFT pathology is closely correlated with both increased

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

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

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

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

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

133 ated tau species but not the accumulation of NFTs.

134 erphosphorylated tau, a primary component of NFTs.

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

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

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

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

139 flect mechanisms underlying the formation of NFTs and their consequences in affected neurons.

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

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

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

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

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

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

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

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

148 ata are the first proteomic investigation of NFTs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

164 th tau hyperphosphorylation, and potentially NFTs formation.

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

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

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

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

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

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

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

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

173 ubset of neuritic plaques, neurons, and some NFTs.

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

175 ive determination of neurofibrillary tangle (NFT) density.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

190 Neurofibrillary tangles (NFT) composed of the microtubule-associated protein tau

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

192 the characteristic neurofibrillary tangles (NFT) of Alzheimer's.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

224 elical filaments of neurofibrillary tangles (NFTs) in AD brain.

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

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

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

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

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

230 The pathogenesis of neurofibrillary tangles (NFTs) in Alzheimer's disease (AD) is poorly understood,

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

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

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

234 e plaques (SPs) and neurofibrillary tangles (NFTs) in vulnerable brain regions.

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

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

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

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

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

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

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

242 , neuritic changes, neurofibrillary tangles (NFTs), and gliosis (reactive astrocytes, activated micro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

258 hological hallmark: neurofibrillary tangles (NFTs).

259 s and intracellular neurofibrillary tangles (NFTs).

260 amyloid plaques and neurofibrillary tangles (NFTs).

261 luble filaments and neurofibrillary tangles (NFTs).

262 sed in neurons with neurofibrillary tangles (NFTs).

263 ed tau protein into neurofibrillary tangles (NFTs).

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

265 ere associated with neurofibrillary tangles (NFTs).

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

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

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

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

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

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

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

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

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

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

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

277 The NFTs were immunopositive, with multiple tau antibodies,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

294 estigating the pathogenesis of diseases with NFT.

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.