ライフサイエンスコーパス: tauopathy

1 eatures of tau present in the brain in human tauopathy.

2 ath in an in vivo model of neurodegenerative tauopathy.

3 autophagic pathways in a Drosophila model of tauopathy.

4 including a Caenorhabditis elegans model of tauopathy.

5 l activity may regulate neurodegeneration in tauopathy.

6 truct does not represent amyloid-independent tauopathy.

7 hich they rescue phenotypes in this model of tauopathy.

8 ced tau pathology in the PS19 mouse model of tauopathy.

9 d from those with severe primary age-related tauopathy.

10 term 'cistauosis', appears long before other tauopathy.

11 eimer's disease (AD) and primary age-related tauopathy.

12 get for the pharmacologic treatment of human tauopathy.

13 memory impairment in an hTau mouse model of tauopathy.

14 limited by constraints of existing models of tauopathy.

15 europrotective role in a Drosophila model of tauopathy.

16 ction and pathological features suggesting a tauopathy.

17 t position 301 (P301L) leads to severe human tauopathy.

18 he effects of MB in the P301S mouse model of tauopathy.

19 ant tau toxicity in the JNPL3 mouse model of tauopathy.

20 amyloid-beta pathology, but also attenuated tauopathy.

21 odegeneration in a transgenic mouse model of tauopathy.

22 tex, which is the common site of age-related tauopathy.

23 S-tg) mouse model of frontotemporal dementia/tauopathy.

24 ity to distinguish TDP-43 proteinopathy from tauopathy.

25 nst neurodegeneration in the setting of pure tauopathy.

26 degenerative disorders collectively known as tauopathies.

27 ntations, similar to those that define human tauopathies.

28 h are characteristic of human AD and related tauopathies.

29 neurodegenerative diseases commonly known as tauopathies.

30 important role in the pathogenesis of human tauopathies.

31 urotoxicity in Alzheimer's disease and other tauopathies.

32 in prognostic and diagnostic approaches for tauopathies.

33 gnitive impairments evident in virtually all tauopathies.

34 strategies for Alzheimer's disease and other tauopathies.

35 subsequent neuropathology in AD and related tauopathies.

36 hts into the molecular mechanisms underlying tauopathies.

37 k1 to be a novel therapeutic entry point for tauopathies.

38 ms and to develop novel treatments for human tauopathies.

39 itical role in Alzheimer disease and related tauopathies.

40 ion of tau aggregates in these non-Alzheimer tauopathies.

41 pic diversity in Alzheimer disease and other Tauopathies.

42 therapeutics for patients with AD and other tauopathies.

43 ing the diversity of neuropathology in human tauopathies.

44 a novel approach for the treatment of human tauopathies.

45 a group of neurodegenerative diseases termed tauopathies.

46 sequences associated with the development of tauopathies.

47 esis of Alzheimer's disease (AD) and related tauopathies.

48 hallmark of Alzheimer's disease and related tauopathies.

49 ansmission contributes to the progression of tauopathies.

50 ly structured amyloid fibril underlies human Tauopathies.

51 hway may offer novel therapeutic targets for tauopathies.

52 a hallmark of Alzheimer's disease and other tauopathies.

53 ay be useful for developing therapeutics for tauopathies.

54 ating tau lesions in Alzheimer's disease and tauopathies.

55 nerative diseases, collectively known as the tauopathies.

56 progression of Alzheimer's disease and other tauopathies.

57 alterations of tau species in other primary tauopathies.

58 a cell, which may mediate progression of the tauopathies.

59 a class of neurodegenerative diseases called tauopathies.

60 be a new therapeutic strategy against human tauopathies.

61 n loss permitted aberrant gene expression in tauopathies.

62 treatment of AD and other neurodegenerative tauopathies.

63 R DNA binding protein 43 proteinopathies and tauopathies.

64 nts for Alzheimer's disease (AD) and related tauopathies.

65 iseases with tau protein aggregates known as tauopathies.

66 umber of neurodegenerative diseases known as tauopathies.

67 lmark of Alzheimer disease (AD), and related tauopathies.

68 tter therapeutic strategies for AD and other tauopathies.

69 hallmark of Alzheimer disease (AD) and other tauopathies.

70 stereotyped progression of neurodegenerative tauopathies.

71 markers for Alzheimer's disease and related tauopathies.

72 plications for Alzheimer's disease and other tauopathies.

73 n the brain in Alzheimer's disease and other tauopathies.

74 chronic traumatic encephalopathy, and other tauopathies.

75 nal death in Alzheimer's disease and related tauopathies.

76 urodegenerative diseases collectively called tauopathies.

77 b, and Lou Gehrig's diseases, as well as the tauopathies.

78 Hsc70 could be therapeutically relevant for tauopathies.

79 ncluding spheroids, typically found in human tauopathies.

80 presents a common pathological event in many tauopathies.

81 roup of neurodegenerative disorders known as tauopathies.

82 pies may be a strategy for the treatment for tauopathies.

83 PTM) in Alzheimer's disease (AD) and related tauopathies.

84 levated in frontotemporal lobar degeneration tauopathies.

85 at identifying tau pathologies in the non-AD tauopathies.

86 lmarks of Alzheimer's disease (AD) and other tauopathies.

87 eutic use of DBS and synaptic stimulation in tauopathies.

88 d ameliorate tau pathology in AD and related tauopathies.

89 r's disease (AD) and other neurodegenerative tauopathies.

90 e of MID1 in the pathology of AD and related tauopathies.

91 d mitigate the levels of tau prions in human tauopathies.

92 ngles (NFTs), which are associated in AD and tauopathies.

93 sease-modifying therapies for AD and related tauopathies.

94 terminus (ie, PAD exposure) occurs in non-AD tauopathies.

95 s may explain the diverse characteristics of tauopathies.

96 widespread relaxation of heterochromatin in tauopathies [1]: age-related progressive neurodegenerati

97 y tangles in the frontal neocortex to severe tauopathy affecting widespread brain regions, including

98 To date, few animal models of tauopathy allow for the potential influence of these pro

99 in Alzheimer and Parkinson diseases and the tauopathies also propagate in a "prion-like" manner.

100 o would help to develop biomarkers for these tauopathies and clinical trials of disease-modifying the

101 ay be part of the early pathology in various Tauopathies and could be exploited therapeutically.

102 is might explain the phenotypic diversity of tauopathies and could enable more effective diagnosis an

103 cific calpain inhibition in the treatment of tauopathies and other neurodegenerative states.

104 study establishes a mouse model of sporadic tauopathies and points to important differences between

105 0 could be a viable therapeutic strategy for tauopathies and possibly lead to new insights in chapero

106 on may occur in a localized fashion in human tauopathies and synucleinopathies, followed by seed-depe

107 In tauopathies and synucleinopathies, the normally soluble

108 ical, pathological, and genetic diversity of tauopathies and the discoveries underlying the emerging

109 mal proteins including TDP-43 proteinopathy, tauopathy and alpha-synucleinopathy.

110 Tau35 mice causes a profound and progressive tauopathy and cognitive changes, which are rescued by ph

111 ronal dysfunction during prodromal stages of tauopathy and define tau-driven pathophysiological chang

112 ease (n = 16) compared to cases with a known tauopathy and healthy controls.

113 n on proteasome function in a mouse model of tauopathy and in a cross to a UPS reporter mouse (line U

114 Ser-324-positive tau both in mouse models of tauopathy and in patients with Alzheimer's disease.

115 n that is associated with the development of tauopathy and is highly phosphorylated.

116 s a mechanism for the pathological spread in tauopathy and other neurodegenerative diseases.

117 e importance of MARK4 as a viable target for Tauopathy and provides fresh insight into the complex me

118 nd exosomes contribute to the progression of tauopathy and that the exosome secretion pathway may be

119 ker that reflects both the progression of AD tauopathy and the emergence of clinical impairment.

120 ptau:ttau ratio in ALS relative to 4-repeat tauopathy and to controls.

121 The 5-LO protein is upregulated in human tauopathy and transgenic tau mice brains.

122 O levels in brain samples from patients with tauopathy and transgenic tau mice, and we evaluated the

123 aetiologic molecules in Alzheimer's disease, tauopathies, and alpha-synucleinopathies, respectively.

124 sible for motor signs observed in some human tauopathies, and for synaptic dysfunction resulting from

125 cumulation is a major contributing factor in tauopathies, and the heat-shock protein 70 (Hsp70) seems

126 previously been evaluated in the context of tauopathy, and here we observed increased deposition of

127 ted with chromosome 17, three unclassifiable tauopathy, and one argyrophilic grain disease); FTLD-TDP

128 rhinal cortex, which exhibits early signs of tauopathy, and the inferior temporal region, which is mo

129 ochemical and neuropathological hallmarks of tauopathies are accurately conserved and are independent

130 Tauopathies are characterized by the progressive accumul

131 Tauopathies are neurodegenerative diseases characterized

132 Tauopathies are neurodegenerative diseases characterized

133 Tauopathies are neurodegenerative disorders that affect

134 Our study provides strong evidence that tauopathies are neurodegenerative laminopathies and iden

135 e exact mechanisms leading to memory loss in tauopathies are not yet known; however, decreased transl

136 The prion-like concept for tauopathies arose initially from the observation that th

137 tic strategy for treating or preventing such tauopathies as frontotemporal dementia, progressive supr

138 that lamin dysfunction is conserved in human tauopathy, as super-resolution microscopy reveals a sign

139 Chronic traumatic encephalopathy is a tauopathy associated with RBT that has become inextricab

140 Our findings relate tauopathy-associated changes in cellular neurophysiology

141 validating hFPPS as a therapeutic target for tauopathy-associated neurodegeneration.

142 homologous and heterologous blockades using tauopathy brain samples.

143 d of straight tau filaments in non-Alzheimer tauopathy brains or to lesions containing beta-amyloid,

144 ce with pathological tau enriched from human tauopathy brains.

145 ers, including Alzheimer's disease and other tauopathies, but the consequences of genotoxic stress to

146 are hallmarks of Alzheimer disease and other tauopathies, but their causative connection is still a m

147 related to the common age-related entorhinal tauopathy, but this dysfunction was independent of amylo

148 ic function in animal and cellular models of tauopathies by promoting the missorting of tau to dendri

149 mpact of LC degeneration in a mouse model of tauopathy by lesioning the LC of male and female P301S t

150 e of straight tau filaments in non-Alzheimer tauopathy cases and to the existence of some [F-18]-AV-1

151 rns in three autopsy-confirmed non-Alzheimer tauopathy cases.

152 gressive supranuclear palsy (PSP), a primary tauopathy characterised by deposition of four microtubul

153 Q) in a well-established Drosophila model of tauopathy characterised by microtubule breakdown and axo

154 Aberrant splicing of TAU exon 10 results in tauopathies characterized by alterations in the proporti

155 Alzheimer disease (AD) is a degenerative tauopathy characterized by aggregation of Tau protein th

156 MAPT P301L mutation carrier had an atypical tauopathy characterized by grain-like tau-containing neu

157 Alzheimer's disease (AD) and related tauopathies comprise a large group of neurodegenerative

158 ked manner during SWRs in the mouse model of tauopathy; conversely, inhibitory interneurons were less

159 ases, including Alzheimer's disease (AD) and tauopathy dementias.

160 Here, we report that the mild tauopathy developing in retinal ganglion cells (RGCs) of

161 ith cis antibody blocks cistauosis, prevents tauopathy development and spread, and restores many TBI-

162 rms in brains of Pick's disease and familial tauopathy due to G272V tau mutation were sensitively det

163 alsy, corticobasal degeneration and familial tauopathy due to N279K tau mutation and 3-repeat isoform

164 Human neurodegenerative tauopathies exhibit pathological tau aggregates in the b

165 au strains from 29 patients with 5 different tauopathies, finding that different diseases are associa

166 otor and memory deficits in a mouse model of tauopathy for 60 d, coincident with rapid reduction of t

167 In tauopathy-frontotemporal dementia mice, both drugs were

168 one of the molecular causes of the inherited tauopathy, FTDP-17.

169 , known as frontotemporal lobar degeneration tauopathy (FTLD-Tau), which presents with dementia and i

170 e [IQR] = 6.0, 12.3; n = 26) compared to the tauopathy group (median = 12.5pg/ml; IQR = 10.7, 15.0; n

171 on of abnormal tau-ribosomal interactions in tauopathies >25 years ago, the consequences of this asso

172 ntation for the neurodegenerative process in tauopathies has yet remained unclear.

173 lzheimer disease (AD), but its role in other tauopathies has yet to be firmly established.

174 However, tauopathy has not been detected in the early stages afte

175 been associated with different phenotypes of tauopathies, has led to controversial assumptions about

176 pathological pathways, Abeta-amyloidosis and Tauopathy, have been considered as therapeutic targets.

177 typically the first brain region affected by tauopathies in AD.

178 est that p25/Cdk5 plays an important role in tauopathy in both mouse and human model systems.

179 rly driver of disease after TBI and leads to tauopathy in chronic traumatic encephalopathy and Alzhei

180 of D2-family dopamine receptors ameliorated tauopathy in multiple models including a Caenorhabditis

181 tic reduction in RanBP9 not only ameliorates tauopathy in Tau-P301S mice but also rescues the deficit

182 Our findings suggest an epilepsy-related tauopathy in temporal lobe epilepsy, which contributes t

183 cline is indicative of accumulation of early tauopathy in the medial temporal lobe, specifically in t

184 clinical Alzheimer's disease, there is focal tauopathy in the medial temporal lobes and adjacent cort

185 We have generated a new mouse model of tauopathy in which this human brain-derived, 35 kDa tau

186 degenerative diseases, collectively known as tauopathies, in which clinical phenotypes manifest as co

187 acellular aggregates of tau proteins, termed tauopathies, include Alzheimer's disease (AD), frontotem

188 that in transgenic rTg4510 mice, a model of tauopathies including Alzheimer's disease, hippocampal n

189 au pathology during the development of human tauopathies including Alzheimer's disease.

190 mer's disease; 2) tau lesions in three other tauopathies including Pick's disease, progressive supran

191 au35 mice recapitulate key features of human tauopathies, including aggregated and abnormally phospho

192 es (NFTs) is a neuropathological hallmark of tauopathies, including Alzheimer's disease (AD) and chro

193 Tauopathies, including Alzheimer's disease (AD) and othe

194 f tau pathology is a major characteristic of tauopathies, including Alzheimer's disease (AD), and pla

195 Tauopathies, including Alzheimer's disease (AD), are ass

196 ogical hallmark of several neurodegenerative tauopathies, including Alzheimer's disease (AD).

197 neurotoxic tau entities in neurodegenerative tauopathies, including Alzheimer's disease (AD).

198 Tauopathies, including Alzheimer's disease and frontotem

199 class of neurodegenerative diseases known as tauopathies, including Alzheimer's disease and related d

200 u leads to dementia and neurodegeneration in tauopathies, including Alzheimer's disease.

201 ssociated protein Tau) defines a spectrum of tauopathies, including Alzheimer's disease.

202 Tauopathies, including frontotemporal dementia (FTD) and

203 displays signature pathological features of tauopathies, including tau accumulation, altered phospho

204 phenotype characteristic of mouse models of tauopathy, including abnormalities in exploration, anxie

205 ential molecular mechanisms by which initial tauopathy induces neuronal dysfunction.

206 mutation eliminating the need of artificial tauopathy induction.

207 neurodegeneration in Alzheimer's disease and tauopathies is generally assumed to start in a normally

208 toms of Alzheimer's disease (AD) and related tauopathies is memory loss.

209 thogenicity in Alzheimer's disease and other tauopathies is thought to involve the generation of hype

210 of JNPL3 mice by overexpressing calpastatin, tauopathy is prevented, including calpain-mediated break

211 early stages after TBI, and how TBI leads to tauopathy is unknown.

212 IFN-gamma in the brains of 2 mouse models of tauopathy: JNPL3 and rTg4510.

213 rphosphorylated tau protein is a hallmark of tauopathies like Alzheimer and many other neurodegenerat

214 g disease-modifying therapeutic strategy for tauopathies like Alzheimer's disease.

215 efining pathologic features of which include tauopathy made of phosphorylated tau protein (P-tau).

216 t the unique features of clinically distinct tauopathies may be a reflection of the strain of misfold

217 stered restored NMNAT2 expression in rTg4510 tauopathy mice to normal levels.

218 a strong in vivo brain signal in transgenic tauopathy mice, but not in wild-type or amyloid-beta pla

219 ed out a detailed time-course study in P301S tauopathy mice, comparing seeding activity versus histol

220 Next, we optimized a SH-SY5Y cell based tauopathy model by introducing a novel 5-fold Tau mutati

221 nds healthy lifespan ( 25%) in wild type and tauopathy model C. elegans at least as effectively as ot

222 The Tg30 murine tauopathy model expresses a human tau protein bearing tw

223 ury and early-stage OSN deficits in a rodent tauopathy model of neurodegenerative disease.

224 We now report the development of a sporadic tauopathy model to study human tau strains by intracereb

225 Alzheimer's disease model), and tau609 mice (tauopathy model).

226 In rTg4510 mice, a Tau-P301L tauopathy model, hippocampal place fields that support s

227 Tauopathy models were used to study the impact of YM-01

228 ploinsufficiency rescued the phenotypes of a tauopathy mouse model.

229 Patients had autopsy-confirmed FTLD with tauopathy (n = 31), TDP-43 proteinopathy (n = 49), or AD

230 thought to explain the progressive spread of tauopathy observed in the brain of patients with Alzheim

231 both neuronal and glial tau aggregations in tauopathies of various etiologies.

232 ease (AD) the impact of amyloid and regional tauopathy on cerebral glucose metabolism and subsequent

233 rm of tau protein, to examine the effects of tauopathy on hippocampal SWRs and associated neuronal fi

234 rm of tau protein, to examine the effects of tauopathy on hippocampal SWRs and associated neuronal fi

235 was disrupted in a transgenic mouse model of tauopathy (one of the major hallmarks of several dementi

236 type C), and is only rarely due to a primary tauopathy or Alzheimer's disease.

237 fact that advanced age, primary age-related tauopathy or comorbidities typical to several types of d

238 able as to whether 5-LO is elevated in human tauopathy or if it directly influences tau pathology in

239 am Alzheimer's disease pathologies including tauopathy or inflammation.

240 proteinopathy of Alzheimer disease and other tauopathies, or tau-mediated neurodegeneration, is not c

241 Most existing mouse models of tauopathy overexpress mutant tau at levels that do not o

242 non-AD pathologies, both primary age-related tauopathy (p < 0.05) and brain arteriolosclerosis pathol

243 Tau model provides mechanistic insights into tauopathy pathogenesis and potential avenues for treatme

244 totemporal lobar degeneration (FTLD) and (2) tauopathy patients have higher phosphorylated-tau levels

245 has enabled visualization of tau lesions in tauopathy patients, but the modes of their binding to di

246 did not synergize with bas-1 suppression of tauopathy phenotypes.

247 decade to suggest that the misfolded tau in tauopathies possesses prion-like features and that such

248 arousal states in the rTg4510 mouse model of tauopathy, prior to significant cell death, when only a

249 e role of TTBK1-induced neuroinflammation in tauopathy-related neuropathogenesis, age-matched TTBK1/J

250 this ligand to bind to tau lesions in other tauopathies remains controversial.

251 al function during early prodromal stages of tauopathy remains unclear.

252 of human tauopathies.SIGNIFICANCE STATEMENT Tauopathies show great clinical and neuropathological he

253 916, and the comparison of ALS with 4-repeat tauopathy showed 92.0% sensitivity and 91.7% specificity

254 egation that underlie the diversity of human tauopathies.SIGNIFICANCE STATEMENT Tauopathies show grea

255 In addition to classic markers of tauopathy, significant neuroinflammation and extensive g

256 to generate a more versatile mouse model of tauopathy, somatic brain transgenesis was utilized to de

257 ysiological changes associated with distinct tauopathy stages to support informed therapeutic decisio

258 RNA) cluster miR-132/212 is downregulated in tauopathies such as AD.

259 In tauopathies such as Alzheimer's disease, this model pred

260 n emission tomography, especially in primary tauopathies such as progressive supranuclear palsy.

261 rain to parameters that discriminate between tauopathies such as regional vulnerability or rate of sp

262 Tauopathies, such as Alzheimer's disease, some cases of

263 on and cognitive decline in AD (3) and other tauopathies, such as frontotemporal dementia (4, 5).

264 ive diseases, including Alzheimer's disease; tauopathies, such as frontotemporal dementia; alpha-synu

265 Studies in animal models of tauopathy suggest that tau oligomers play a key role in

266 been found in several sporadic and inherited tauopathies, suggesting that dysregulation of tau exon 1

267 eeding is thus an early and robust marker of tauopathy, suggesting a proximal role for tau seeds in n

268 atients with AD, as well as a mouse model of tauopathy, suggesting that loss of acetylation on KXGS m

269 that drive the development of AD, including tauopathy, synaptic dysfunction, and neurodegeneration.

270 to three categories: amyloid deposition (A), tauopathy (T), and neurodegeneration or neuronal injury

271 In Alzheimer's disease and tauopathies, tau protein aggregates into neurofibrillary

272 like prion diseases, synucleinopathies, and tauopathies that are collectively termed protein misfold

273 th S320F), we generated aggressive models of tauopathy that do not require exogenous seeding.

274 lates in neurodegenerative diseases known as tauopathies, the most common being Alzheimer's disease.

275 d amyloid deposits is a primary pathology in tauopathies, the most common of which is Alzheimer's dis

276 ggregates that promote cognitive deficits in tauopathies, the most common of which is Alzheimer's dis

277 In Alzheimer's disease (AD) and other tauopathies, the tau protein forms fibrils, which are be

278 In individuals with a sporadic primary tauopathy, the presence of an epsilon4 allele is associa

279 work shows that in a relevant model of early tauopathy, the retina of the P301S mutant human tau tran

280 loid interacts with hippocampal and cortical tauopathy to affect neurodegeneration.

281 have used a Caenorhabditis elegans model of tauopathy to screen a drug library containing 1120 compo

282 ogenic tau levels is a rational strategy for tauopathy treatment, but therapeutic targets with clinic

283 ogenic tau levels is a rational strategy for tauopathy treatment.

284 It is not clearly understood why tauopathies vary greatly in the neuroanatomical and hist

285 s with a disorder associated with a 4-repeat tauopathy was conducted at an academic medical center.

286 Neocortical tauopathy was positively associated with metabolism in i

287 Here, to address the role of p25/Cdk5 in tauopathy, we generated double-transgenic mice by crossi

288 To further validate the role of p25/Cdk5 in tauopathy, we used frontotemporal dementia patient-deriv

289 Microglial activation, amyloidopathy, and tauopathy were enhanced by surgery as compared with desf

290 26S proteasomes from mice with tauopathy were physically associated with tau and were l

291 Thus, in tauopathies, where MT injury would be detrimental to neu

292 l neurodegenerative disorders referred to as tauopathies, which include Alzheimer's disease, frontote

293 cell death in this novel AAV-based model of tauopathy, which offers exceptional versatility and spee

294 au-induced toxicity in a C. elegans model of tauopathy, while loss of no other dopamine or serotonin

295 r's disease and to distinguish it from other tauopathies with distinct clinical and pathological char

296 The existence of multiple human Tauopathies with distinct fibril morphologies has led to

297 tion (CBD) are neurodegenerative four-repeat tauopathies with no cure.

298 encephalopathy (CTE) is an acquired primary tauopathy with a variety of cognitive, behavioral, and m

299 essed CSF tau protein abnormalities in AD, a tauopathy with prominent Abeta pathology, and progressiv

300 y model of stroke that combines high age and tauopathy with thromboembolic cerebral ischemia.