ライフサイエンスコーパス: supranuclear

1 which appeared in a punctate pattern in the supranuclear and apical cytoplasm of acini.

2 The cellular localization of OPN was supranuclear and apical, and responding cells were diffu

3 These supranuclear cataracts colocalised with enhanced Abeta i

4 We consistently saw equatorial supranuclear cataracts in lenses from people with Alzhei

5 gation, extracerebral amyloid formation, and supranuclear cataracts.

6 se early zymogen activation takes place in a supranuclear compartment that overlaps in distribution w

7 sits located exclusively in the cytoplasm of supranuclear/deep cortical lens fibre cells (n=4).

8 d vestibular rehabilitation of patients with supranuclear eye movement disorders.

9 on's syndrome have delayed onset of vertical supranuclear gaze palsy (>3 years after onset of first s

10 Whipple's disease can present with supranuclear gaze palsy and characteristic oculomasticat

11 s defined by its akinetic rigidity, vertical supranuclear gaze palsy and falls, cognitive impairments

12 terized by akinetic-rigid features, falls, a supranuclear gaze palsy and subcortical dementia.

13 ear mutism, dysphagia with choking, vertical supranuclear gaze palsy or slowing, balance difficulties

14 dementia with an akinetic rigid syndrome and supranuclear gaze palsy or Steele-Richardson-Olszewski d

15 clinical description of PSP, which includes supranuclear gaze palsy, early falls and dementia, does

16 stability, early unexplained falls, vertical supranuclear gaze palsy, symmetric motor disability and

17 d retraction, frequent square-wave jerks and supranuclear gaze palsy.

18 bility, which leads to falls, and a vertical supranuclear-gaze palsy.

19 system can be divided into broad categories: supranuclear, internuclear, nuclear, and gaze-holding sy

20 o-phagolysosomal aggregates in vitro and the supranuclear melanin cap in situ.

21 To determine whether the supranuclear melanin cap of transferred, phagocytosed me

22 osomes, participates in the formation of the supranuclear melanin cap or "microparasol" and serves as

23 ging studies are providing new insights into supranuclear ocular motor circuitry.

24 This work reviews supranuclear ocular motor disorders, highlighting new da

25 her with brainstem encephalitis reflected by supranuclear ophtalmoparesis and rapid eye movement slee

26 %), Alzheimer disease (AD, 23%), progressive supranuclear palsy (13%), and frontotemporal lobar degen

27 nd the most common tauopathy was progressive supranuclear palsy (16 cases).

28 l degeneration (5 patients), and progressive supranuclear palsy (5 patients).

29 wy body disease (12.8%; n = 26), progressive supranuclear palsy (6.4%; n = 13), cerebrovascular disea

30 icity, 97% PPV, and 83% NPV) and progressive supranuclear palsy (88% sensitivity, 94% specificity, 91

31 mpared with the 13 patients with progressive supranuclear palsy (baseline area under the receiver ope

32 , multiple system atrophy (MSA), progressive supranuclear palsy (MSP)).

33 ate multiple system atrophy from progressive supranuclear palsy (multiple system atrophy versus progr

34 ents subsequently diagnosed with progressive supranuclear palsy (n = 16, seven males, age at death 68

35 and in vivo volume loss in both progressive supranuclear palsy (n = 340 regions; beta 0.155; 95% CI:

36 icobasal degeneration (n = 5) or progressive supranuclear palsy (n = 4).

37 th Parkinson's disease (n = 15), progressive supranuclear palsy (n = 9) and healthy age- and gender-m

38 ltiple system atrophy (n=372) or progressive supranuclear palsy (n=311) from the Neuroprotection and

39 repeats with the development of progressive supranuclear palsy (OR = 5.83; P= 0.004; repeat length >

40 95% CI: 2.5-19.5, P < 0.01) and progressive supranuclear palsy (OR: 3.1, 95% CI: 1.1-8.9, P = 0.032)

41 95% CI: 3.2-24.2, P < 0.01) and progressive supranuclear palsy (OR: 4.8, 95% CI: 1.7-13.6, P < 0.01)

42 d a movement disorder resembling progressive supranuclear palsy (PSP) and associated with dementia.

43 Progressive supranuclear palsy (PSP) and corticobasal degeneration (

44 f the neurodegenerative diseases progressive supranuclear palsy (PSP) and corticobasal degeneration (

45 Progressive supranuclear palsy (PSP) and corticobasal degeneration (

46 Studies of progressive supranuclear palsy (PSP) and corticobasal degeneration (

47 ver-represented in patients with progressive supranuclear palsy (PSP) and corticobasal degeneration.

48 FTD-s) disorders, including FTD, progressive supranuclear palsy (PSP) and corticobasal syndrome, and

49 ude a limited number of cases of progressive supranuclear palsy (PSP) and dementia with Lewy bodies;

50 nclude Alzheimer's disease (AD), progressive supranuclear palsy (PSP) and frontotemporal lobar degene

51 nd The differential diagnosis of progressive supranuclear palsy (PSP) and Lewy body disorders, which

52 ictors have not been defined for progressive supranuclear palsy (PSP) and multiple system atrophy (MS

53 clinical disease progression in progressive supranuclear palsy (PSP) and multiple system atrophy (MS

54 sh Parkinson's disease (PD) from progressive supranuclear palsy (PSP) and multiple system atrophy (MS

55 rs and survival in patients with progressive supranuclear palsy (PSP) and multiple system atrophy (MS

56 8Q polymorphism for DJ-1, and in progressive supranuclear palsy (PSP) brains.

57 ticobasal degeneration (CBD) and progressive supranuclear palsy (PSP) can sometimes present with a pr

58 ostmortem brain samples from two progressive supranuclear palsy (PSP) cases and a MAPT P301L mutation

59 for association of CBD with top progressive supranuclear palsy (PSP) GWAS single-nucleotide polymorp

60 A diagnosis of progressive supranuclear palsy (PSP) had been considered in all thre

61 gh pathological heterogeneity of progressive supranuclear palsy (PSP) has also been established, atte

62 Progressive supranuclear palsy (PSP) has been conceptualized as a la

63 ing binding to tau aggregates in progressive supranuclear palsy (PSP) have yielded mixed results.

64 estimate the point prevalence of progressive supranuclear palsy (PSP) in the UK at national, regional

65 Progressive supranuclear palsy (PSP) is a movement disorder characte

66 Progressive supranuclear palsy (PSP) is a neurodegenerative disorder

67 Progressive supranuclear palsy (PSP) is a progressive neurodegenerat

68 Progressive supranuclear palsy (PSP) is a rare and progressive neuro

69 Because progressive supranuclear palsy (PSP) is linked to tau pathology, dav

70 generative tauopathies, of which progressive supranuclear palsy (PSP) is one of the most common, are

71 Progressive supranuclear palsy (PSP) is usually sporadic, but few pe

72 with patients with diagnoses of progressive supranuclear palsy (PSP) or Alzheimer's disease (AD) or

73 progressive aphasia (nfvPPA) and progressive supranuclear palsy (PSP) or corticobasal degeneration (C

74 We devised a Progressive Supranuclear Palsy (PSP) Rating Scale comprising 28 item

75 The clinical diagnosis of progressive supranuclear palsy (PSP) relies on the identification of

76 ]AV-1451 PET in 17 patients with progressive supranuclear palsy (PSP) Richardson's syndrome.

77 nant AD and subcortical-dominant progressive supranuclear palsy (PSP) tau topologies.

78 ultiple-system atrophy (MSA) and progressive supranuclear palsy (PSP) than in Parkinson disease (PD),

79 ultiple system atrophy (MSA) and progressive supranuclear palsy (PSP) were 85.7 (30 out of 35) and 80

80 ultiple system atrophy (MSA) and progressive supranuclear palsy (PSP) where nigral dopaminergic neuro

81 arkinson's disease (PD), 30 with progressive supranuclear palsy (PSP), 19 with corticobasal degenerat

82 h prominent Abeta pathology, and progressive supranuclear palsy (PSP), a primary tauopathy characteri

83 Multiple-system atrophy (MSA), progressive supranuclear palsy (PSP), and corticobasal syndrome (CBS

84 luding Alzheimer's disease (AD), progressive supranuclear palsy (PSP), and frontotemporal dementia (F

85 ypical, pathologically diagnosed progressive supranuclear palsy (PSP), and investigated their genetic

86 ticobasal degeneration (CBD) and progressive supranuclear palsy (PSP), are neurodegenerative tauopath

87 corticobasal syndrome (CBS) and progressive supranuclear palsy (PSP), both of which have prominent e

88 nsonian syndromes (APSs) such as progressive supranuclear palsy (PSP), multiple system atrophy (MSA)

89 Progressive supranuclear palsy (PSP), multiple system atrophy (MSA)

90 Progressive supranuclear palsy (PSP), previously believed to be a co

91 ticobasal degeneration (CBD) and progressive supranuclear palsy (PSP), tau also aggregates in astrocy

92 ultiple system atrophy (MSA) and progressive supranuclear palsy (PSP), the most common atypical parki

93 ontotemporal dementia (FTD), and progressive supranuclear palsy (PSP).

94 (CBS) but is not specific versus progressive supranuclear palsy (PSP).

95 eurological disorders, including progressive supranuclear palsy (PSP).

96 ng the neurodegenerative disease progressive supranuclear palsy (PSP).

97 ticobasal degeneration (CBD) and progressive supranuclear palsy (PSP).

98 pathological features similar to progressive supranuclear palsy (PSP).

99 ultiple-system atrophy (MSA) and progressive supranuclear palsy (PSP).

100 of H1 haplotype is increased in progressive supranuclear palsy (PSP).

101 etic determinants of survival in progressive supranuclear palsy (PSP).

102 sessed as a prognostic factor in progressive supranuclear palsy (PSP).

103 both Alzheimer disease (AD) and progressive supranuclear palsy (PSP).

104 his review provides an update on progressive supranuclear palsy (PSP, or Steele-Richardson-Olszewski

105 ostmortem brains of AD (AD-tau), progressive supranuclear palsy (PSP-tau), and corticobasal degenerat

106 nson's disease (PD; n = 32), and progressive supranuclear palsy (PSP; n = 31), were included in our c

107 tients with clinically diagnosed progressive supranuclear palsy (Richardson's syndrome), 24 patients

108 from multiple system atrophy and progressive supranuclear palsy (the two most common atypical parkins

109 We recruited 23 patients with progressive supranuclear palsy (using clinical diagnostic criteria,

110 alternative causes for dementia (progressive supranuclear palsy = 1, Lewy body disease = 1, vascular

111 rodegeneration severity, in both progressive supranuclear palsy [n = 340 regions; beta 0.036; 95% con

112 taucipir-PET and died with FTLD (progressive supranuclear palsy [PSP], n = 10; corticobasal degenerat

113 present in 75% of patients with progressive supranuclear palsy and 15% of patients with Parkinson's

114 served in 62.0% of patients with progressive supranuclear palsy and 31.8% of those with multiple syst

115 ing was, however, found on human progressive supranuclear palsy and corticobasal degeneration brain s

116 were higher in autopsy-confirmed progressive supranuclear palsy and corticobasal degeneration than in

117 tangles in Alzheimer's disease, progressive supranuclear palsy and corticobasal degeneration, and in

118 s including Alzheimer's disease, progressive supranuclear palsy and corticobasal degeneration, which

119 ar degeneration, Pick's disease, progressive supranuclear palsy and corticobasal degeneration.

120 ther forms of tauopathy, such as progressive supranuclear palsy and corticobasal degeneration.

121 Lewy bodies but is not found in progressive supranuclear palsy and corticobasal degeneration.

122 rodegeneration and tau burden in progressive supranuclear palsy and corticobasal degeneration.

123 athies including Pick's disease, progressive supranuclear palsy and corticobasal degeneration; 3) alp

124 Many patients with progressive supranuclear palsy and corticobasal syndrome had languag

125 imary progressive aphasia (PPA), progressive supranuclear palsy and corticobasal syndrome.

126 ple system atrophy compared with progressive supranuclear palsy and corticobasal syndrome.

127 ants of frontotemporal dementia, progressive supranuclear palsy and corticobasal syndrome.

128 -independent social cognition in progressive supranuclear palsy and explore the neural correlates for

129 ently examined the MAPT locus in progressive supranuclear palsy and found that a haplotype (H1c) on t

130 au haplotype over-represented in progressive supranuclear palsy and further extend the similarity in

131 ecruited cohort of patients with progressive supranuclear palsy and multiple system atrophy studied t

132 ied new genetic risk factors for progressive supranuclear palsy and new genetic conditions presenting

133 Progressive supranuclear palsy and Parkinson's disease have distinct

134 supranuclear palsy, all of whom had vertical supranuclear palsy and seven had falls within the first

135 Moreover, there was an upgaze supranuclear palsy and slow saccades on vertical plane.

136 se, multiple system atrophy, and progressive supranuclear palsy and to accurately distinguish between

137 esented with an atypical form of progressive supranuclear palsy and two others with either severe pos

138 sease, relative to patients with progressive supranuclear palsy and with control subjects, in the hip

139 or dementia with Lewy bodies) or progressive supranuclear palsy are misdiagnosed as having multiple s

140 ation have been revised, and for progressive supranuclear palsy are under revision.

141 the 179 pathologically diagnosed progressive supranuclear palsy cases (3%).

142 ripts performed by patients with progressive supranuclear palsy did not exhibit decrements in script

143 Donors with progressive supranuclear palsy exhibited more variation in inhibitor

144 ith corticobasal degeneration or progressive supranuclear palsy fell outside 95% of the normal mean,

145 Progressive supranuclear palsy filaments contain 4R tau.

146 r a clinical test to distinguish progressive supranuclear palsy from Lewy body disorders.

147 rved in approximately 57% of the progressive supranuclear palsy group and 20% of the multiple system

148 87% of finger tap trials in the progressive supranuclear palsy group and only 12% in the Parkinson's

149 Although the progressive supranuclear palsy group performed worse overall, the co

150 eatures and 30% of patients with progressive supranuclear palsy had corticobasal syndrome-like featur

151 with frontotemporal dementia and progressive supranuclear palsy had impaired response inhibition, wit

152 We conclude that patients with progressive supranuclear palsy have a multimodal deficit in social c

153 In conclusion, patients with progressive supranuclear palsy have a specific finger tap pattern of

154 not known whether patients with progressive supranuclear palsy have criteria-defined bradykinesia.

155 h as multiple system atrophy and progressive supranuclear palsy have elevated free-water in the subst

156 phy versus Lewy body disease and progressive supranuclear palsy if a patient developed orthostatic hy

157 e corticobasal degeneration from progressive supranuclear palsy in patients with Richardson syndrome.

158 n and caudate, and increased for progressive supranuclear palsy in the putamen, caudate, thalamus, an

159 ology in Alzheimer's disease and progressive supranuclear palsy in vivo would help to develop biomark

160 Progressive supranuclear palsy is a 4R tauopathy with neuronal and g

161 Progressive supranuclear palsy is a rare neurodegenerative disease a

162 Although progressive supranuclear palsy is considered an atypical parkinsonia

163 Although progressive supranuclear palsy is defined by its akinetic rigidity,

164 a rare clinical presentation of progressive supranuclear palsy occurring in only 6 of the 179 pathol

165 vascular dementia (AUC=92.13%), progressive supranuclear palsy or corticobasal syndrome (AUC=88.47%)

166 ure closely resembling classical progressive supranuclear palsy or Richardson's syndrome, and we prop

167 e value of 23.8%; six others had progressive supranuclear palsy pathology, five had Alzheimer's disea

168 supranuclear palsy syndrome with progressive supranuclear palsy pathology.

169 icobasal syndrome had underlying progressive supranuclear palsy pathology.

170 in any corticobasal syndrome and progressive supranuclear palsy patients or controls.

171 latency to residential care than progressive supranuclear palsy patients, whereas patients with Lewy

172 ases presented clinically with a progressive supranuclear palsy phenotype and 29% of cases with corti

173 Thus, the R5L mutation causes a progressive supranuclear palsy phenotype, presumably by a gain-of-fu

174 rols from the PIck's disease and Progressive supranuclear palsy Prevalence and INcidence study (PiPPI

175 nts with Alzheimer's disease and progressive supranuclear palsy relative to controls [main effect of

176 roving detection sensitivity for progressive supranuclear palsy seeds by ~10(6) Hofmeister analysis a

177 The corticobasal degeneration/progressive supranuclear palsy set showed white matter abnormalities

178 a (the corticobasal degeneration/progressive supranuclear palsy set), anterior temporal lobes in sema

179 with multiple system atrophy and progressive supranuclear palsy shared several symptoms and signs, at

180 , P < 0.04); while patients with progressive supranuclear palsy showed, relative to controls, increas

181 (R5L) was identified in a single progressive supranuclear palsy subject that was not in the other pro

182 ubject that was not in the other progressive supranuclear palsy subjects or in 96 controls.

183 was screened for mutations in 96 progressive supranuclear palsy subjects.

184 The progressive supranuclear palsy subtype of FTLD-tau consistently caus

185 ated with Pick, corticobasal and progressive supranuclear palsy subtypes of tau pathology, respective

186 f FTD, corticobasal syndrome and progressive supranuclear palsy syndrome were identified out of the 9

187 ntia with FUS pathology; and the progressive supranuclear palsy syndrome with progressive supranuclea

188 frontotemporal dementia and the progressive supranuclear palsy syndrome, corticobasal syndrome, and

189 ined frontotemporal dementia and progressive supranuclear palsy syndrome.

190 availability of binding sites on progressive supranuclear palsy tau deposits for 11C-PBB3 than 18F-AV

191 pt size' are also more common in progressive supranuclear palsy than in Parkinson's disease.

192 e, corticobasal degeneration and progressive supranuclear palsy using the Interpersonal Reactivity In

193 e finger separation amplitude in progressive supranuclear palsy was less than half of that in control

194 The average amplitude slope in progressive supranuclear palsy was nearly zero (0.01 degrees /cycle)

195 controls, Parkinson's disease or progressive supranuclear palsy was observed.

196 But patients with progressive supranuclear palsy were strongly biased towards a pro-sa

197 a, corticobasal degeneration and progressive supranuclear palsy were, with one exception, associated

198 years with probable or possible progressive supranuclear palsy with a score of 20 or greater on the

199 N in multiple system atrophy and progressive supranuclear palsy with an identical localisation of the

200 ients with pathologically proven progressive supranuclear palsy with Richardson syndrome (n = 15).

201 in corticobasal degeneration and progressive supranuclear palsy without labeling the predominant glia

202 pathic Parkinson's Disease(IPD), Progressive Supranuclear Palsy(PSP) or Multiple System Atrophy(MSA).

203 iple system atrophy, and 13 with progressive supranuclear palsy) who were followed up for 5 to 9 year

204 ndrome), a rare complex disease (progressive supranuclear palsy), and a common complex disease (Alzhe

205 o-morbid FTD-spectrum pathology (progressive supranuclear palsy).

206 ltiple system atrophy and 50% in progressive supranuclear palsy).

207 , dementia with Lewy bodies, and progressive supranuclear palsy).

208 multiple system atrophy, 34 with progressive supranuclear palsy, 15 with corticobasal degeneration, 5

209 en subjects (4 controls, 6 AD, 3 progressive supranuclear palsy, 2 cortico basal syndrome) underwent

210 en subjects (4 controls, 6 AD, 3 progressive supranuclear palsy, 2 cortico basal syndrome) underwent

211 , 16 semantic dementia [SD]), 22 progressive supranuclear palsy, 50 Alzheimer disease, 6 Parkinson di

212 isk SNPs in STX6 are shared with progressive supranuclear palsy, a neurodegenerative disease associat

213 not in controls or patients with progressive supranuclear palsy, a type of FTLD-tau.

214 had been clinically diagnosed as progressive supranuclear palsy, all of whom had vertical supranuclea

215 ve impairment), 19 patients with progressive supranuclear palsy, and 13 age- and sex-matched controls

216 basal syndrome, 31 patients with progressive supranuclear palsy, and 222 control subjects.

217 tients with Alzheimer's disease, progressive supranuclear palsy, and a control case to assess the 18F

218 , including Alzheimer's disease, progressive supranuclear palsy, and cases of frontotemporal dementia

219 ies such as Alzheimer's disease, progressive supranuclear palsy, and chronic traumatic encephalopathy

220 ermined for Alzheimer's disease, progressive supranuclear palsy, and corticobasal degeneration patien

221 gnosing multiple-system atrophy, progressive supranuclear palsy, and corticobasal degeneration was co

222 hronic traumatic encephalopathy, progressive supranuclear palsy, and corticobasal degeneration.

223 rgyrophilic grain disease (AGD), progressive supranuclear palsy, and corticobasal degeneration.

224 g frontotemporal dementia (FTD), progressive supranuclear palsy, and corticobasal degeneration.

225 cluding multiple-system atrophy, progressive supranuclear palsy, and corticobasal degeneration.

226 , including Alzheimer's disease, progressive supranuclear palsy, and dementia with Lewy bodies, we fo

227 the brains of patients with Down's syndrome, supranuclear palsy, and prion disease.

228 a, corticobasal degeneration and progressive supranuclear palsy, are characterized by aggregates of t

229 itive impairment associated with progressive supranuclear palsy, but also point to comparable dysfunc

230 both multiple system atrophy and progressive supranuclear palsy, but not Parkinson's disease, showed

231 hardson syndrome presentation of progressive supranuclear palsy, characterized by postural instabilit

232 ion causing Alzheimer's disease, progressive supranuclear palsy, chronic traumatic encephalopathy, an

233 f 4-repeat isoforms in brains of progressive supranuclear palsy, corticobasal degeneration and famili

234 peat (4R) tauopathies, including progressive supranuclear palsy, corticobasal degeneration, and argyr

235 brain tissue from Pick disease, progressive supranuclear palsy, corticobasal degeneration, and chron

236 Mean SUVRs were calculated for progressive supranuclear palsy, corticobasal degeneration, and neuro

237 e had non-Alzheimer tauopathies (progressive supranuclear palsy, corticobasal degeneration, argyrophi

238 DNA binding protein 43 (TDP-43), progressive supranuclear palsy, corticobasal degeneration, dementia

239 ia disorders (Parkinson disease, progressive supranuclear palsy, corticobasal degeneration, multiple

240 egenerative disorders, including progressive supranuclear palsy, corticobasal degeneration, Parksinso

241 trophy, frontotemporal dementia, progressive supranuclear palsy, corticobasal syndrome and controls.

242 corticobasal degeneration, nine progressive supranuclear palsy, eight Pick's disease, three frontote

243 Like progressive supranuclear palsy, globular glial tauopathy and argyrop

244 one of the 298 controls, who had progressive supranuclear palsy, had IgLON5 antibodies.

245 at corticobasal degeneration and progressive supranuclear palsy, in particular, might be identifiable

246 ntotemporal dementia and 18 with progressive supranuclear palsy, including both Richardson's syndrome

247 , corticobasal degeneration, and progressive supranuclear palsy, likely representing a major regulato

248 tter in a subset of 70 patients (progressive supranuclear palsy, n = 22; corticobasal syndrome, n = 1

249 hies as frontotemporal dementia, progressive supranuclear palsy, or Alzheimer's disease.

250 es but not in Alzheimer disease, progressive supranuclear palsy, or multiple system atrophy.

251 inopathies: Alzheimer's disease, progressive supranuclear palsy, Parkinson's disease, dementia with L

252 Compared with progressive supranuclear palsy, patients with corticobasal degenerat

253 neuronal tau pathologies in CBD, progressive supranuclear palsy, PiD, and frontotemporal dementia wit

254 e partly resembled those seen in progressive supranuclear palsy, presenting these animals as a model

255 stem atrophy (P < 0.001) but not progressive supranuclear palsy, presumably because of the overlap (

256 Conversely, in patients with progressive supranuclear palsy, relative to patients with Alzheimer'

257 In progressive supranuclear palsy, the mean amplitude was not correlate

258 thout decrement in patients with progressive supranuclear palsy, which differed from the finger tap p

259 in corticobasal degeneration and progressive supranuclear palsy-a pathologically proven feature of th

260 g both Richardson's syndrome and progressive supranuclear palsy-frontal subtypes) and 20 healthy cont

261 s with corticobasal syndrome had progressive supranuclear palsy-like features and 30% of patients wit

262 evolve and develop a devastating progressive supranuclear palsy-like syndrome approximately 5 years a

263 symptoms that had evolved into a progressive supranuclear palsy-like syndrome; they showed a combinat

264 palsy-tau pathology now include progressive supranuclear palsy-parkinsonism (PSP-P), in addition to

265 e, and vergence dysfunction, and progressive supranuclear palsy-related lid retraction, frequent squa

266 rticobasal degeneration- and the progressive supranuclear palsy-related metabolic topographies.

267 alues for a previously validated progressive supranuclear palsy-related pattern provided excellent sp

268 variant of MSA (MSA-C), 17 with progressive supranuclear palsy-Richardson syndrome (PSP-RS), and 10

269 inical syndromes associated with progressive supranuclear palsy-tau pathology now include progressive

270 and in all regions examined for progressive supranuclear palsy.

271 se, multiple system atrophy, and progressive supranuclear palsy.

272 ing and caring for patients with progressive supranuclear palsy.

273 xamine brainstem pathogenesis of progressive supranuclear palsy.

274 in corticobasal degeneration and progressive supranuclear palsy.

275 eatment of Alzheimer disease and progressive supranuclear palsy.

276 t of frontotemporal dementia and progressive supranuclear palsy.

277 degenerative diseases, including progressive supranuclear palsy.

278 eimer disease, Pick disease, and progressive supranuclear palsy.

279 se of multiple system atrophy or progressive supranuclear palsy.

280 se, multiple system atrophy, and progressive supranuclear palsy.

281 is also associated with risk for progressive supranuclear palsy.

282 l tolerated in participants with progressive supranuclear palsy.

283 NFTs in Alzheimer's disease and progressive supranuclear palsy.

284 y of BIIB092 in individuals with progressive supranuclear palsy.

285 a potential novel treatment for progressive supranuclear palsy.

286 such as Alzheimer's disease and progressive supranuclear palsy.

287 as Alzheimer's disease (AD) and progressive supranuclear palsy.

288 latively little loss, as seen in progressive supranuclear palsy.

289 ological characteristics such as progressive supranuclear palsy.

290 hology, but less specifically in progressive supranuclear palsy.

291 y in primary tauopathies such as progressive supranuclear palsy.

292 cortico basal syndrome, but not progressive supranuclear palsy.

293 Subgroup classifications of progressive supranuclear palsy/corticobasal degeneration (PSP/CBD) o

294 orticobasal degeneration: 92.7%; progressive supranuclear palsy: 94.1%) in classifying 58 testing sub

295 ; multiple system atrophy versus progressive supranuclear palsy: OR: 11.2, 95% CI: 3.2-39.2, P < 0.01

296 (multiple system atrophy versus progressive supranuclear palsy: OR: 3.4, 95% CI: 1.2-9.7, P = 0.023)

297 proteins and lipids from each intermixing in supranuclear recycling endosomes (REs).

298 l layers, whereas GalNAc-T2 was found in the supranuclear region of the basal cell layers of both cor

299 luding oculomotor nerves or nuclei, vertical supranuclear saccadic centres, and convergence neurons.

300 rly onset of postural instability and falls, supranuclear vertical gaze palsy and cognitive dysfuncti