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 f melanin to keratinocytes and formation of "supranuclear caps," as occurs in naturally pigmented ski

4 ible cellular mechanism for the formation of supranuclear cataract.

5 These supranuclear cataracts colocalised with enhanced Abeta i

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

7 gation, extracerebral amyloid formation, and supranuclear cataracts.

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

9 orting cells; ubiquitin IR was confined to a supranuclear cone-shaped region.

10 ss certain but may be the result of abnormal supranuclear control of the superior colliculus resultin

11 Diffuse or supranuclear cytoplasmic staining occurred in about one

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

13 The dextran remains in the large supranuclear EEA1-positive early endosomes while recycli

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

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

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

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

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

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

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

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

22 a patient with any combination of dementia, supranuclear gaze palsy, hypothalamic manifestations, my

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

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

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

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

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

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

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

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

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

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

33 iple neurological symptoms, such as vertical supranuclear ophthalmoplegia, progressive ataxia, and de

34 %), Alzheimer disease (AD, 23%), progressive supranuclear palsy (13%), and frontotemporal lobar degen

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

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

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

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

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

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

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

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

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

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

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

46 Progressive supranuclear palsy (PSP) and corticobasal degeneration (

47 imer disease (AD), Pick disease, progressive supranuclear palsy (PSP) and corticobasal degeneration (

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

49 Progressive supranuclear palsy (PSP) and corticobasal degeneration (

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

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

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

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

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

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

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

57 The prevalence of progressive supranuclear palsy (PSP) and multiple system atrophy (MS

58 8Q polymorphism for DJ-1, and in progressive supranuclear palsy (PSP) brains.

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

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

61 e excessively represented in the progressive supranuclear palsy (PSP) group, compared with the age-ma

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

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

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

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

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

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

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

69 Progressive supranuclear palsy (PSP) is a progressive neurodegenerat

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

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

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

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

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

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

76 The clinical features of progressive supranuclear palsy (PSP) overlap with other parkinsonian

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

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

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

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

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

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

83 urological conditions, including progressive supranuclear palsy (PSP), a late-onset atypical parkinso

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

85 In this review, we will focus on progressive supranuclear palsy (PSP), a rare parkinsonian disorder w

86 rophy (MSA), pure akinesia (PA), progressive supranuclear palsy (PSP), and cortical-basal ganglionic

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

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

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

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

91 ver-represented in patients with progressive supranuclear palsy (PSP), extending earlier reports of a

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

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

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

95 In Alzheimer's disease and progressive supranuclear palsy (PSP), tau proteins assemble into str

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

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

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

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

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

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

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

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

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

105 he difficulty in differentiating progressive supranuclear palsy (PSP, also called Steele-Richardson-O

106 ntington's disease (HD, n = 11), progressive supranuclear palsy (PSP, n = 11), young adult normal con

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

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

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

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

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

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

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 with AD, Parkinson's disease, or progressive supranuclear palsy and control subjects seen at a large

116 The implications of considering progressive supranuclear palsy and corticobasal degeneration as tauo

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

118 of neuronal involvement found in progressive supranuclear palsy and corticobasal degeneration may hel

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

120 vidual patients using 1H-MRSI in progressive supranuclear palsy and corticobasal degeneration, detect

121 enetic risk factors for sporadic progressive supranuclear palsy and corticobasal degeneration, tau ab

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

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

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

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

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

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 l and pathologic overlap between progressive supranuclear palsy and other disorders remains.

134 Progressive supranuclear palsy and Parkinson's disease have distinct

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

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

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

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

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

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

141 ile both Parkinson's disease and progressive supranuclear palsy brains showed marked depletion.

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

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

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

145 Progressive supranuclear palsy filaments contain 4R tau.

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

147 87% of finger tap trials in the progressive supranuclear palsy group and only 12% in the Parkinson's

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

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

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

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

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

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

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

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

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

157 Although progressive supranuclear palsy is considered an atypical parkinsonia

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

159 d to control tissue, and also in progressive supranuclear palsy nigra, but not Parkinson's disease ni

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

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

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

163 supranuclear palsy syndrome with progressive supranuclear palsy pathology.

164 icobasal syndrome had underlying progressive supranuclear palsy pathology.

165 he possible misclassification of progressive supranuclear palsy patients as Parkinson's disease, but

166 t may contribute toward managing progressive supranuclear palsy patients better are discussed and the

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

168 Progressive supranuclear palsy patients, compared with control subje

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

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

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

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

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

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

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

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

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

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

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

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

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

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

183 ined frontotemporal dementia and progressive supranuclear palsy syndrome.

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

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

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

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

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

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

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

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

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

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

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

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

196 al Disorders and the Society for Progressive Supranuclear Palsy) diagnostic criteria for PSP were app

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

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

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

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

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

202 study included 12 patients with progressive supranuclear palsy, 10 with Parkinson's disease, nine wi

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

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

205 , 16 semantic dementia [SD]), 22 progressive supranuclear palsy, 50 Alzheimer disease, 6 Parkinson di

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

207 ropathologic phenotype resembles progressive supranuclear palsy, an alternative consideration is that

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

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

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

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

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

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

214 nsonism linked to chromosome 17, progressive supranuclear palsy, and corticobasal degeneration.

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

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

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

218 radic corticobasal degeneration, progressive supranuclear palsy, and Pick's disease, as well as by he

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

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

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

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

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

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

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

226 sorders, such as Pick's disease, progressive supranuclear palsy, corticobasal degeneration and famili

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

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

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

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

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

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

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

234 e forms of subcortical dementia (progressive supranuclear palsy, Huntington's and Parkinson's disease

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

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

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

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

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

240 cortical neuronal involvement in progressive supranuclear palsy, Parkinson's disease and corticobasal

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

242 Compared with progressive supranuclear palsy, patients with corticobasal degenerat

243 ommon neurodegenerative diseases-progressive supranuclear palsy, Pick's disease, and corticobasal deg

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

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

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

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

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

249 In sporadic cases of progressive supranuclear palsy, the presence of the H1 haplotype was

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

251 the clinicopathologic markers of progressive supranuclear palsy, which have helped establish standard

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

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

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

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

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

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

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

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

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

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

262 ing and caring for patients with progressive supranuclear palsy.

263 xamine brainstem pathogenesis of progressive supranuclear palsy.

264 in corticobasal degeneration and progressive supranuclear palsy.

265 eatment of Alzheimer disease and progressive supranuclear palsy.

266 degenerative diseases, including progressive supranuclear palsy.

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

268 se of multiple system atrophy or progressive supranuclear palsy.

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

270 ological characteristics such as progressive supranuclear palsy.

271 is also associated with risk for progressive supranuclear palsy.

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

273 hology, but less specifically in progressive supranuclear palsy.

274 a common genetic background with progressive supranuclear palsy.

275 er or a spectrum of disease with progressive supranuclear palsy.

276 y in primary tauopathies such as progressive supranuclear palsy.

277 ibution similar to that found in progressive supranuclear palsy.

278 on, and Parkinson's disease with progressive supranuclear palsy.

279 cortico basal syndrome, but not progressive supranuclear palsy.

280 and in all regions examined for progressive supranuclear palsy.

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

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

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

284 ous cytoplasmic plaques mostly stored in the supranuclear part of the hair cells.

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

286 ining localized the protein primarily to the supranuclear region of colon carcinoma cells, whereas no

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

288 eactivity was localized in the dendritic and supranuclear regions.

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

290 patients, the main ocular motor finding was supranuclear vertical gaze impairment with slow vertical

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

292 Supranuclear vertical gaze palsy and increased age at sy

293 Supranuclear vertical gaze palsy, gait instability and t

294 Supranuclear vertical gaze palsy, moderate or severe pos

295 ed systemic symptoms and neurological signs (supranuclear vertical gaze palsy, rhythmic myoclonus, de

296 f patients, and were always accompanied by a supranuclear vertical gaze palsy.