ライフサイエンスコーパス: supranuclear palsy

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

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

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

4 and in all regions examined for progressive supranuclear palsy.

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

6 ing and caring for patients with progressive supranuclear palsy.

7 xamine brainstem pathogenesis of progressive supranuclear palsy.

8 in corticobasal degeneration and progressive supranuclear palsy.

9 eatment of Alzheimer disease and progressive supranuclear palsy.

10 degenerative diseases, including progressive supranuclear palsy.

11 t of frontotemporal dementia and progressive supranuclear palsy.

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

13 se of multiple system atrophy or progressive supranuclear palsy.

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

15 is also associated with risk for progressive supranuclear palsy.

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

17 l tolerated in participants with progressive supranuclear palsy.

18 a common genetic background with progressive supranuclear palsy.

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

20 y of BIIB092 in individuals with progressive supranuclear palsy.

21 ibution similar to that found in progressive supranuclear palsy.

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

23 a potential novel treatment for progressive supranuclear palsy.

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

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

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

27 ological characteristics such as progressive supranuclear palsy.

28 hology, but less specifically in progressive supranuclear palsy.

29 y in primary tauopathies such as progressive supranuclear palsy.

30 cortico basal syndrome, but not progressive supranuclear palsy.

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

32 %), Alzheimer disease (AD, 23%), progressive supranuclear palsy (13%), and frontotemporal lobar degen

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

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

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

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

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

38 , 16 semantic dementia [SD]), 22 progressive supranuclear palsy, 50 Alzheimer disease, 6 Parkinson di

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

72 Progressive supranuclear palsy and Parkinson's disease have distinct

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

118 Donors with progressive supranuclear palsy exhibited more variation in inhibitor

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

120 Progressive supranuclear palsy filaments contain 4R tau.

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

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

123 Like progressive supranuclear palsy, globular glial tauopathy and argyrop

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

125 87% of finger tap trials in the progressive supranuclear palsy group and only 12% in the Parkinson's

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

141 Progressive supranuclear palsy is a rare neurodegenerative disease a

142 Although progressive supranuclear palsy is considered an atypical parkinsonia

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 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)

163 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)

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

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

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

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

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

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

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

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

172 supranuclear palsy syndrome with progressive supranuclear palsy pathology.

173 icobasal syndrome had underlying progressive supranuclear palsy pathology.

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

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

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

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

178 Compared with progressive supranuclear palsy, patients with corticobasal degenerat

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

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

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

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

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

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

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

186 Progressive supranuclear palsy (PSP) and corticobasal degeneration (

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

188 Progressive supranuclear palsy (PSP) and corticobasal degeneration (

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

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

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

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

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

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

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

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

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

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

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

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

201 8Q polymorphism for DJ-1, and in progressive supranuclear palsy (PSP) brains.

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

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

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

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

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

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

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

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

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

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

212 Progressive supranuclear palsy (PSP) is a neurodegenerative disorder

213 Progressive supranuclear palsy (PSP) is a progressive neurodegenerat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

280 ined frontotemporal dementia and progressive supranuclear palsy syndrome.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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