ライフサイエンスコーパス: progressive supranuclear palsy

1 ad primary co-morbid FTD-spectrum pathology (progressive supranuclear palsy).

2 s (22% in multiple system atrophy and 50% in progressive supranuclear palsy).

3 er's disease, dementia with Lewy bodies, and progressive supranuclear palsy).

4 tem atrophy, and in all regions examined for progressive supranuclear palsy.

5 nson's disease, multiple system atrophy, and progressive supranuclear palsy.

6 those managing and caring for patients with progressive supranuclear palsy.

7 a model to examine brainstem pathogenesis of progressive supranuclear palsy.

8 e pathology in corticobasal degeneration and progressive supranuclear palsy.

9 s for the treatment of Alzheimer disease and progressive supranuclear palsy.

10 other neurodegenerative diseases, including progressive supranuclear palsy.

11 rug treatment of frontotemporal dementia and progressive supranuclear palsy.

12 cluding Alzheimer disease, Pick disease, and progressive supranuclear palsy.

13 milar to those of multiple system atrophy or progressive supranuclear palsy.

14 nson's disease, multiple system atrophy, and progressive supranuclear palsy.

15 n that SNP6 is also associated with risk for progressive supranuclear palsy.

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

17 rs to be well tolerated in participants with progressive supranuclear palsy.

18 tion shares a common genetic background with progressive supranuclear palsy.

19 arate disorder or a spectrum of disease with progressive supranuclear palsy.

20 tolerability of BIIB092 in individuals with progressive supranuclear palsy.

21 with a distribution similar to that found in progressive supranuclear palsy.

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

23 assessed as a potential novel treatment for progressive supranuclear palsy.

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

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

26 sease, to relatively little loss, as seen in progressive supranuclear palsy.

27 cal and pathological characteristics such as progressive supranuclear palsy.

28 ated tau pathology, but less specifically in progressive supranuclear palsy.

29 y, especially in primary tauopathies such as progressive supranuclear palsy.

30 e extent for cortico basal syndrome, but not progressive supranuclear palsy.

31 2 (23%) had alternative causes for dementia (progressive supranuclear palsy = 1, Lewy body disease =

32 were CBD (35%), Alzheimer disease (AD, 23%), progressive supranuclear palsy (13%), and frontotemporal

33 se, 34 with multiple system atrophy, 34 with progressive supranuclear palsy, 15 with corticobasal deg

34 20 cases), and the most common tauopathy was progressive supranuclear palsy (16 cases).

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

36 thods: Fifteen subjects (4 controls, 6 AD, 3 progressive supranuclear palsy, 2 cortico basal syndrome

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

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

39 including Lewy body disease (12.8%; n = 26), progressive supranuclear palsy (6.4%; n = 13), cerebrova

40 , 96% specificity, 97% PPV, and 83% NPV) and progressive supranuclear palsy (88% sensitivity, 94% spe

41 ecificity (corticobasal degeneration: 92.7%; progressive supranuclear palsy: 94.1%) in classifying 58

42 Risk SNPs in STX6 are shared with progressive supranuclear palsy, a neurodegenerative dise

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

44 tter lesion in corticobasal degeneration and progressive supranuclear palsy-a pathologically proven f

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

46 and the neuropathologic phenotype resembles progressive supranuclear palsy, an alternative considera

47 pt size, was present in 75% of patients with progressive supranuclear palsy and 15% of patients with

48 rment was observed in 62.0% of patients with progressive supranuclear palsy and 31.8% of those with m

49 om patients with AD, Parkinson's disease, or progressive supranuclear palsy and control subjects seen

50 temporal lobar degeneration, Pick's disease, progressive supranuclear palsy and corticobasal degenera

51 cal regions were higher in autopsy-confirmed progressive supranuclear palsy and corticobasal degenera

52 other tauopathies including Pick's disease, progressive supranuclear palsy and corticobasal degenera

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

54 nks FTD to other forms of tauopathy, such as progressive supranuclear palsy and corticobasal degenera

55 ementia with Lewy bodies but is not found in progressive supranuclear palsy and corticobasal degenera

56 pear to be genetic risk factors for sporadic progressive supranuclear palsy and corticobasal degenera

57 The implications of considering progressive supranuclear palsy and corticobasal degenera

58 between individual patients using 1H-MRSI in progressive supranuclear palsy and corticobasal degenera

59 nal pattern of neuronal involvement found in progressive supranuclear palsy and corticobasal degenera

60 ons from neurodegeneration and tau burden in progressive supranuclear palsy and corticobasal degenera

61 tive diseases including Alzheimer's disease, progressive supranuclear palsy and corticobasal degenera

62 pecific binding was, however, found on human progressive supranuclear palsy and corticobasal degenera

63 riants of primary progressive aphasia (PPA), progressive supranuclear palsy and corticobasal syndrome

64 Many patients with progressive supranuclear palsy and corticobasal syndrome

65 CK1 in multiple system atrophy compared with progressive supranuclear palsy and corticobasal syndrome

66 anguage variants of frontotemporal dementia, progressive supranuclear palsy and corticobasal syndrome

67 of modality-independent social cognition in progressive supranuclear palsy and explore the neural co

68 We have recently examined the MAPT locus in progressive supranuclear palsy and found that a haplotyp

69 ous to the tau haplotype over-represented in progressive supranuclear palsy and further extend the si

70 spectively recruited cohort of patients with progressive supranuclear palsy and multiple system atrop

71 tudy identified new genetic risk factors for progressive supranuclear palsy and new genetic condition

72 the clinical and pathologic overlap between progressive supranuclear palsy and other disorders remai

73 Progressive supranuclear palsy and Parkinson's disease h

74 nson's disease, multiple system atrophy, and progressive supranuclear palsy and to accurately disting

75 dividuals presented with an atypical form of progressive supranuclear palsy and two others with eithe

76 zheimer's disease, relative to patients with progressive supranuclear palsy and with control subjects

77 he testes syndrome), a rare complex disease (progressive supranuclear palsy), and a common complex di

78 mild cognitive impairment), 19 patients with progressive supranuclear palsy, and 13 age- and sex-matc

79 with corticobasal syndrome, 31 patients with progressive supranuclear palsy, and 222 control subjects

80 ssue from patients with Alzheimer's disease, progressive supranuclear palsy, and a control case to as

81 ive diseases, including Alzheimer's disease, progressive supranuclear palsy, and cases of frontotempo

82 led tauopathies such as Alzheimer's disease, progressive supranuclear palsy, and chronic traumatic en

83 n disease, chronic traumatic encephalopathy, progressive supranuclear palsy, and corticobasal degener

84 k disease, argyrophilic grain disease (AGD), progressive supranuclear palsy, and corticobasal degener

85 ia and parkinsonism linked to chromosome 17, progressive supranuclear palsy, and corticobasal degener

86 es, including frontotemporal dementia (FTD), progressive supranuclear palsy, and corticobasal degener

87 yndromes, including multiple-system atrophy, progressive supranuclear palsy, and corticobasal degener

88 ics were determined for Alzheimer's disease, progressive supranuclear palsy, and corticobasal degener

89 PET for diagnosing multiple-system atrophy, progressive supranuclear palsy, and corticobasal degener

90 tauopathies, including Alzheimer's disease, progressive supranuclear palsy, and dementia with Lewy b

91 ified by sporadic corticobasal degeneration, progressive supranuclear palsy, and Pick's disease, as w

92 n's disease or dementia with Lewy bodies) or progressive supranuclear palsy are misdiagnosed as havin

93 asal degeneration have been revised, and for progressive supranuclear palsy are under revision.

94 oral dementia, corticobasal degeneration and progressive supranuclear palsy, are characterized by agg

95 F pattern compared with the 13 patients with progressive supranuclear palsy (baseline area under the

96 subjects, while both Parkinson's disease and progressive supranuclear palsy brains showed marked depl

97 evel of cognitive impairment associated with progressive supranuclear palsy, but also point to compar

98 ntia nigra, both multiple system atrophy and progressive supranuclear palsy, but not Parkinson's dise

99 n only 6 of the 179 pathologically diagnosed progressive supranuclear palsy cases (3%).

100 with the Richardson syndrome presentation of progressive supranuclear palsy, characterized by postura

101 urodegeneration causing Alzheimer's disease, progressive supranuclear palsy, chronic traumatic enceph

102 ve response DNA binding protein 43 (TDP-43), progressive supranuclear palsy, corticobasal degeneratio

103 tiple neurodegenerative disorders, including progressive supranuclear palsy, corticobasal degeneratio

104 Mean SUVRs were calculated for progressive supranuclear palsy, corticobasal degeneratio

105 thology, nine had non-Alzheimer tauopathies (progressive supranuclear palsy, corticobasal degeneratio

106 with four-repeat (4R) tauopathies, including progressive supranuclear palsy, corticobasal degeneratio

107 basal ganglia disorders (Parkinson disease, progressive supranuclear palsy, corticobasal degeneratio

108 dementing disorders, such as Pick's disease, progressive supranuclear palsy, corticobasal degeneratio

109 mortem human brain tissue from Pick disease, progressive supranuclear palsy, corticobasal degeneratio

110 comprised of 4-repeat isoforms in brains of progressive supranuclear palsy, corticobasal degeneratio

111 ple system atrophy, frontotemporal dementia, progressive supranuclear palsy, corticobasal syndrome an

112 Subgroup classifications of progressive supranuclear palsy/corticobasal degeneration

113 f Neurological Disorders and the Society for Progressive Supranuclear Palsy) diagnostic criteria for

114 Most scripts performed by patients with progressive supranuclear palsy did not exhibit decrement

115 D-tau (34 10 corticobasal degeneration, nine progressive supranuclear palsy, eight Pick's disease, th

116 Donors with progressive supranuclear palsy exhibited more variation

117 ry patient with corticobasal degeneration or progressive supranuclear palsy fell outside 95% of the n

118 Progressive supranuclear palsy filaments contain 4R tau.

119 oundation for a clinical test to distinguish progressive supranuclear palsy from Lewy body disorders.

120 sy, including both Richardson's syndrome and progressive supranuclear palsy-frontal subtypes) and 20

121 Like progressive supranuclear palsy, globular glial tauopathy

122 ent was observed in approximately 57% of the progressive supranuclear palsy group and 20% of the mult

123 dentified in 87% of finger tap trials in the progressive supranuclear palsy group and only 12% in the

124 Although the progressive supranuclear palsy group performed worse ove

125 palsy-like features and 30% of patients with progressive supranuclear palsy had corticobasal syndrome

126 articipants with frontotemporal dementia and progressive supranuclear palsy had impaired response inh

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

128 We conclude that patients with progressive supranuclear palsy have a multimodal deficit

129 In conclusion, patients with progressive supranuclear palsy have a specific finger ta

130 drome, it is not known whether patients with progressive supranuclear palsy have criteria-defined bra

131 isorders such as multiple system atrophy and progressive supranuclear palsy have elevated free-water

132 system atrophy versus Lewy body disease and progressive supranuclear palsy if a patient developed or

133 differentiate corticobasal degeneration from progressive supranuclear palsy in patients with Richards

134 n the putamen and caudate, and increased for progressive supranuclear palsy in the putamen, caudate,

135 of tau pathology in Alzheimer's disease and progressive supranuclear palsy in vivo would help to dev

136 indicate that corticobasal degeneration and progressive supranuclear palsy, in particular, might be

137 variant frontotemporal dementia and 18 with progressive supranuclear palsy, including both Richardso

138 Progressive supranuclear palsy is a 4R tauopathy with ne

139 Progressive supranuclear palsy is a rare neurodegenerati

140 Although progressive supranuclear palsy is considered an atypical

141 Although progressive supranuclear palsy is defined by its akineti

142 t of patients with corticobasal syndrome had progressive supranuclear palsy-like features and 30% of

143 ill rapidly evolve and develop a devastating progressive supranuclear palsy-like syndrome approximate

144 gression of symptoms that had evolved into a progressive supranuclear palsy-like syndrome; they showe

145 disease (AD), corticobasal degeneration, and progressive supranuclear palsy, likely representing a ma

146 erosis (ALS), multiple system atrophy (MSA), progressive supranuclear palsy (MSP)).

147 n differentiate multiple system atrophy from progressive supranuclear palsy (multiple system atrophy

148 for 27 patients subsequently diagnosed with progressive supranuclear palsy (n = 16, seven males, age

149 degeneration and in vivo volume loss in both progressive supranuclear palsy (n = 340 regions; beta 0.

150 either corticobasal degeneration (n = 5) or progressive supranuclear palsy (n = 4).

151 patients with Parkinson's disease (n = 15), progressive supranuclear palsy (n = 9) and healthy age-

152 of either multiple system atrophy (n=372) or progressive supranuclear palsy (n=311) from the Neuropro

153 ndent of neurodegeneration severity, in both progressive supranuclear palsy [n = 340 regions; beta 0.

154 and white matter in a subset of 70 patients (progressive supranuclear palsy, n = 22; corticobasal syn

155 igra compared to control tissue, and also in progressive supranuclear palsy nigra, but not Parkinson'

156 syndrome is a rare clinical presentation of progressive supranuclear palsy occurring in only 6 of th

157 ss cohorts), vascular dementia (AUC=92.13%), progressive supranuclear palsy or corticobasal syndrome

158 linical picture closely resembling classical progressive supranuclear palsy or Richardson's syndrome,

159 panded ATXN2 repeats with the development of progressive supranuclear palsy (OR = 5.83; P= 0.004; rep

160 se (OR: 7.0, 95% CI: 2.5-19.5, P < 0.01) and progressive supranuclear palsy (OR: 3.1, 95% CI: 1.1-8.9

161 se (OR: 8.8, 95% CI: 3.2-24.2, P < 0.01) and progressive supranuclear palsy (OR: 4.8, 95% CI: 1.7-13.

162 such tauopathies as frontotemporal dementia, progressive supranuclear palsy, or Alzheimer's disease.

163 from PD cases but not in Alzheimer disease, progressive supranuclear palsy, or multiple system atrop

164 7, P = 0.021; multiple system atrophy versus progressive supranuclear palsy: OR: 11.2, 95% CI: 3.2-39

165 uclear palsy (multiple system atrophy versus progressive supranuclear palsy: OR: 3.4, 95% CI: 1.2-9.7

166 ical and subcortical neuronal involvement in progressive supranuclear palsy, Parkinson's disease and

167 and synucleinopathies: Alzheimer's disease, progressive supranuclear palsy, Parkinson's disease, dem

168 supranuclear palsy-tau pathology now include progressive supranuclear palsy-parkinsonism (PSP-P), in

169 ve predictive value of 23.8%; six others had progressive supranuclear palsy pathology, five had Alzhe

170 progressive supranuclear palsy syndrome with progressive supranuclear palsy pathology.

171 es with corticobasal syndrome had underlying progressive supranuclear palsy pathology.

172 usting for the possible misclassification of progressive supranuclear palsy patients as Parkinson's d

173 Factors that may contribute toward managing progressive supranuclear palsy patients better are discu

174 ot detected in any corticobasal syndrome and progressive supranuclear palsy patients or controls.

175 Progressive supranuclear palsy patients, compared with c

176 and longer latency to residential care than progressive supranuclear palsy patients, whereas patient

177 Compared with progressive supranuclear palsy, patients with corticobas

178 generation cases presented clinically with a progressive supranuclear palsy phenotype and 29% of case

179 Thus, the R5L mutation causes a progressive supranuclear palsy phenotype, presumably by

180 f glial and neuronal tau pathologies in CBD, progressive supranuclear palsy, PiD, and frontotemporal

181 ansgenic mice partly resembled those seen in progressive supranuclear palsy, presenting these animals

182 multiple system atrophy (P < 0.001) but not progressive supranuclear palsy, presumably because of th

183 and 50 controls from the PIck's disease and Progressive supranuclear palsy Prevalence and INcidence

184 II) developed a movement disorder resembling progressive supranuclear palsy (PSP) and associated with

185 Progressive supranuclear palsy (PSP) and corticobasal de

186 ic feature of the neurodegenerative diseases progressive supranuclear palsy (PSP) and corticobasal de

187 type H1 is over-represented in patients with progressive supranuclear palsy (PSP) and corticobasal de

188 Progressive supranuclear palsy (PSP) and corticobasal de

189 ent in Alzheimer disease (AD), Pick disease, progressive supranuclear palsy (PSP) and corticobasal de

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

191 a-spectrum (FTD-s) disorders, including FTD, progressive supranuclear palsy (PSP) and corticobasal sy

192 says to include a limited number of cases of progressive supranuclear palsy (PSP) and dementia with L

193 ies, which include Alzheimer's disease (AD), progressive supranuclear palsy (PSP) and frontotemporal

194 Background The differential diagnosis of progressive supranuclear palsy (PSP) and Lewy body disor

195 gnostic predictors have not been defined for progressive supranuclear palsy (PSP) and multiple system

196 ationship to clinical disease progression in progressive supranuclear palsy (PSP) and multiple system

197 The prevalence of progressive supranuclear palsy (PSP) and multiple system

198 at distinguish Parkinson's disease (PD) from progressive supranuclear palsy (PSP) and multiple system

199 nostic factors and survival in patients with progressive supranuclear palsy (PSP) and multiple system

200 ease with R98Q polymorphism for DJ-1, and in progressive supranuclear palsy (PSP) brains.

201 nts with corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP) can sometimes prese

202 rements in postmortem brain samples from two progressive supranuclear palsy (PSP) cases and a MAPT P3

203 alleles were excessively represented in the progressive supranuclear palsy (PSP) group, compared wit

204 Testing for association of CBD with top progressive supranuclear palsy (PSP) GWAS single-nucleot

205 A diagnosis of progressive supranuclear palsy (PSP) had been considered

206 Although pathological heterogeneity of progressive supranuclear palsy (PSP) has also been estab

207 Progressive supranuclear palsy (PSP) has been conceptual

208 udies assessing binding to tau aggregates in progressive supranuclear palsy (PSP) have yielded mixed

209 a study to estimate the point prevalence of progressive supranuclear palsy (PSP) in the UK at nation

210 Progressive supranuclear palsy (PSP) is a movement disor

211 Progressive supranuclear palsy (PSP) is a neurodegenerat

212 Progressive supranuclear palsy (PSP) is a progressive ne

213 Progressive supranuclear palsy (PSP) is a rare and progr

214 Because progressive supranuclear palsy (PSP) is linked to tau pa

215 Neurodegenerative tauopathies, of which progressive supranuclear palsy (PSP) is one of the most

216 Progressive supranuclear palsy (PSP) is usually sporadic

217 PD compared with patients with diagnoses of progressive supranuclear palsy (PSP) or Alzheimer's dise

218 tic primary progressive aphasia (nfvPPA) and progressive supranuclear palsy (PSP) or corticobasal deg

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

220 We devised a Progressive Supranuclear Palsy (PSP) Rating Scale compri

221 The clinical diagnosis of progressive supranuclear palsy (PSP) relies on the ident

222 and [(18) F]AV-1451 PET in 17 patients with progressive supranuclear palsy (PSP) Richardson's syndro

223 ortical-dominant AD and subcortical-dominant progressive supranuclear palsy (PSP) tau topologies.

224 systems in multiple-system atrophy (MSA) and progressive supranuclear palsy (PSP) than in Parkinson d

225 agnosis of multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) were 85.7 (30 out o

226 occurs in multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) where nigral dopami

227 idiopathic Parkinson's disease (PD), 30 with progressive supranuclear palsy (PSP), 19 with corticobas

228 ariety of neurological conditions, including progressive supranuclear palsy (PSP), a late-onset atypi

229 auopathy with prominent Abeta pathology, and progressive supranuclear palsy (PSP), a primary tauopath

230 In this review, we will focus on progressive supranuclear palsy (PSP), a rare parkinsonia

231 Multiple-system atrophy (MSA), progressive supranuclear palsy (PSP), and corticobasal s

232 sorders, including Alzheimer's disease (AD), progressive supranuclear palsy (PSP), and frontotemporal

233 pical and atypical, pathologically diagnosed progressive supranuclear palsy (PSP), and investigated t

234 ncluding corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP), are neurodegenerat

235 nically with corticobasal syndrome (CBS) and progressive supranuclear palsy (PSP), both of which have

236 nificantly over-represented in patients with progressive supranuclear palsy (PSP), extending earlier

237 ypical parkinsonian syndromes (APSs) such as progressive supranuclear palsy (PSP), multiple system at

238 Progressive supranuclear palsy (PSP), multiple system at

239 Progressive supranuclear palsy (PSP), previously believe

240 while in corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP), tau also aggregate

241 In Alzheimer's disease and progressive supranuclear palsy (PSP), tau proteins assem

242 (IPD) from multiple system atrophy (MSA) and progressive supranuclear palsy (PSP), the most common at

243 ase (AD), frontotemporal dementia (FTD), and progressive supranuclear palsy (PSP).

244 in certain neurological disorders, including progressive supranuclear palsy (PSP).

245 al syndrome (CBS) but is not specific versus progressive supranuclear palsy (PSP).

246 of developing the neurodegenerative disease progressive supranuclear palsy (PSP).

247 FTLD-U), corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP).

248 es has histopathological features similar to progressive supranuclear palsy (PSP).

249 studies of multiple-system atrophy (MSA) and progressive supranuclear palsy (PSP).

250 he frequency of H1 haplotype is increased in progressive supranuclear palsy (PSP).

251 identify genetic determinants of survival in progressive supranuclear palsy (PSP).

252 cifically assessed as a prognostic factor in progressive supranuclear palsy (PSP).

253 pathology of both Alzheimer disease (AD) and progressive supranuclear palsy (PSP).

254 The difficulty in differentiating progressive supranuclear palsy (PSP, also called Steele-

255 This review provides an update on progressive supranuclear palsy (PSP, or Steele-Richardso

256 acted from postmortem brains of AD (AD-tau), progressive supranuclear palsy (PSP-tau), and corticobas

257 = 30), Parkinson's disease (PD; n = 32), and progressive supranuclear palsy (PSP; n = 31), were inclu

258 (18) F]-flortaucipir-PET and died with FTLD (progressive supranuclear palsy [PSP], n = 10; corticobas

259 rely in Idiopathic Parkinson's Disease(IPD), Progressive Supranuclear Palsy(PSP) or Multiple System A

260 ed blink rate, and vergence dysfunction, and progressive supranuclear palsy-related lid retraction, f

261 tween the corticobasal degeneration- and the progressive supranuclear palsy-related metabolic topogra

262 expression values for a previously validated progressive supranuclear palsy-related pattern provided

263 living patients with Alzheimer's disease and progressive supranuclear palsy relative to controls [mai

264 Conversely, in patients with progressive supranuclear palsy, relative to patients wit

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

266 e cerebellar variant of MSA (MSA-C), 17 with progressive supranuclear palsy-Richardson syndrome (PSP-

267 assays, improving detection sensitivity for progressive supranuclear palsy seeds by ~10(6) Hofmeiste

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

269 ssive aphasia (the corticobasal degeneration/progressive supranuclear palsy set), anterior temporal l

270 gh patients with multiple system atrophy and progressive supranuclear palsy shared several symptoms a

271 ain (t = 2.1, P < 0.04); while patients with progressive supranuclear palsy showed, relative to contr

272 nt mutation (R5L) was identified in a single progressive supranuclear palsy subject that was not in t

273 lear palsy subject that was not in the other progressive supranuclear palsy subjects or in 96 control

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

275 The progressive supranuclear palsy subtype of FTLD-tau consi

276 tion, associated with Pick, corticobasal and progressive supranuclear palsy subtypes of tau pathology

277 e variants of FTD, corticobasal syndrome and progressive supranuclear palsy syndrome were identified

278 emporal dementia with FUS pathology; and the progressive supranuclear palsy syndrome with progressive

279 der the term frontotemporal dementia and the progressive supranuclear palsy syndrome, corticobasal sy

280 inically defined frontotemporal dementia and progressive supranuclear palsy syndrome.

281 and higher availability of binding sites on progressive supranuclear palsy tau deposits for 11C-PBB3

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

283 ment in script size' are also more common in progressive supranuclear palsy than in Parkinson's disea

284 egeneration from multiple system atrophy and progressive supranuclear palsy (the two most common atyp

285 In progressive supranuclear palsy, the mean amplitude was n

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

287 mer's disease, corticobasal degeneration and progressive supranuclear palsy using the Interpersonal R

288 We recruited 23 patients with progressive supranuclear palsy (using clinical diagnosti

289 Average finger separation amplitude in progressive supranuclear palsy was less than half of tha

290 The average amplitude slope in progressive supranuclear palsy was nearly zero (0.01 deg

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

292 But patients with progressive supranuclear palsy were strongly biased towa

293 ssive apraxia, corticobasal degeneration and progressive supranuclear palsy were, with one exception,

294 pokinesia without decrement in patients with progressive supranuclear palsy, which differed from the

295 evaluating the clinicopathologic markers of progressive supranuclear palsy, which have helped establ

296 11 with multiple system atrophy, and 13 with progressive supranuclear palsy) who were followed up for

297 s aged 41-86 years with probable or possible progressive supranuclear palsy with a score of 20 or gre

298 sed in the SN in multiple system atrophy and progressive supranuclear palsy with an identical localis

299 red with patients with pathologically proven progressive supranuclear palsy with Richardson syndrome

300 l pathology in corticobasal degeneration and progressive supranuclear palsy without labeling the pred