ライフサイエンスコーパス: supranuclear palsy

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

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

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

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

5 ing and caring for patients with progressive supranuclear palsy.

6 xamine brainstem pathogenesis of progressive supranuclear palsy.

7 in corticobasal degeneration and progressive supranuclear palsy.

8 eatment of Alzheimer disease and progressive supranuclear palsy.

9 degenerative diseases, including progressive supranuclear palsy.

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

11 se of multiple system atrophy or progressive supranuclear palsy.

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

13 is also associated with risk for progressive supranuclear palsy.

14 ological characteristics such as progressive supranuclear palsy.

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

16 a common genetic background with progressive supranuclear palsy.

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

18 ibution similar to that found in progressive supranuclear palsy.

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

20 hology, but less specifically in progressive supranuclear palsy.

21 y in primary tauopathies such as progressive supranuclear palsy.

22 cortico basal syndrome, but not progressive supranuclear palsy.

23 and in all regions examined for progressive supranuclear palsy.

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

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

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

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

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

31 , 16 semantic dementia [SD]), 22 progressive supranuclear palsy, 50 Alzheimer disease, 6 Parkinson di

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

58 Progressive supranuclear palsy and Parkinson's disease have distinct

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 Progressive supranuclear palsy filaments contain 4R tau.

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

100 87% of finger tap trials in the progressive supranuclear palsy group and only 12% in the Parkinson's

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

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

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

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

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

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

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

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

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

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

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

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

113 Although progressive supranuclear palsy is considered an atypical parkinsonia

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

133 supranuclear palsy syndrome with progressive supranuclear palsy pathology.

134 icobasal syndrome had underlying progressive supranuclear palsy pathology.

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

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

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

138 Progressive supranuclear palsy patients, compared with control subje

139 Compared with progressive supranuclear palsy, patients with corticobasal degenerat

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

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

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

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

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

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

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

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

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

149 Progressive supranuclear palsy (PSP) and corticobasal degeneration (

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

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

152 Progressive supranuclear palsy (PSP) and corticobasal degeneration (

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

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

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

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

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

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

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

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

161 8Q polymorphism for DJ-1, and in progressive supranuclear palsy (PSP) brains.

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

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

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

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

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

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

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

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

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

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

172 Progressive supranuclear palsy (PSP) is a progressive neurodegenerat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

231 ined frontotemporal dementia and progressive supranuclear palsy syndrome.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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