ライフサイエンスコーパス: primary progressive

1 was derived at autopsy from 54 patients (17 primary progressive, 30 secondary progressive and 7 cont

2 secondary-progressive (49.0 +/- 7.0 mM) and primary-progressive (49.3 +/- 8.0 mM) compared with rela

3 Motor disability in the primary progressive and secondary progressive groups was

4 ical studies comparing axonal damage between primary progressive and secondary progressive multiple s

5 er of corticospinal axons was equally low in primary progressive and secondary progressive multiple s

6 substrate of progressive disability in both primary progressive and secondary progressive multiple s

7 ting, 10 with secondary progressive, 16 with primary progressive and three with transitional multiple

8 h MS (30 relapsing-remitting, 6 secondary or primary progressive) and 15 healthy individuals serving

9 Patients with logopenic variant primary progressive aphasia ('language variant of Alzhei

10 frontotemporal dementia and semantic variant primary progressive aphasia (also called semantic dement

11 in a consecutive series of 18 patients with primary progressive aphasia (eight with semantic variant

12 sive aphasia (nonfluent PPA; n = 15), fluent primary progressive aphasia (fluent PPA; n = 7), and amy

13 different to that seen in the fluent form of primary progressive aphasia (fPPA), a neurodegenerative

14 y and executive deficits), logopenic variant primary progressive aphasia (language deficits), and pos

15 Most subjects with logopenic variant of primary progressive aphasia (lvPPA) have beta-amyloid (A

16 n participants with the logopenic variant of primary progressive aphasia (lvPPA) performed a recognit

17 sterior cortical atrophy (PCA), 12 logopenic primary progressive aphasia (lvPPA), 20 behavioural vari

18 's disease, semantic dementia and non-fluent primary progressive aphasia (n = 9 each) were contrasted

19 The non-fluent/agrammatic variant of primary progressive aphasia (naPPA) is a young-onset neu

20 ture of the non-fluent/agrammatic variant of primary progressive aphasia (naPPA), but well-controlled

21 hology in patients with nonfluent/agrammatic primary progressive aphasia (nfvPPA) and progressive sup

22 sive aphasia (svPPA), (4) non-fluent variant primary progressive aphasia (nfvPPA) or (5) early onset

23 phasia (svPPA), five with non-fluent variant primary progressive aphasia (nfvPPA)) and 17 healthy con

24 ed in difficulty, in patients with nonfluent primary progressive aphasia (nonfluent PPA; n = 15), flu

25 ral variant frontotemporal dementia (bvFTD), primary progressive aphasia (PPA) and corticobasal syndr

26 The dementia syndrome of primary progressive aphasia (PPA) can be caused by 1 of

27 Primary Progressive Aphasia (PPA) is a behaviorally foca

28 Primary progressive aphasia (PPA) is a clinical dementia

29 Primary progressive aphasia (PPA) is a clinical syndrome

30 Primary progressive aphasia (PPA) is a focal dementia ch

31 Primary progressive aphasia (PPA) is a neurodegenerative

32 Primary progressive aphasia (PPA) is a neurodegenerative

33 Primary progressive aphasia (PPA) is a progressive langu

34 Noninvasive brain stimulation in primary progressive aphasia (PPA) is a promising approac

35 Primary progressive aphasia (PPA) is an uncommon degener

36 Primary progressive aphasia (PPA) is characterized by an

37 The semantic variant of primary progressive aphasia (PPA) is characterized by th

38 Primary progressive aphasia (PPA) refers to a disorder o

39 diagnosis in a large cohort of patients with primary progressive aphasia (PPA) variants defined by cu

40 aging, and genetic study of 31 patients with primary progressive aphasia (PPA), a decline in language

41 Primary progressive aphasia (PPA), a selective neurodege

42 autopsy in up to one third of patients with primary progressive aphasia (PPA), but clinical features

43 In the nonfluent variant of primary progressive aphasia (PPA), degeneration of the p

44 D), amyotrophic lateral sclerosis (ALS), and primary progressive aphasia (PPA), including 281 AD, 256

45 In primary progressive aphasia (PPA), speech and language d

46 Impaired word retrieval is a main symptom of primary progressive aphasia (PPA).

47 hemisphere-dominant pattern of deposition in primary progressive aphasia (PPA).

48 The semantic variant of primary progressive aphasia (svPPA) is typically associa

49 al dementia (rtFTD), (3) semantic variant of primary progressive aphasia (svPPA), (4) non-fluent vari

50 ementia (bvFTD), eight with semantic variant primary progressive aphasia (svPPA), five with non-fluen

51 dementia, including the semantic variant of primary progressive aphasia (svPPA), is strongly associa

52 operculum and caudate nucleus in non-fluent primary progressive aphasia (the corticobasal degenerati

53 in a consecutive series of 20 patients with primary progressive aphasia [12 with progressive non-flu

54 Patients with logopenic variant primary progressive aphasia also showed significant hype

55 eed region derived from the semantic variant primary progressive aphasia analysis was strongly connec

56 5 years), 12 patients with logopenic variant primary progressive aphasia and 13 patients with posteri

57 Thirty-five patients with primary progressive aphasia and 29 control subjects were

58 We asked 15 patients with semantic variant primary progressive aphasia and 57 patients with Alzheim

59 We found that both semantic variant primary progressive aphasia and Alzheimer's disease are

60 We conclude that both semantic variant primary progressive aphasia and Alzheimer's disease are

61 Both semantic variant primary progressive aphasia and Alzheimer's disease had

62 Logopenic variant primary progressive aphasia and developmental dyslexia b

63 t tract underlies verbal fluency deficits in primary progressive aphasia and further confirm the role

64 However, recent primary progressive aphasia and normal neurophysiologica

65 n-verbal sound perception and recognition in primary progressive aphasia and specific disorders at pe

66 tegrity of these impacted neural networks in primary progressive aphasia are lacking.

67 characteristics of early and mild disease in primary progressive aphasia are poorly understood.

68 Revisions of criteria for logopenic primary progressive aphasia are proposed to address thes

69 Fifty-eight autopsies of patients with primary progressive aphasia are reported.

70 re the evolution of the logopenic variant of primary progressive aphasia as a distinct clinical entit

71 ed greater leftward asymmetry for tangles in primary progressive aphasia but not in the amnestic Alzh

72 A review of published primary progressive aphasia cases with adequate clinical

73 nships are not universal and that individual primary progressive aphasia cases with Alzheimer patholo

74 rnia San Francisco Memory and Aging Center's primary progressive aphasia cohort (n = 198) for history

75 0.001), while patients with semantic variant primary progressive aphasia discounted delayed rewards m

76 The Alzheimer's disease pathology in primary progressive aphasia displayed multiple atypical

77 er neocortical-to-entorhinal tangle ratio in primary progressive aphasia establishes clinical concord

78 a core central auditory impairment exists in primary progressive aphasia for non-linguistic stimuli.

79 s for distinguishing the semantic variant of primary progressive aphasia from the partially overlappi

80 Moreover, patients with semantic variant primary progressive aphasia had a significantly more pro

81 Patients with primary progressive aphasia had deficits of non-verbal s

82 follow-up, all participants with non-fluent primary progressive aphasia had evolved either corticoba

83 of neurodevelopmental learning disability in primary progressive aphasia has been reported.

84 The connected speech of patients with primary progressive aphasia has often been dichotomized

85 ment before making a definitive diagnosis of primary progressive aphasia has promoted diagnostic spec

86 Observations in semantic variant primary progressive aphasia have inspired an alternative

87 Patients with logopenic and nonfluent primary progressive aphasia have some deficits recognizi

88 s been associated with syntactic deficits in primary progressive aphasia in a number of structural an

89 co-pathological relationships in subtypes of primary progressive aphasia in hopes of utilizing langua

90 We examined 39 patients with primary progressive aphasia including logopenic variant

91 Patient presenting with logopenic variant primary progressive aphasia initially thought to be due

92 Primary progressive aphasia is a clinical syndrome defin

93 Primary progressive aphasia is a clinical syndrome that

94 Primary progressive aphasia is a neurodegenerative clini

95 Primary progressive aphasia is a neurodegenerative syndr

96 Primary progressive aphasia is a syndrome characterized

97 icits may contribute to the phenomenology of primary progressive aphasia is not established.

98 irment for natural kinds in semantic variant primary progressive aphasia is related in part to diseas

99 st that cortical atrophy in semantic variant primary progressive aphasia may follow connectional path

100 sed on larger groups of patients with either primary progressive aphasia or a typical amnestic dement

101 Cases with predominant primary progressive aphasia or extra-pyramidal syndromes

102 frontotemporal dementia and semantic variant primary progressive aphasia patients alone confirmed thi

103 odulated to a lesser extent or not at all in primary progressive aphasia patients whose syntax was re

104 tly limbic and symmetric pathology cause the primary progressive aphasia phenotype, characterized by

105 est that syntactic comprehension deficits in primary progressive aphasia reflect not only structural

106 t language network for the logopenic variant primary progressive aphasia region of interest, and the

107 sion in the non-fluent/agrammatic variant of primary progressive aphasia relates to the strength of c

108 individual patients in both semantic variant primary progressive aphasia samples.

109 of atrophy in non-fluent/agrammatic variant primary progressive aphasia spreads over time from a syn

110 p that was matched in age and gender to each primary progressive aphasia subgroup (n = 20, age = 65 +

111 ty had a predilection for one or more of the primary progressive aphasia subtypes.

112 rity of white matter tracts in the different primary progressive aphasia subtypes.

113 f resting state neuronal synchronizations in primary progressive aphasia syndromes.

114 patients with bvFTD and semantic variant of primary progressive aphasia than in those with AD and is

115 Within semantic variant primary progressive aphasia the right-handed and non-rig

116 These findings expand the differential of primary progressive aphasia to include prion disease.

117 yses related performance in semantic variant primary progressive aphasia to ventral and medial portio

118 istent region of atrophy in semantic variant primary progressive aphasia using cortical thickness ana

119 s of regional spectral power changes in each primary progressive aphasia variant, compared to age-mat

120 Each of the primary progressive aphasia variants showed different pa

121 trols showed significant differences between primary progressive aphasia variants themselves.

122 of network-specific neuronal dysfunction in primary progressive aphasia variants.

123 ntre of the non-fluent/agrammatic variant of primary progressive aphasia was derived in a group of 10

124 No subject with a diagnosis of primary progressive aphasia was identified with this mut

125 feature for all pathologies associated with primary progressive aphasia was the asymmetric prominenc

126 frontotemporal dementia and semantic variant primary progressive aphasia were most likely to exhibit

127 ntroversy were addressed in 72 patients with primary progressive aphasia who collectively displayed a

128 The association of logopenic primary progressive aphasia with Alzheimer's disease pat

129 ing research has associated semantic variant primary progressive aphasia with distributed cortical at

130 Behaviourally, patients with primary progressive aphasia with non-semantic subtypes w

131 ing in healthy controls and in patients with primary progressive aphasia with relatively spared synta

132 thology displays an atypical distribution in primary progressive aphasia yielded inconclusive results

133 rior cortical atrophy than logopenic variant primary progressive aphasia) and higher-order visual net

134 et Alzheimer's disease and logopenic variant primary progressive aphasia), with a trend towards lower

135 dementia, 14 patients with semantic variant primary progressive aphasia, 25 patients with Alzheimer'

136 hy, 4 subjects with the logopenic variant of primary progressive aphasia, 6 age-matched patients with

137 This study used patients with primary progressive aphasia, a clinical dementia syndrom

138 striking gains of function in a patient with primary progressive aphasia, a degenerative disease of t

139 analysed speech samples for 50 patients with primary progressive aphasia, along with neurodegenerativ

140 Patients with the semantic variant of primary progressive aphasia, also known as semantic deme

141 bvFTD), 89 patients with semantic variant of primary progressive aphasia, and 30 patients with Huntin

142 tia, semantic variant and non-fluent variant primary progressive aphasia, and 46 healthy controls) de

143 89 patients (27.0%) with semantic variant of primary progressive aphasia, and 6 of 30 patients (20%)

144 osterior cortical atrophy, logopenic variant primary progressive aphasia, and corticobasal syndrome).

145 nnected speech production in each variant of primary progressive aphasia, by quantifying speech outpu

146 ntactic comprehension in 51 individuals with primary progressive aphasia, composed of all clinical va

147 diagnoses included frontotemporal dementia, primary progressive aphasia, corticobasal syndrome, and

148 ortical atrophy and the logopenic variant of primary progressive aphasia, differ from amnestic AD in

149 mage and syntactic deficits in patients with primary progressive aphasia, using multimodal neuroimagi

150 sis of patients with the semantic subtype of primary progressive aphasia, which is associated with ma

151 in 43 of type C consistently led to semantic primary progressive aphasia.

152 ropsychological and neuroimaging features of primary progressive aphasia.

153 to verbal fluency and grammar impairment in primary progressive aphasia.

154 s within language network in each variant of primary progressive aphasia.

155 e left language network in logopenic variant primary progressive aphasia.

156 semantic memory deficit in semantic variant primary progressive aphasia.

157 subjects and patients with semantic variant primary progressive aphasia.

158 temporoparietal regions in logopenic variant primary progressive aphasia.

159 tients represent a fourth variant of 'mixed' primary progressive aphasia.

160 atrophy, making this syndrome distinct from primary progressive aphasia.

161 language tests; hence, none met criteria for primary progressive aphasia.

162 matter changes that occur in the variants of primary progressive aphasia.

163 l in the multimodal diagnostic evaluation of primary progressive aphasia.

164 ed through detailed studies of patients with primary progressive aphasia.

165 tributed atrophy pattern in semantic variant primary progressive aphasia.

166 nges in the non-fluent/agrammatic variant of primary progressive aphasia.

167 ical atrophy and eight for logopenic variant primary progressive aphasia.

168 cits are highly variable in individuals with primary progressive aphasia.

169 seen in most patients with semantic variant primary progressive aphasia.

170 ndrome, n = 13; behavioural variant, n = 14; primary progressive aphasias, n = 21) and 27 control sub

171 luent (n = 54) and semantic (n = 96) variant primary progressive aphasias.

172 t the processing of non-verbal sounds in the primary progressive aphasias.

173 ferences between the speech patterns of each primary progressive aphasic variant adequately, and to r

174 Eleven of 69 prospectively enrolled primary progressive aphasics were selected for this stud

175 e findings help improve our understanding of primary progressive apraxia of speech and provide some i

176 These subjects with primary progressive apraxia of speech included eight fem

177 Primary progressive apraxia of speech is a recently desc

178 Thirteen subjects with primary progressive apraxia of speech underwent two seri

179 findings demonstrate that some subjects with primary progressive apraxia of speech will rapidly evolv

180 sychological impairment in the subjects with primary progressive apraxia of speech, but there was ind

181 her the increase was actually related to the primary progressive apraxia of speech.

182 l and radiological features of patients with primary progressive compared with secondary progressive

183 ; 11 had a relapsing-remitting course, one a primary progressive course and one a secondary progressi

184 f patients with multiple sclerosis (MS) have primary progressive disease (PPMS).

185 apse was longer (5 vs 2.6 years, p=0.04) and primary progressive disease was less common (0.9% vs 8.5

186 her mammals, tree kangaroos commonly develop primary progressive disease with MAC from random sources

187 ed with treatment failure, of whom eight had primary progressive disease, seven had early relapse (<

188 The primary progressive form of multiple sclerosis is charac

189 ely depletes CD20-expressing B cells, in the primary progressive form of the disease.

190 he major symptoms of Parkinson's disease and primary progressive freezing gait.

191 No classifiers could differentiate primary progressive from secondary progressive MS better

192 s, whereas it was absent in individuals with primary progressive MS (PP-MS).

193 We evaluated rituximab in adults with primary progressive MS (PPMS) through 96 weeks and safet

194 , 17 secondary progressive MS [SPMS], and 40 primary progressive MS [PPMS]) from C1 to T10.

195 thy donors, whereas levels were unchanged in primary progressive MS and neuromyelitis optica patients

196 greatest challenges remain in the subset of primary progressive MS clinical trials in which brain at

197 significant DRB1*15 association observed in primary progressive MS families (P=0.0004), similar to r

198 ts not previously affected by ON, but not in primary progressive MS patients, compared with controls.

199 ant, where significant reduction was seen in primary progressive MS versus controls and in secondary

200 uced in secondary progressive MS, but not in primary progressive MS when compared with control RNFL t

201 with primary progressive multiple sclerosis (primary progressive MS) (13 male; 10 female; mean age 52

202 emitting, 28% secondary progressive and 4.2% primary progressive MS) and 69 healthy controls.

203 we review some basic and clinical aspects of primary progressive MS, and describe how the disorder in

204 elapsing/remitting MS, glatiramer acetate in primary progressive MS, and intravenous immunoglobulin i

205 e MS versus controls and in secondary versus primary progressive MS.

206 optic nerve, in secondary progressive MS and primary progressive MS.

207 progressive MS (P < 0.05), and not at all in primary progressive MS.

208 was observed between relapsing-onset MS and primary progressive MS.

209 erebellum and most apparent in patients with primary progressive MS.

210 -remitting MS cases (RRMS), those developing primary-progressive MS (PPMS) scored a significant 4.6 t

211 ting patients as compared with patients with primary-progressive MS.

212 Primary progressive multiple sclerosis (MS) has long bee

213 allergic encephalomyelitis (EAE), a model of primary progressive multiple sclerosis (MS).

214 lei, and spinal cord damage in patients with primary progressive multiple sclerosis (PP-MS) provides

215 emitting multiple sclerosis (RR-MS; n = 52), primary progressive multiple sclerosis (PP-MS; n = 21),

216 Longitudinal imaging studies of primary progressive multiple sclerosis (PPMS) have shown

217 The unique clinical characteristics of primary progressive multiple sclerosis (PPMS) pose parti

218 eported brain atrophy in the early stages of primary progressive multiple sclerosis (PPMS), affecting

219 gnetic resonance imaging (MRI) parameters in primary progressive multiple sclerosis (PPMS).

220 ically isolated syndrome (RIS) who evolve to primary progressive multiple sclerosis (PPMS).

221 ular volume were studied in 23 patients with primary progressive multiple sclerosis (primary progress

222 tiple sclerosis, compared with patients with primary progressive multiple sclerosis and healthy subje

223 r the treatment of relapsing, remitting, and primary progressive multiple sclerosis and Huntington's

224 oglobulin abnormalities who met criteria for primary progressive multiple sclerosis and whose son die

225 axonal loss within areas of demyelination in primary progressive multiple sclerosis could explain hig

226 rial, we randomly assigned 732 patients with primary progressive multiple sclerosis in a 2:1 ratio to

227 f perivascular and meningeal inflammation in primary progressive multiple sclerosis in order to under

228 Therapeutic strategies for primary progressive multiple sclerosis might need differ

229 imilar across groups and representative of a primary progressive multiple sclerosis population (48% w

230 ntrolled parallel-group study, patients with primary progressive multiple sclerosis recruited across

231 ts and expands the differential diagnosis of primary progressive multiple sclerosis to include proteo

232 Patients with primary progressive multiple sclerosis underwent serial

233 of amiloride in a cohort of 14 patients with primary progressive multiple sclerosis using magnetic re

234 A total of 943 patients with primary progressive multiple sclerosis were randomized t

235 Furthermore, cases with primary progressive multiple sclerosis with extensive me

236 Data from 21 patients with primary progressive multiple sclerosis within 6 years of

237 were age 25-65 years, clinical diagnosis of primary progressive multiple sclerosis, 1 year or more o

238 ergic pathways in the cervical cord of early primary progressive multiple sclerosis, in the absence o

239 This applies to all subgroups except for primary progressive multiple sclerosis, in which none of

240 Among patients with primary progressive multiple sclerosis, ocrelizumab was

241 In patients with primary progressive multiple sclerosis, we observed a si

242 ective effects of amiloride in patients with primary progressive multiple sclerosis.

243 post-mortem brain tissue from 26 cases with primary progressive multiple sclerosis.

244 an increased rate of clinical progression in primary progressive multiple sclerosis.

245 d to demonstrate a treatment effect of GA on primary progressive multiple sclerosis.

246 iple sclerosis, but has not been assessed in primary progressive multiple sclerosis.

247 and efficacy of fingolimod in patients with primary progressive multiple sclerosis.

248 MEV-IDD), a well-established animal model of primary progressive multiple sclerosis.

249 ngolimod did not slow disease progression in primary progressive multiple sclerosis.

250 No treatments have been approved for primary progressive multiple sclerosis.

251 nal cord and have yet to be applied in early primary progressive multiple sclerosis.

252 t of disability progression in patients with primary progressive multiple sclerosis.

253 /- 2.84 versus 44.75 +/- 3.10, P < 0.01) and primary-progressive multiple sclerosis (46.99 +/- 3.78 v

254 gressive (coefficient = -0.51, P < 0.01) and primary-progressive multiple sclerosis (coefficient = -0

255 in networks underlying cognitive deficits in primary-progressive multiple sclerosis (PP-MS) and to ex

256 neurological disability, a disorder known as primary-progressive multiple sclerosis (PPMS).

257 g, 23 with secondary-progressive and 20 with primary-progressive multiple sclerosis.

258 g, 28 with secondary-progressive and 28 with primary-progressive multiple sclerosis.

259 f relapses and can occur with disease onset (primary progressive) or can be preceded by a relapsing d

260 gher in secondary progressive (P < 0.01) and primary progressive (P < 0.05) disease, suggesting alter

261 g the different forms of multiple sclerosis, primary progressive (PP) and secondary progressive (SP)

262 The relative rarity of primary progressive (PP) and transitional progressive (T

263 One assessed the efficacy of rituximab for primary progressive (PP) MS while the other three focuse

264 1), secondary progressive (SP) MS (n=13) and primary progressive (PP)-MS; n=6) MS; first demyelinatin

265 ine ratios (UNCRs) were measured daily in 10 primary progressive (PP).

266 g (RR), 21 secondary progressive (SP) and 10 primary progressive (PP)] and 51 neurological control pa

267 h secondary-progressive [SP] MS, and 37 with primary-progressive [PP] MS) studied in two centers.

268 shed RRMS, secondary progressive (SPMS), and primary progressive (PPMS) MS from both healthy controls

269 al neuropsychological data of an exclusively primary progressive series are available.

270 lapsing-remitting, secondary progressive and primary progressive subgroups.

271 e matter was significantly more extensive in primary progressive versus secondary progressive patient