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 tients comprising 58 relapsing-remitting, 28 primary progressive and 36 secondary progressive.

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

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

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

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

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 Eight patients with the nonfluent variant of primary progressive aphasia (age, 67.0 +/- 7.4 y; 4 wome

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

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

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

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

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

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

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

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

19 nestic variants, including logopenic-variant primary progressive aphasia (n = 25), posterior cortical

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

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

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

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

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

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

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

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

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

29 Primary Progressive Aphasia (PPA) is a behaviorally foca

30 Primary progressive aphasia (PPA) is a clinical dementia

31 Primary progressive aphasia (PPA) is a clinical syndrome

32 Primary progressive aphasia (PPA) is a neurodegenerative

33 Primary progressive aphasia (PPA) is a neurodegenerative

34 Primary progressive aphasia (PPA) is a progressive langu

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

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 mentia, non-fluent, and semantic variants of primary progressive aphasia (PPA), progressive supranucl

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

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

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

49 ific language functions and often damaged in primary progressive aphasia (PPA).

50 The semantic variant of primary progressive aphasia (svPPA) is a clinical syndro

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

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

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

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

55 offered by patients with semantic variant of primary progressive aphasia (svPPA).

56 mporal dementia (bvFTD) and semantic variant primary progressive aphasia (svPPA).

57 ed a right-sided variant of semantic variant primary progressive aphasia (svPPA).

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

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

60 9 (7.0) years], nine with non-fluent variant primary progressive aphasia [five female; 67.4 (8.1) yea

61 64.8 (6.8) years], 12 with semantic variant primary progressive aphasia [four female; 66.9 (7.0) yea

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

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

64 5 years), 12 patients with logopenic variant primary progressive aphasia and 13 patients with posteri

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

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

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

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

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

70 temporal regions, and both semantic variant primary progressive aphasia and behavioural variant fron

71 Logopenic variant primary progressive aphasia and developmental dyslexia b

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

73 However, recent primary progressive aphasia and normal neurophysiologica

74 l-variant FTD, non-fluent/agrammatic variant primary progressive aphasia and semantic variant PPA.

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

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

77 gh some phenotypes such as logopenic variant primary progressive aphasia are more commonly associated

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

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

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

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

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

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

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

85 51 binding was increased in semantic variant primary progressive aphasia compared to controls in the

86 0.001), while patients with semantic variant primary progressive aphasia discounted delayed rewards m

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

103 Primary progressive aphasia is a clinical syndrome defin

104 Primary progressive aphasia is a clinical syndrome that

105 Primary progressive aphasia is a neurodegenerative clini

106 Primary progressive aphasia is a neurodegenerative syndr

107 Primary progressive aphasia is a syndrome characterized

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 Each of the primary progressive aphasia variants showed different pa

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

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

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

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

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

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

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

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

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

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

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

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

144 : emotion recognition in semantic variant of primary progressive aphasia', by Bertoux et al. (doi:10.

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

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

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

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

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

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

151 work is affected in the nonfluent variant of primary progressive aphasia, a neurodegenerative disorde

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

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

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

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

156 89 patients (27.0%) with semantic variant of primary progressive aphasia, and 6 of 30 patients (20%)

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

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

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

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

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

162 -stroke aphasia, PSA) and neurodegeneration (primary progressive aphasia, PPA) have overlapping sympt

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

164 ical diagnosis of frontotemporal dementia or primary progressive aphasia, we included 70 subjects wit

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

166 ate to syndrome-specific atrophy patterns in primary progressive aphasia.

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

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

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

170 ropsychological and neuroimaging features of primary progressive aphasia.

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

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

173 semantic memory deficit in semantic variant primary progressive aphasia.

174 subjects and patients with semantic variant primary progressive aphasia.

175 temporoparietal regions in logopenic variant primary progressive aphasia.

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

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

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

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

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

181 (n = 45) and non-fluent (n = 39) variants of primary progressive aphasia.

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

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

184 tributed atrophy pattern in semantic variant primary progressive aphasia.

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

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

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

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

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

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

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

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

193 Primary progressive apraxia of speech is a recently desc

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

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

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

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

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

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

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

201 of earlier intervention with ocrelizumab in primary progressive disease, progression remains an impo

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

203 The primary progressive form of multiple sclerosis is charac

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

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

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

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

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

209 data in 58 relapsing-remitting MS (RRMS), 28 primary progressive MS (PPMS), 36 secondary progressive

210 Gal-9 pathway, in particular, is impaired in primary progressive MS (PPMS).

211 -diseased controls (n = 8) and patients with primary progressive MS (PPMS, n = 19) and either a rapid

212 , 17 secondary progressive MS [SPMS], and 40 primary progressive MS [PPMS]) from C1 to T10.

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

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

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

216 s with relapsing multiple sclerosis (MS) and primary progressive MS has led to a conceptual shift in

217 multiple sclerosis [MS] n = 110, HD n = 110; primary progressive MS n = 9; secondary progressive MS n

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

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

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

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

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

223 orbent assay in 105 MS patients (73 RRMS, 12 primary progressive MS, 20 secondary progressive MS) and

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

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

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

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

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

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

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

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

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

233 Primary progressive multiple sclerosis (MS) has long bee

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

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

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

237 nt stem cell (iPSC) lines from patients with primary progressive multiple sclerosis (PPMS) failed to

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

239 se of patients with a confirmed diagnosis of primary progressive multiple sclerosis (PPMS) is uncerta

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

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

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

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

244 Patients with primary progressive multiple sclerosis aged 18-55 years

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

246 ion activity predict clinical progression in primary progressive multiple sclerosis and may qualify a

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

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

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

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

251 Therapeutic strategies for primary progressive multiple sclerosis might need differ

252 ocrelizumab on this outcome in patients with primary progressive multiple sclerosis participating in

253 prognostic factor and therapeutic target in primary progressive multiple sclerosis patients', by Mal

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

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

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

257 Patients with primary progressive multiple sclerosis underwent serial

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

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

260 The safety and efficacy of ocrelizumab in primary progressive multiple sclerosis were shown in the

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

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

263 -remitting, 84 secondary progressive, and 73 primary progressive multiple sclerosis) from 13 clinical

264 sing remitting, 39 secondary progressive, 31 primary progressive multiple sclerosis) from eight sites

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

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

267 In a phase 2 trial of patients with primary progressive multiple sclerosis, laquinimod also

268 Among patients with primary progressive multiple sclerosis, ocrelizumab was

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

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

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

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

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

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

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

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

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

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

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

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

281 /- 2.84 versus 44.75 +/- 3.10, P < 0.01) and primary-progressive multiple sclerosis (46.99 +/- 3.78 v

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

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

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

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

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

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

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

289 icospinal tracts was higher in secondary and primary progressive patients (mean = 3.6 +/- 2.7% and 2.

290 comparable between white and grey matter in primary progressive patients.

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

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

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

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

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

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

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

298 d area was more often affected by lesions in primary progressive than relapse-remitting patients (P <

299 in heterogeneous clinical outcomes including primary progressive tuberculosis and latent Mtb infectio

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