ライフサイエンスコーパス: multiple system atrophy

1 H (8 with pure autonomic failure and 11 with multiple-system atrophy).

2 son's disease, dementia with Lewy bodies and multiple system atrophy.

3 be used to predict survival in patients with multiple system atrophy.

4 d progression of the parkinsonian variant of multiple system atrophy.

5 s Parkinson disease, Lewy body dementia, and multiple system atrophy.

6 role in the developmental and progression of multiple system atrophy.

7 c symptoms, on the survival in patients with multiple system atrophy.

8 Parkinson's disease, Lewy body dementia, and multiple system atrophy.

9 multiple system atrophy, and 91 for possible multiple system atrophy.

10 basis of frontal-subcortical dysfunction in multiple system atrophy.

11 disease modifying therapies in patients with multiple system atrophy.

12 ampicin does not slow or halt progression of multiple system atrophy.

13 and efficacy of rifampicin in patients with multiple system atrophy.

14 affect cognitive impairment in patients with multiple system atrophy.

15 a with Lewy bodies, Parkinson's disease, and multiple system atrophy.

16 in differentiating Parkinson's disease from multiple system atrophy.

17 rom patients with Alzheimer disease (AD) and multiple system atrophy.

18 substantial proportion of the patients with multiple system atrophy.

19 on's disease, dementia with Lewy bodies, and multiple system atrophy.

20 e supranuclear palsy and 31.8% of those with multiple system atrophy.

21 eases, such as dementia with Lewy bodies and multiple system atrophy.

22 ronal alpha-synuclein positive inclusions in multiple system atrophy.

23 inclusions in dementia with Lewy bodies and multiple system atrophy.

24 n indication of a different disease, such as multiple system atrophy.

25 on's disease, dementia with Lewy bodies, and multiple system atrophy.

26 e, Alzheimer's disease, Down's syndrome, and multiple system atrophy.

27 ele-Richardson-Olszewski syndrome (SRO), and multiple system atrophy.

28 evere bladder dysfunction that characterizes multiple system atrophy.

29 with the occurrence of memory impairment in multiple system atrophy.

30 's disease (PD) and glial cell inclusions in multiple system atrophy.

31 glial and neuronal cytoplasmic inclusions in multiple system atrophy.

32 tonomic and motor deficits characteristic of multiple system atrophy.

33 n volumes, similar to those seen in sporadic multiple system atrophy.

34 distinguish between Parkinson's disease and multiple system atrophy.

35 saic SVs in brain tissue from a patient with multiple system atrophy.

36 son's disease, dementia with Lewy bodies and multiple system atrophy.

37 discriminate between Parkinson's disease and multiple system atrophy.

38 rocess is centred around oligodendrocytes in multiple system atrophy.

39 igns, ataxia and stridor were more common in multiple system atrophy.

40 reach multiple milestones than patients with multiple system atrophy.

41 val in patients with Parkinson's disease and multiple system atrophy.

42 sed in life and had pathologically confirmed multiple system atrophy.

43 on's disease, dementia with Lewy bodies, and multiple system atrophy.

44 prove the ante-mortem diagnostic accuracy of multiple system atrophy.

45 odendrocytes in the putamen of patients with multiple system atrophy.

46 ls with glucagon-like peptide-1 analogues in multiple system atrophy.

47 disease, progressive supranuclear palsy, or multiple system atrophy.

48 brain levels in a transgenic mouse model of multiple system atrophy.

49 inson disease, dementia with Lewy bodies, or multiple system atrophy.

50 on's disease, dementia with Lewy bodies, and multiple system atrophy.

51 on's disease, dementia with Lewy bodies, and multiple-system atrophy.

52 nally impaired, are associated with sporadic multiple-system atrophy.

53 on's disease, dementia with Lewy bodies, and multiple-system atrophy.

54 Parkinson's disease, Lewy body dementia, and multiple systems atrophy.

55 on's disease, dementia with Lewy bodies, and multiple systems atrophy.

56 son's disease, dementia with Lewy bodies and multiple system atrophy(1).

57 cohol excess (12%) and cerebellar variant of multiple system atrophy (11%).

58 um of neuronal pathology in 35 patients with multiple system atrophy (20 male, 15 female; mean age at

59 nopathy patients (34 Parkinson's disease, 54 multiple system atrophy, 20 pure autonomic failure) and

60 mentia, 70 with Parkinson's disease, 34 with multiple system atrophy, 34 with progressive supranuclea

61 gic presynaptic terminals in 4 patients with multiple system atrophy, 8 with sporadic olivopontocereb

62 aging classifications were also accurate for multiple system atrophy (85% sensitivity, 96% specificit

63 and, PD could be clearly differentiated from multiple system atrophy, a disease that overlaps with PD

64 tle is known about extracellular vesicles in multiple system atrophy, a disease that, like Parkinson'

65 s disease, dementia without parkinsonism and multiple system atrophy accounted for all but 14% of the

66 th Parkinson disease, Lewy body dementia, or multiple system atrophy, alpha-synuclein pathology accum

67 tract abnormalities suggests a diagnosis of multiple system atrophy, although pathological verificat

68 that it may share pathogenic mechanisms with multiple system atrophy, Alzheimer's disease and prion d

69 was evident even in the early stages (22% in multiple system atrophy and 50% in progressive supranucl

70 Parkinson's disease, Lewy body dementia, and multiple system atrophy and animal disease models; 2) pr

71 these neurons are depleted in patients with multiple system atrophy and bladder dysfunction.

72 orticobasal degeneration as tauopathies, and multiple system atrophy and dementia with Lewy bodies as

73 cal pathogenic event in Parkinson's disease, multiple system atrophy and dementia with Lewy bodies.

74 ive disease, especially Parkinson's disease, multiple system atrophy and dementia, and neurologists s

75 Multiple system atrophy and idiopathic Parkinson's disea

76 gain observed in a transgenic mouse model of multiple system atrophy and in primary oligodendrocyte c

77 a-SYN) filamentous deposits are prominent in multiple system atrophy and neuronal alpha-SYN inclusion

78 ypometabolism in a pattern found in sporadic multiple system atrophy and not in dominantly inherited

79 across the spectrum of Parkinson's disease, multiple system atrophy and other proteinopathies.

80 is that other parkinsonian disorders such as multiple system atrophy and progressive supranuclear pal

81 Beyond the substantia nigra, both multiple system atrophy and progressive supranuclear pal

82 discriminated corticobasal degeneration from multiple system atrophy and progressive supranuclear pal

83 n expression was also decreased in the SN in multiple system atrophy and progressive supranuclear pal

84 Although patients with multiple system atrophy and progressive supranuclear pal

85 The Parkinson's disease, multiple system atrophy and pure autonomic failure group

86 n's disease and two other synucleinopathies, multiple system atrophy and pure autonomic failure.

87 new-onset parkinsonism (104 with PD, 11 with multiple system atrophy, and 13 with progressive supranu

88 re identified; 594 met criteria for probable multiple system atrophy, and 91 for possible multiple sy

89 in (alphaSyn) occurs in Parkinson's disease, multiple system atrophy, and dementia with Lewy bodies.

90 mark of pathogenesis in Parkinson's disease, multiple system atrophy, and dementia with Lewy bodies.

91 y, Lewy body variant of Alzheimer's disease, multiple system atrophy, and Hallervorden-Spatz disease,

92 pranuclear palsy, corticobasal degeneration, multiple system atrophy, and Huntington disease), the sp

93 subthalamic nucleus, and corpus callosum of multiple system atrophy, and in all regions examined for

94 of multiple system atrophy (MSA-P subtype), multiple system atrophy, and methamphetamine addiction.

95 obe epilepsy, amyotrophic lateral sclerosis, multiple system atrophy, and other neurodegenerative dis

96 ior substantia nigra of Parkinson's disease, multiple system atrophy, and progressive supranuclear pa

97 atients with idiopathic Parkinson's disease, multiple system atrophy, and progressive supranuclear pa

98 the substantia nigra in Parkinson's disease, multiple system atrophy, and progressive supranuclear pa

99 ognitive impairment, 50 with AD, and 32 with multiple-system atrophy, and 137 healthy control individ

100 ith dementia, dementia with Lewy bodies, and multiple system atrophy; and 4) TDP-43 lesions in two TD

101 a with Lewy bodies, Parkinson's disease, and Multiple System Atrophy are age-related neurodegenerativ

102 disease (PD), dementia with Lewy bodies, and multiple system atrophy are alpha-synucleinopathies char

103 son's disease, dementia with Lewy bodies and multiple system atrophy are characterised by abnormal ne

104 disease, dementia with Lewy bodies (DLB) and multiple system atrophy are characterized by the formati

105 son's disease, dementia with Lewy bodies and multiple system atrophy are megadalton alpha-synuclein-r

106 on's disease, dementia with Lewy bodies, and multiple system atrophy, are neurodegenerative disorders

107 uggests impaired insulin/IGF-1 signalling in multiple system atrophy, as corroborated by increased in

108 kinson's disease, dementia with Lewy bodies, multiple system atrophy, as well as Huntington's disease

109 ome (AUC=88.47%), and Parkinson's disease or multiple systems atrophy (AUC=81.90%).

110 d be further explored for their potential as multiple system atrophy biomarkers.

111 mutation can result in a disorder similar to multiple system atrophy, both clinically and neuropathol

112 ewy body variant of Alzheimer's disease, and multiple system atrophy brains.

113 ating its value not only in the diagnosis of multiple system atrophy but also as prognostic marker.

114 tem studies reported 22-37% of patients with multiple system atrophy can develop cognitive impairment

115 the largest number of pathologically proven multiple system atrophy cases described to date, we prov

116 lar-predominant and parkinsonism-predominant multiple system atrophy cases had FGF14 expansions.

117 Among 218 autopsy-proven multiple system atrophy cases reviewed, 177 (81.2%) were

118 In all multiple system atrophy cases, there was a severe deplet

119 Average age of onset was earlier in multiple system atrophy-cerebellar ataxia (58.4 years) c

120 (multiple system atrophy-parkinsonism versus multiple system atrophy-cerebellar ataxia), age of onset

121 sal degeneration, dementia with Lewy bodies, multiple system atrophy, cerebral amyloid angiopathy and

122 disease (PD), dementia with Lewy bodies and multiple system atrophy, collectively referred to as syn

123 group levels of FGF-5, FGF-19 and SPOCK1 in multiple system atrophy compared with progressive supran

124 ts and 4 patients with clinical diagnosis of multiple system atrophy, confirmed neuropathologically.

125 nical Parkinson's disease when compared with multiple system atrophy, controls or other neurodegenera

126 are associated with Parkinson's disease and multiple system atrophy correspond to different conforma

127 More patients with multiple system atrophy developed ataxia, stridor, dysph

128 orrelated with worse clinical progression of multiple system atrophy (e.g. change in Unified Multiple

129 ing to differentiate Parkinson's disease and multiple system atrophy, especially at the early stages

130 All cases of multiple system atrophy evaluated at Mayo Clinic, Roches

131 rment appears consistent with a diagnosis of multiple system atrophy, even early in the disease, with

132 Lewy body-like inclusions in multiple system atrophy followed the stepwise anatomic p

133 pid eye movement (REM) sleep disorder and/or multiple system atrophy, following optimization of its p

134 but identification of seeds associated with multiple system atrophy for diagnostic purposes has prov

135 e first 3 years from onset can differentiate multiple system atrophy from progressive supranuclear pa

136 s aged 30-80 years with possible or probable multiple system atrophy from ten US medical centres.

137 specificity in differentiating patients with multiple-system atrophy from those with AD or PD and con

138 kinson's disease, dementia with Lewy bodies, multiple system atrophy, frontotemporal dementia, progre

139 sive supranuclear palsy group and 20% of the multiple system atrophy group.

140 ar K1 was not significantly decreased in the multiple system atrophy group.

141 Patients with multiple system atrophy had shorter latency to reach use

142 Patients with multiple system atrophy had T1 and T2 shortening in the

143 Patients who phenoconverted to multiple system atrophy had younger age at onset of auto

144 from a member of a multiplex family in whom multiple-system atrophy had been diagnosed on autopsy.

145 morphs trigger either Parkinson's disease or multiple system atrophy hallmarks in vivo.

146 recent consensus in diagnostic criteria for multiple system atrophy has been achieved.

147 Although the precise definition of multiple system atrophy has been difficult, a recent con

148 leinopathies such as Parkinson's disease and multiple system atrophy have been postulated to stem fro

149 ly diagnosed and pathologically confirmed as multiple system atrophy (i.e. typical cases), while the

150 in 11, dementia with Lewy bodies in 13, and multiple system atrophy in 1) with mean latency of 3.2 +

151 upranuclear palsy are misdiagnosed as having multiple system atrophy in life.

152 suggest that insulin resistance may occur in multiple system atrophy in regions where the neurodegene

153 ctional anisotropy values were increased for multiple system atrophy in the putamen and caudate, and

154 e first prospective natural history study of multiple system atrophy in the USA, and the effects of p

155 Q2 were associated with an increased risk of multiple-system atrophy in multiplex families and patien

156 nclusion pathology in 25.7% of patients with multiple system atrophy, including a patient with visual

157 showed neuropathological changes typical of multiple system atrophy, including glial cytoplasmic inc

158 totic neurodegeneration with a corresponding multiple system atrophy indicative of Shy-Drager syndrom

159 Multiple system atrophy is a complex neurodegenerative d

160 Multiple system atrophy is a fatal sporadic adult-onset

161 Probable multiple system atrophy is a late-stage disease with sho

162 Multiple system atrophy is a rare, fatal neurodegenerati

163 Multiple system atrophy is a sporadic alpha-synucleinopa

164 Multiple system atrophy is a sporadic progressive neurol

165 We here tested the hypothesis that multiple system atrophy is associated with brain insulin

166 Clinical diagnosis of multiple system atrophy is challenging and many patients

167 Multiple system atrophy is characterized by autonomic fa

168 Pathologically, multiple system atrophy is characterized by glial cytopl

169 The cytopathological hallmark of multiple system atrophy is the accumulation of alpha-syn

170 Multiple-system atrophy is an intractable neurodegenerat

171 Although multiple-system atrophy is widely considered to be a non

172 ure, a phenotype that is consistent with the multiple system atrophy-like neurodegeneration that has

173 lin resistance in the striatum of transgenic multiple system atrophy mice and further demonstrate tha

174 with survival of nigral dopamine neurons in multiple system atrophy mice treated with exendin-4.

175 In the multiple system atrophy mixed pathological subgroup, whi

176 33 clinically probable cerebellar variant of multiple system atrophy MSA-C) and 44 patients with spor

177 Here we report a family with coexistence of multiple system atrophy (MSA) and amyotrophic lateral sc

178 uch as progressive supranuclear palsy (PSP), multiple system atrophy (MSA) and corticobasal syndrome

179 rders, we examined brains from patients with multiple system atrophy (MSA) and detected alpha-synucle

180 Progressive supranuclear palsy (PSP), multiple system atrophy (MSA) and idiopathic Parkinson's

181 f primary degenerative dysautonomias such as multiple system atrophy (MSA) and Parkinson's disease (P

182 n of idiopathic Parkinson disease (IPD) from multiple system atrophy (MSA) and progressive supranucle

183 specific to PD or whether it also occurs in multiple system atrophy (MSA) and progressive supranucle

184 predictive values of a clinical diagnosis of multiple system atrophy (MSA) and progressive supranucle

185 sease (PD), dementia with Lewy bodies (DLB), multiple system atrophy (MSA) and pure autonomic failure

186 e (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA) are characterized by patho

187 Parkinson's disease (PD) and multiple system atrophy (MSA) are distinct clinical synd

188 ht limbic or neocortical stage LBD and eight multiple system atrophy (MSA) cases, confirmed neuropath

189 ), one case of familial PD, and six cases of multiple system atrophy (MSA) for their ability to induc

190 Multiple system atrophy (MSA) has varying clinical (MSA-

191 of progressive supranuclear palsy (PSP) and multiple system atrophy (MSA) in the general population

192 Multiple system atrophy (MSA) is a disorder that may man

193 Multiple system atrophy (MSA) is a neurodegenerative dis

194 Multiple system atrophy (MSA) is a neurodegenerative dis

195 Multiple system atrophy (MSA) is a neurodegenerative dis

196 Multiple system atrophy (MSA) is a progressive neurodege

197 Multiple system atrophy (MSA) is a progressive, neurodeg

198 Multiple system atrophy (MSA) is a sporadic orphan neuro

199 Multiple system atrophy (MSA) is a sporadic progressive

200 We report here that multiple system atrophy (MSA) is caused by a different h

201 in progressive supranuclear palsy (PSP) and multiple system atrophy (MSA) is not clear.

202 Besides PD and DLB, multiple system atrophy (MSA) is the third major synucle

203 In patients with multiple system atrophy (MSA) or pure autonomic failure

204 n tomography in 7 normal control subjects, 8 multiple system atrophy (MSA) patients with predominantl

205 he synucleinopathies Parkinson's disease and multiple system atrophy (MSA) share a common genetic eti

206 these neurons are more severely involved in multiple system atrophy (MSA) than in Parkinson's diseas

207 plasmic inclusions (GCI) are the hallmark of multiple system atrophy (MSA), a rare movement disorder

208 ure in 10 normal volunteers, 9 patients with multiple system atrophy (MSA), and 8 patients with pure

209 r are shown here to recapitulate features of multiple system atrophy (MSA), including the accumulatio

210 Synucleinopathies, which include multiple system atrophy (MSA), Parkinson's disease, Park

211 (FTD), amyotrophic lateral sclerosis (ALS), multiple system atrophy (MSA), progressive supranuclear

212 ian syndromes: idiopathic parkinsonism (PD), multiple system atrophy (MSA), pure akinesia (PA), progr

213 rom progressive supranuclear palsy (PSP) and multiple system atrophy (MSA), which have similar charac

214 ing features of Parkinson's disease (PD) and multiple system atrophy (MSA).

215 Parkinson's disease, Lewy body dementia, and multiple system atrophy (MSA).

216 for progressive supranuclear palsy (PSP) and multiple system atrophy (MSA).

217 ne-vasopressin (AVP) synthesizing neurons in multiple system atrophy (MSA).

218 ullary serotonergic neurons were affected in multiple system atrophy (MSA).

219 se (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA).

220 with other parkinsonian syndromes, including multiple system atrophy (MSA).

221 thogenesis of the neurodegenerative disorder multiple system atrophy (MSA).

222 hies, including Parkinson's disease (PD) and multiple system atrophy (MSA).

223 e disorders are Parkinson's disease (PD) and Multiple System Atrophy (MSA).

224 se (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA).

225 ith progressive supranuclear palsy (PSP) and multiple system atrophy (MSA).

226 lude PD, dementia with Lewy bodies (DLB) and multiple system atrophy (MSA).

227 e (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA).

228 ease without parkinsonism); in patients with multiple system atrophy (MSA, a non-Lewy body synucleino

229 Pick's disease (n = 8) and multiple system atrophy (MSA, n = 15).

230 l-DOPA-unresponsive parkinsonism subtype of multiple system atrophy (MSA-P subtype), multiple system

231 (PD), nine with the parkinsonian variant of multiple system atrophy (MSA-P), seven with the cerebell

232 hese functions are affected in patients with multiple systems atrophy (MSA) with autonomic failure, w

233 has been observed in (123)I-MIBG studies of multiple-system atrophy (MSA) and progressive supranucle

234 generation of other monoaminergic systems in multiple-system atrophy (MSA) and progressive supranucle

235 palsy/corticobasal degeneration (PSP/CBD) or multiple-system atrophy (MSA) by PET and clinical follow

236 Multiple-system atrophy (MSA), progressive supranuclear

237 sh from other parkinsonian syndromes such as multiple-system atrophy (MSA).

238 IPD), Progressive Supranuclear Palsy(PSP) or Multiple System Atrophy(MSA).

239 on test for the diagnosis of cerebellar-type multiple system atrophy (MSAc) in patients with ataxia.

240 dies (n = 13), Parkinson disease (n = 6), or multiple system atrophy (n = 6).

241 patients with a clinical diagnosis of either multiple system atrophy (n=372) or progressive supranucl

242 Within both the multiple system atrophy (n=5) and pure autonomic failure

243 apies for spinocerebellar ataxias (SCAs) and multiple system atrophy of the cerebellar type (MSA-C) i

244 We recruited participants with probable multiple system atrophy-of either the parkinsonism subty

245 an present with symptoms similar to those of multiple system atrophy or progressive supranuclear pals

246 c autonomic failure (pure autonomic failure, multiple system atrophy, or autonomic failure in Parkins

247 nuclein disorder, such as Parkinson disease, multiple-system atrophy, or dementia with Lewy bodies.

248 neration was successfully distinguished from multiple system atrophy (P < 0.001) but not progressive

249 erence in survival between motor subtypes of multiple system atrophy (P = 0.232).

250 Midbrain sections from patients with multiple system atrophy-Parkinsonian type (MSA-P) and de

251 y-cerebellar ataxia (58.4 years) compared to multiple system atrophy-parkinsonism (62.3 years; P < 0.

252 clinical features, including motor subtype (multiple system atrophy-parkinsonism versus multiple sys

253 Multiple system atrophy-parkinsonism was the predominant

254 d insulin and IGF-1 plasma concentrations in multiple system atrophy patients and reduced IGF-1 brain

255 r observation of brain insulin resistance in multiple system atrophy patients and transgenic mice tog

256 he striatum was significantly reduced in the multiple system atrophy patients as compared with the no

257 Multiple system atrophy patients with predominant parkin

258 patients, 27 Parkinson's disease patients, 4 multiple system atrophy patients, and 44 controls using

259 rations of OEMVs were significantly lower in multiple system atrophy patients, compared to Parkinson'

260 d atypical parkinsonian syndromes, including multiple-system atrophy, progressive supranuclear palsy,

261 specificity of (18)F-FDG PET for diagnosing multiple-system atrophy, progressive supranuclear palsy,

262 3 types of confirmed autonomic dysfunction (multiple system atrophy, pure autonomic failure, and bar

263 lysis) from baseline to 12 months in Unified Multiple System Atrophy Rating Scale (UMSARS) I score, a

264 from baseline to study end in total Unified Multiple System Atrophy Rating Scale (UMSARS) score (par

265 l questionnaires and scales (reduced Unified Multiple System Atrophy Rating Scale (UMSARS), Montreal

266 r 5 years and assessed them with the Unified Multiple System Atrophy Rating Scale part I (UMSARS I; a

267 tiple system atrophy (e.g. change in Unified Multiple System Atrophy Rating Scale).

268 nsylvania Smell Identification Test, Unified Multiple System Atrophy Rating Scale, Mini-Mental State

269 amined 12 features supporting a diagnosis of multiple system atrophy (red flag features: orofacial dy

270 y bodies and glial cell inclusions in PD and multiple system atrophy, respectively, as well as alpha-

271 In a mouse model of multiple system atrophy, rifampicin inhibited formation

272 survival in a large cohort of patients with multiple system atrophy seen at a single referral centre

273 ents with progressive supranuclear palsy and multiple system atrophy studied to date, the existence o

274 disease (synuclein A53T mutation) as well as multiple system atrophy, suggesting a common pathogenic

275 In multiple system atrophy, the deficit is mild and indisti

276 rms the sensitivity of clinical outcomes for multiple system atrophy to detect clinically significant

277 phenotype displaying Parkinson's disease and multiple system atrophy traits.

278 of patients with the parkinsonian variant of multiple system atrophy, treatment with rasagiline 1 mg

279 on analysis revealed increased likelihood of multiple system atrophy versus Lewy body disease and pro

280 with the requirement for urinary catheters [multiple system atrophy versus Lewy body disease: odds r

281 onfidence interval (CI): 1.1-3.7, P = 0.021; multiple system atrophy versus progressive supranuclear

282 atrophy from progressive supranuclear palsy (multiple system atrophy versus progressive supranuclear

283 erebellar ataxia (SCA) types 1, 2, and 6 and multiple system atrophy, we identified CF degeneration w

284 Five of the 14 patients with multiple system atrophy were female, and thus the strong

285 th possible or probable parkinsonian variant multiple system atrophy were randomly assigned (1:1), vi

286 of 203 patients with a clinical diagnosis of multiple system atrophy were reviewed to identify diagno

287 secutive patients with pathologically proven multiple system atrophy were reviewed.

288 lable treatments slow or halt progression of multiple system atrophy, which is a rare, progressive, f

289 By contrast, patients with multiple system atrophy, which is difficult to distingui

290 other proteinopathies with AUC=0.98 and from multiple system atrophy with AUC=0.94.

291 Patients with multiple system atrophy with parkinsonism (hazard ratio,

292 Parkinson disease dementia, and 16 [3.5%] of multiple system atrophy with parkinsonism).

293 Individuals with multiple system atrophy with parkinsonism, dementia with

294 The number of red flag features in multiple system atrophy with predominant cerebellar sign

295 ncluded patients with parkinsonian type MSA (multiple-system atrophy with predominantly parkinsonism

296 ncluded patients with parkinsonian type MSA (multiple-system atrophy with predominantly parkinsonism

297 son's disease and samples from patients with multiple system atrophy, with an overall sensitivity of

298 son's disease, dementia with Lewy bodies and multiple system atrophy, with hereditary mutations in al

299 rvous system include Parkinson's disease and multiple system atrophy, with the most serious manifesta

300 e disorders, such as Parkinson's disease and multiple system atrophy, yet its functions remain obscur