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

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

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

5 substantial proportion of the patients with multiple system atrophy.

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

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

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

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

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

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

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

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

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

15 evere bladder dysfunction that characterizes multiple system atrophy.

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

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

18 glial and neuronal cytoplasmic inclusions in multiple system atrophy.

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

20 tonomic and motor deficits characteristic of multiple system atrophy.

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

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

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

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

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

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

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

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

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

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

31 disease modifying therapies in patients with multiple system atrophy.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

53 Multiple system atrophy and idiopathic Parkinson's disea

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

111 Multiple system atrophy is a complex neurodegenerative d

112 Multiple system atrophy is a fatal sporadic adult-onset

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

114 Multiple system atrophy is a rare, fatal neurodegenerati

115 Multiple system atrophy is a sporadic alpha-synucleinopa

116 Multiple system atrophy is a sporadic progressive neurol

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

118 Multiple system atrophy is characterized by autonomic fa

119 Pathologically, multiple system atrophy is characterized by glial cytopl

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

121 Multiple-system atrophy is an intractable neurodegenerat

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

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

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

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

126 33 clinically probable cerebellar variant of multiple system atrophy MSA-C) and 44 patients with spor

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

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

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

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

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

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

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

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

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

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

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

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

139 Multiple system atrophy (MSA) is a neurodegenerative dis

140 Multiple system atrophy (MSA) is a neurodegenerative dis

141 Multiple system atrophy (MSA) is a progressive neurodege

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

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

144 Multiple system atrophy (MSA) is a sporadic progressive

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

190 Multiple system atrophy-parkinsonism was the predominant

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

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

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

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

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

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

197 3 types of confirmed autonomic dysfunction (multiple system atrophy, pure autonomic failure, and bar

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

217 Individuals with multiple system atrophy with parkinsonism, dementia with

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

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

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

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