ライフサイエンスコーパス: corticobasal

1 e, with one exception, associated with Pick, corticobasal and progressive supranuclear palsy subtypes

2 ents with Alzheimer's disease (10 patients), corticobasal degeneration (5 patients), and progressive

3 To highlight the fact that patients with corticobasal degeneration (CBD) and progressive supranuc

4 quitin-only-immunoreactive changes (FTLD-U), corticobasal degeneration (CBD) and progressive supranuc

5 Frontotemporal dementias (FTDs), including corticobasal degeneration (CBD) and progressive supranuc

6 Progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) are neurodegenerative fo

7 Progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) are sporadic neurodegene

8 Corticobasal degeneration (CBD) is a complex neurodegene

9 Corticobasal degeneration (CBD) is a neurodegenerative d

10 Corticobasal degeneration (CBD) is an adult-onset progre

11 and progressive supranuclear palsy (PSP) or corticobasal degeneration (CBD) proved by autopsy.

12 of progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) suggest that mitigating

13 itrated tau in the insoluble fraction of AD, corticobasal degeneration (CBD), and Pick's disease (PiD

14 ses progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD).

15 ease (AD), frontotemporal dementia (FTD) and corticobasal degeneration (CBD).

16 se, progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD).

17 other neurodegenerative disorders, including corticobasal degeneration (CBD).

18 ders, including Alzheimer's disease (AD) and corticobasal degeneration (CBD).

19 other neurodegenerative disorders, including corticobasal degeneration (CBD).

20 rogressive supranuclear palsy (PSP), 19 with corticobasal degeneration (CBD).

21 rogressive supranuclear palsy (PSP-tau), and corticobasal degeneration (CBD-tau) patients into differ

22 neuropathologically, including PSP (n = 24), corticobasal degeneration (n = 11), Parkinson's disease

23 imary progressive aphasia had evolved either corticobasal degeneration (n = 5) or progressive supranu

24 ifications of progressive supranuclear palsy/corticobasal degeneration (PSP/CBD) or multiple-system a

25 alsy, 10 with Parkinson's disease, nine with corticobasal degeneration and 11 age-matched normal cont

26 cal temporal lobe atrophy and the third with corticobasal degeneration and biparietal atrophy-on test

27 k's disease, progressive supranuclear palsy, corticobasal degeneration and familial frontotemporal de

28 in brains of progressive supranuclear palsy, corticobasal degeneration and familial tauopathy due to

29 insights into early pathological features of corticobasal degeneration and its progression.

30 h diagnoses of multiple sclerosis, dementia, corticobasal degeneration and new variant CJD have been

31 individual patients included Pick's disease, corticobasal degeneration and other tauopathies, Lewy bo

32 e, it detects only the neuronal pathology in corticobasal degeneration and progressive supranuclear p

33 123 patients with FTLD, Alzheimer's disease, corticobasal degeneration and progressive supranuclear p

34 ease, some cases of frontotemporal dementia, corticobasal degeneration and progressive supranuclear p

35 is report presents evidence to indicate that corticobasal degeneration and progressive supranuclear p

36 ion of this extensive white matter lesion in corticobasal degeneration and progressive supranuclear p

37 and also thioflavin-S-negative pathology in corticobasal degeneration and progressive supranuclear p

38 Clinical diagnoses of progressive apraxia, corticobasal degeneration and progressive supranuclear p

39 Corticobasal degeneration and PSP are neurodegenerative

40 rogressive supranuclear palsy, patients with corticobasal degeneration and Richardson syndrome had le

41 ditory "oddball" paradigm were found only in corticobasal degeneration and SRO.

42 lesions in the typically affected regions in corticobasal degeneration and the pathognomonic astrocyt

43 is strongly associated with the risk of PSP, corticobasal degeneration and, to a lesser extent, AD an

44 The pathological findings of corticobasal degeneration are associated with several di

45 nsidering progressive supranuclear palsy and corticobasal degeneration as tauopathies, and multiple s

46 on human progressive supranuclear palsy and corticobasal degeneration brain slices.

47 Although definitive diagnosis of corticobasal degeneration can only be made at post-morte

48 Corticobasal degeneration can present very commonly with

49 Patients with corticobasal degeneration can present with several diffe

50 ases and was moderate to severe in end-stage corticobasal degeneration cases (P < 0.05).

51 Three preclinical corticobasal degeneration cases and six age-matched end-

52 Fourty-two per cent of corticobasal degeneration cases presented clinically wit

53 Corticobasal degeneration cases were also compared with

54 neration cases and six age-matched end-stage corticobasal degeneration cases were included in this st

55 (sum of all regional tau load) of end-stage corticobasal degeneration cases were nine times greater

56 Of 19 pathologically confirmed corticobasal degeneration cases, only five had been diag

57 cases was 12-fold greater than in end-stage corticobasal degeneration cases.

58 es for this pattern accurately discriminated corticobasal degeneration from multiple system atrophy a

59 fic network that can be used to discriminate corticobasal degeneration from other atypical parkinsoni

60 tential neuroimaging marker to differentiate corticobasal degeneration from progressive supranuclear

61 Eight cases of corticobasal degeneration had been clinically diagnosed

62 h clinical PSP and pathological diagnosis of corticobasal degeneration had severe tau pathology in PS

63 The clinical criteria for diagnosis of corticobasal degeneration have been revised, and for pro

64 obasal syndrome or pathological diagnosis of corticobasal degeneration in an attempt to identify the

65 ese diagnostic difficulties we conclude that corticobasal degeneration is a discrete clinicopathologi

66 Corticobasal degeneration is a progressive neurodegenera

67 Corticobasal degeneration is an uncommon parkinsonian va

68 In conclusion, corticobasal degeneration is associated with a reproduci

69 For example, the tau pathology in corticobasal degeneration is distinct from that of an AD

70 neuronal lesions leads one to speculate that corticobasal degeneration may begin as an astrogliopathy

71 found in progressive supranuclear palsy and corticobasal degeneration may help in the diagnostic eva

72 , although the values for every patient with corticobasal degeneration or progressive supranuclear pa

73 osis of corticobasal syndrome, only five had corticobasal degeneration pathology, giving a positive p

74 can be helpful pointers to their underlying corticobasal degeneration pathology.

75 However, one patient had corticobasal degeneration pathology.

76 disease, progressive supranuclear palsy, and corticobasal degeneration patient brain tissue slices us

77 Corticobasal degeneration patients, compared with contro

78 In the parietal cortex of corticobasal degeneration patients, NA/Cho was significa

79 of this study was to identify differences in corticobasal degeneration presenting with corticobasal s

80 This opens the question of whether corticobasal degeneration represents a separate disorder

81 Corticobasal degeneration shares a common genetic backgr

82 The patient with corticobasal degeneration showed poor novel tool selecti

83 ing with either a frontotemporal dementia or corticobasal degeneration syndrome with a mean age of on

84 s included dementia with spastic paraplegia, corticobasal degeneration syndrome, and stroke disorders

85 atrophy, progressive supranuclear palsy, and corticobasal degeneration was consistently shown to be h

86 Based upon this measure, corticobasal degeneration was successfully distinguished

87 ile pathologically proven Pick's disease and corticobasal degeneration were clinically heterogeneous,

88 Abnormalities in corticobasal degeneration were present under "less-atten

89 me-like condition, Christianson syndrome and corticobasal degeneration with tau deposition, with each

90 ns in GLT-1 expression were also observed in corticobasal degeneration, a tauopathy with prominent pa

91 s, including progressive supranuclear palsy, corticobasal degeneration, and argyrophilic grain diseas

92 ick disease, progressive supranuclear palsy, corticobasal degeneration, and chronic traumatic encepha

93 disease, progressive supranuclear palsy and corticobasal degeneration, and in the glial and neuronal

94 , non-amnestic as frontotemporal dementia or corticobasal degeneration, and non-specific as dementia

95 all patient groups, Parkinson's disease with corticobasal degeneration, and Parkinson's disease with

96 causes, including dementia with Lewy bodies, corticobasal degeneration, and prion disease, have also

97 ific modification in Alzheimer disease (AD), corticobasal degeneration, and progressive supranuclear

98 show additional similarities between PSP and corticobasal degeneration, but unlike corticobasal degen

99 obar dementias, including Pick's disease and corticobasal degeneration, by the absence of abnormally

100 clinical phenotype originally described for corticobasal degeneration, characterized by asymmetric r

101 43 (TDP-43), progressive supranuclear palsy, corticobasal degeneration, dementia with Lewy bodies, mu

102 H-MRSI in progressive supranuclear palsy and corticobasal degeneration, detection of specific cortica

103 both the variability of presentation of true corticobasal degeneration, for example as a dementing il

104 metric, predominantly extratemporal atrophy (corticobasal degeneration, fused-in-sarcoma pathology).

105 SP and corticobasal degeneration, but unlike corticobasal degeneration, more abundant white matter ta

106 son disease, progressive supranuclear palsy, corticobasal degeneration, multiple system atrophy, and

107 nfluent aphasia, n = 8), and motor variants (corticobasal degeneration, n = 9; and motor neuron disea

108 TLD were distributed between FTLD-tau (34 10 corticobasal degeneration, nine progressive supranuclear

109 s, including progressive supranuclear palsy, corticobasal degeneration, Parksinson's disease and poss

110 nerative tauopathies exemplified by sporadic corticobasal degeneration, progressive supranuclear pals

111 Cases with corticobasal degeneration, regardless of presentation, s

112 ars duration: idiopathic Parkinson's disease corticobasal degeneration, Steele-Richardson-Olszewski s

113 sporadic progressive supranuclear palsy and corticobasal degeneration, tau abnormalities are linked

114 disease, progressive supranuclear palsy and corticobasal degeneration, which are characterized by in

115 approximately 24%) that existed between the corticobasal degeneration- and the progressive supranucl

116 sive supranuclear palsy, Pick's disease, and corticobasal degeneration-illustrates the types of analy

117 the combined group to identify a significant corticobasal degeneration-related metabolic pattern that

118 The presence of this corticobasal degeneration-related metabolic topography w

119 mputing hemispheric asymmetry scores for the corticobasal degeneration-related pattern on a prospecti

120 liest neural network connections affected by corticobasal degeneration-related tau pathology.

121 chardson's syndrome, and we propose the term corticobasal degeneration-Richardson's syndrome for this

122 Cases of corticobasal degeneration-Richardson's syndrome have del

123 pathology, including Alzheimer's disease and corticobasal degeneration.

124 l tau deposition in a pattern reminiscent of corticobasal degeneration.

125 atrophy, progressive supranuclear palsy, and corticobasal degeneration.

126 , such as progressive supranuclear palsy and corticobasal degeneration.

127 ith progressive supranuclear palsy (PSP) and corticobasal degeneration.

128 found in progressive supranuclear palsy and corticobasal degeneration.

129 some 17, progressive supranuclear palsy, and corticobasal degeneration.

130 s a neurodegenerative disease that resembles corticobasal degeneration.

131 ce of alien limb syndorme separated PSP from corticobasal degeneration.

132 supranuclear palsy, Parkinson's disease and corticobasal degeneration.

133 lopathy, progressive supranuclear palsy, and corticobasal degeneration.

134 disease, progressive supranuclear palsy and corticobasal degeneration.

135 uals were diagnosed clinically with probable corticobasal degeneration.

136 e (AGD), progressive supranuclear palsy, and corticobasal degeneration.

137 can be a clinicopathological presentation of corticobasal degeneration.

138 non-fluent primary progressive aphasia (the corticobasal degeneration/progressive supranuclear palsy

139 The corticobasal degeneration/progressive supranuclear palsy

140 ated pattern provided excellent specificity (corticobasal degeneration: 92.7%; progressive supranucle

141 disease, progressive supranuclear palsy and corticobasal degeneration; 3) alpha-synuclein inclusion

142 Motor thalamus (Mthal) is a key node in the corticobasal ganglia (BG) loop that controls complex, co

143 the frontal cortex, forming the last link in corticobasal ganglia circuitry.

144 nt insights into the role of oscillations in corticobasal ganglia circuits, both in health and in neu

145 the modulation of specific loops in parallel corticobasal ganglia circuits.

146 synchronized oscillatory activity within the corticobasal ganglia loop may play a key role in the pat

147 by changes in the degree to which neurons in corticobasal ganglia loops synchronize their activity wi

148 (PD) patients are not processed by the same corticobasal ganglia network as movements in the waking

149 ated movements are not processed by the same corticobasal ganglia network as movements in the waking

150 ized, recent description of discrete frontal corticobasal ganglia networks in a range of species has

151 Corticobasal ganglia neuronal ensembles bring automatic

152 The architecture of corticobasal ganglia pathways allows for many routes to

153 stent with abnormalities in corticocortical, corticobasal ganglia, mesocortical dopamine, and cerebel

154 t is concluded that segregation of different corticobasal ganglia-cortical pathways is maintained in

155 ns (NAc) are both integral components of the corticobasal ganglia-thalamic circuitry that regulates a

156 nt medication may reduce connectivity within corticobasal ganglia-thalamo-cortical circuits in OCD.

157 ole for the striatum, as part of the complex corticobasal ganglia-thalamocortical circuitry, in the o

158 is that the AFP corresponds to the mammalian corticobasal ganglia-thalamocortical loop.

159 In this model, reverberant activity in corticobasal-ganglia circuits reaches a threshold level

160 dementia with swollen achromatic neurons and corticobasal inclusion bodies is a neurodegenerative dis

161 ural syndrome of frontotemporal dementia and corticobasal pathology in four others with clinical fron

162 clusions, parkinsonism and apraxia predicted corticobasal pathology, and nonfluent aphasia predicted

163 ration (FTLD) often overlaps clinically with corticobasal syndrome (CBS) and progressive supranuclear

164 lsy (PSP), multiple system atrophy (MSA) and corticobasal syndrome (CBS) carry a poor prognosis, comp

165 Corticobasal syndrome (CBS) is associated with asymmetri

166 s, notably posterior cortical atrophy (PCA), corticobasal syndrome (CBS), behavioural variant frontot

167 vFTD), primary progressive aphasia (PPA) and corticobasal syndrome (CBS).

168 in corticobasal degeneration presenting with corticobasal syndrome (n = 11) or Richardson syndrome (n

169 concepts in patients with FTLD (n = 29) and corticobasal syndrome (n = 18).

170 syndromes, such as frontotemporal dementia, corticobasal syndrome and apraxia of speech, there is gr

171 bjects); however, it was not detected in any corticobasal syndrome and progressive supranuclear palsy

172 Patients with a corticobasal syndrome but without CBD pathology all (14/

173 FTLD and corticobasal syndrome groups performed equally poorly on

174 In particular, those with corticobasal syndrome had greater tau pathology in the p

175 uclear palsy phenotype and 29% of cases with corticobasal syndrome had underlying progressive supranu

176 several distinct clinical syndromes, and the corticobasal syndrome has been linked with a number of d

177 Queen Square Brain Bank archival collection, corticobasal syndrome is a rare clinical presentation of

178 Corticobasal syndrome is the clinical phenotype original

179 r period with either a clinical diagnosis of corticobasal syndrome or pathological diagnosis of corti

180 onounced impairments on social concepts than corticobasal syndrome patients.

181 zheimer disease, 6 Parkinson disease, and 17 corticobasal syndrome patients.

182 FTD-amyotrophic lateral sclerosis (ALS), and corticobasal syndrome were assessed at FRONTIER.

183 CBD often presents with a 'corticobasal syndrome' including impairments of movement

184 nic variant primary progressive aphasia, and corticobasal syndrome).

185 In addition, we genotyped 21 patients with corticobasal syndrome, 31 patients with progressive supr

186 TD, progressive supranuclear palsy (PSP) and corticobasal syndrome, and a common extended haplotype s

187 poral dementia, primary progressive aphasia, corticobasal syndrome, and Alzheimer's disease.

188 the progressive supranuclear palsy syndrome, corticobasal syndrome, and motor neuron disease.

189 awareness and control of voluntary action in corticobasal syndrome, and provide candidate markers to

190 mb and apraxia are a defining feature of the corticobasal syndrome, but a limited understanding of th

191 nts (progressive supranuclear palsy, n = 22; corticobasal syndrome, n = 13; behavioural variant, n =

192 nd, of 21 cases with a clinical diagnosis of corticobasal syndrome, only five had corticobasal degene

193 dementia, progressive supranuclear palsy and corticobasal syndrome.

194 against the clinical volitional disorders of corticobasal syndrome.

195 hanism of impairments in voluntary action in corticobasal syndrome.

196 normal cognition, Alzheimer's disease, or a corticobasal syndrome.

197 F1R mutation in an individual diagnosed with corticobasal syndrome.

198 However, patients with similar corticobasal syndromes can have neurodegenerative pathol