ライフサイエンスコーパス: corticobasal degeneration

1 burden in progressive supranuclear palsy and corticobasal degeneration.

2 , such as progressive supranuclear palsy and corticobasal degeneration.

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

4 found in progressive supranuclear palsy and corticobasal degeneration.

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

6 s a neurodegenerative disease that resembles corticobasal degeneration.

7 a (FTD), progressive supranuclear palsy, and corticobasal degeneration.

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

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

10 including progressive supranuclear palsy and corticobasal degeneration.

11 disease, progressive supranuclear palsy, and corticobasal degeneration.

12 instead resembling the four-layered fold of corticobasal degeneration.

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

14 atrophy, progressive supranuclear palsy, and corticobasal degeneration.

15 lopathy, progressive supranuclear palsy, and corticobasal degeneration.

16 disease, progressive supranuclear palsy and corticobasal degeneration.

17 uals were diagnosed clinically with probable corticobasal degeneration.

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

19 can be a clinicopathological presentation of corticobasal degeneration.

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

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

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

23 (3), chronic traumatic encephalopathy(4) and corticobasal degeneration(5) are distinct.

24 with progressive supranuclear palsy, 15 with corticobasal degeneration, 50 with Alzheimer's disease,

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

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

27 fer to the amyloid-negative cohort as having corticobasal degeneration, although we acknowledge other

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

29 k's disease, progressive supranuclear palsy, corticobasal degeneration and argyrophilic grain disease

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

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

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

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

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

35 r's disease, progressive supranuclear palsy, corticobasal degeneration and other sporadic neurodegene

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

37 r's disease, progressive supranuclear palsy, corticobasal degeneration and Pick's disease.

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

39 123 patients with FTLD, Alzheimer's disease, corticobasal degeneration and progressive supranuclear p

40 Corticobasal degeneration and progressive supranuclear p

41 in Huntington's chorea, Parkinson's disease, corticobasal degeneration and progressive supranuclear p

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

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

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

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

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

47 Corticobasal degeneration and PSP are neurodegenerative

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

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

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

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

52 hies (eg, progressive supranuclear palsy and corticobasal degeneration), and the MAPT H2 haplotype is

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

54 teins; in this family are Alzheimer disease, corticobasal degeneration, and chronic traumatic encepha

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

56 disease, progressive supranuclear palsy and corticobasal degeneration, and forms amyloid-like filame

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

58 lculated for progressive supranuclear palsy, corticobasal degeneration, and neurofibrillary tangle Br

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

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

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

62 gregates extracted from Alzheimer's disease, corticobasal degeneration, and progressive supranuclear

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

64 ; phonetic subtype and younger age predicted corticobasal degeneration, and prosodic subtype and olde

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

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

67 tauopathies (progressive supranuclear palsy, corticobasal degeneration, argyrophilic grain disease, a

68 and include progressive supranuclear palsy, corticobasal degeneration, argyrophilic grain disease, g

69 athies of progressive supranuclear palsy and corticobasal degeneration as a function of disease sever

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

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

72 51 binding in progressive supranuclear palsy/corticobasal degeneration, but this association diminish

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

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

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

76 Corticobasal degeneration can present very commonly with

77 Patients with corticobasal degeneration can present with several diffe

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

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

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

81 Corticobasal degeneration cases were also compared with

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

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

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

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

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

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

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

89 se (AD), tau aggregates in neurons, while in corticobasal degeneration (CBD) and progressive supranuc

90 Progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) are 4-repeat (4R) tauopa

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

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

93 ), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD) brain with [(3)H]1 provi

94 in progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) form amyloid-like fibrou

95 termine the structures of tau filaments from corticobasal degeneration (CBD) human brain tissue.

96 Corticobasal degeneration (CBD) is a complex neurodegene

97 Corticobasal degeneration (CBD) is a neurodegenerative d

98 Corticobasal degeneration (CBD) is a neurodegenerative t

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

100 of progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) is hampered by imperfect

101 Corticobasal degeneration (CBD) is one of the most commo

102 ), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD) post-mortem brain tissue

103 sed by mutations in MAPT (R406W & P301L) and corticobasal degeneration (CBD) postmortem brain tissues

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

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

106 , including patient-derived fibrils from AD, corticobasal degeneration (CBD), and frontotemporal deme

107 (AD), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and Pick disease (PiD).

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

109 heimer's disease (AD), Pick's disease (PiD), corticobasal degeneration (CBD), and progressive supranu

110 and MTBR-tau(282)) increase in the brains of corticobasal degeneration (CBD), progressive supranuclea

111 as progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD), which are difficult to

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

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

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

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

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

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

118 he role of CgA in Tau pathogenesis in AD and corticobasal degeneration (CBD).

119 with AD, frontotemporal dementia (FTD), and corticobasal degeneration (CBD).

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

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

122 rogressive supranuclear palsy [PSP], n = 10; corticobasal degeneration [CBD], n = 10; FTLD-TDP, n = 3

123 are progressive supranuclear palsy (PSP) and corticobasal degeneration characterized by subcortical t

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

125 43 (TDP-43), progressive supranuclear palsy, corticobasal degeneration, dementia with Lewy bodies, mu

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

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

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

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

130 tential neuroimaging marker to differentiate corticobasal degeneration from progressive supranuclear

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

132 Eight cases of corticobasal degeneration had been clinically diagnosed

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

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

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

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

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

138 Corticobasal degeneration is a progressive neurodegenera

139 Corticobasal degeneration is an uncommon parkinsonian va

140 In conclusion, corticobasal degeneration is associated with a reproduci

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

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

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

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

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

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

147 athology interval = 670.2 +/- 425.1 days) or corticobasal degeneration (n = 11, two males, age at dea

148 interval (CI): 0.001, 0.072; P = 0.046] and corticobasal degeneration (n = 215 regions; beta 0.044;

149 on and intrinsic connectivity dysfunction in corticobasal degeneration (n = 215 regions; beta 0.074;

150 0.155; 95% CI: 0.061, 0.248; P = 0.001) and corticobasal degeneration (n = 215 regions; beta 0.277;

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

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

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

154 s (including progressive supranuclear palsy, corticobasal degeneration or Pick's disease), and 69 wit

155 ase neuropathological changes (ADNC) in 42%, corticobasal degeneration or progressive supranuclear pa

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

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

158 al atrophy in areas commonly associated with corticobasal degeneration pathology than healthy control

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

160 However, one patient had corticobasal degeneration pathology.

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

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

163 Corticobasal degeneration patients had faster rates of d

164 brains derived from Pick's disease, PSP, and corticobasal degeneration patients who underwent PET sca

165 Corticobasal degeneration patients, compared with contro

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

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

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

169 20 showed Tau binding on brain sections from corticobasal degeneration, progressive supranuclear pals

170 or frontal but not temporoparietal cortex in corticobasal degeneration/progressive supranuclear palsy

171 Cortical atrophy was smallest in corticobasal degeneration/progressive supranuclear palsy

172 logopenics had ADNC, 56% of agrammatics had corticobasal degeneration/progressive supranuclear palsy

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

174 The corticobasal degeneration/progressive supranuclear palsy

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

176 Cases with corticobasal degeneration, regardless of presentation, s

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

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

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

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

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

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

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

184 Corticobasal degeneration shares a common genetic backgr

185 The patient with corticobasal degeneration showed poor novel tool selecti

186 ncluding three with pathologically confirmed corticobasal degeneration, showed greater regional 18F-A

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

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

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

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

191 confirmed progressive supranuclear palsy and corticobasal degeneration than in controls, but were sim

192 g to AD, progressive supranuclear palsy, and corticobasal degeneration tissues as well as PD and MSA

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

194 Based upon this measure, corticobasal degeneration was successfully distinguished

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

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

197 ns characterize corticobasal syndrome due to corticobasal degeneration, whereas the cortical retentio

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

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