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 same or different neural populations in this corticobasal circuitry.

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

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

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

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

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

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

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

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

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

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

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

14 Corticobasal degeneration (CBD) is a complex neurodegene

15 Corticobasal degeneration (CBD) is a neurodegenerative d

16 Corticobasal degeneration (CBD) is a neurodegenerative t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

43 0.155; 95% CI: 0.061, 0.248; P = 0.001) and corticobasal degeneration (n = 215 regions; beta 0.277;

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 123 patients with FTLD, Alzheimer's disease, corticobasal degeneration and progressive supranuclear p

62 Corticobasal degeneration and progressive supranuclear p

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

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

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

66 Corticobasal degeneration and PSP are neurodegenerative

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

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

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

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

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

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

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

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

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

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

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

89 tential neuroimaging marker to differentiate corticobasal degeneration from progressive supranuclear

90 Eight cases of corticobasal degeneration had been clinically diagnosed

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

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

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

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

95 Corticobasal degeneration is a progressive neurodegenera

96 Corticobasal degeneration is an uncommon parkinsonian va

97 In conclusion, corticobasal degeneration is associated with a reproduci

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

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

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

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

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

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

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

105 However, one patient had corticobasal degeneration pathology.

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

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

108 Corticobasal degeneration patients had faster rates of d

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

110 Corticobasal degeneration patients, compared with contro

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

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

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

114 Corticobasal degeneration shares a common genetic backgr

115 The patient with corticobasal degeneration showed poor novel tool selecti

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

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

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

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

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

121 Based upon this measure, corticobasal degeneration was successfully distinguished

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

144 51 binding in progressive supranuclear palsy/corticobasal degeneration, but this association diminish

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

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

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

148 43 (TDP-43), progressive supranuclear palsy, corticobasal degeneration, dementia with Lewy bodies, mu

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

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

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

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

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

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

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

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

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

158 20 showed Tau binding on brain sections from corticobasal degeneration, progressive supranuclear pals

159 Cases with corticobasal degeneration, regardless of presentation, s

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

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

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

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

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

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

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

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

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

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

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

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

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

173 can be a clinicopathological presentation of corticobasal degeneration.

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

175 , such as progressive supranuclear palsy and corticobasal degeneration.

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

177 found in progressive supranuclear palsy and corticobasal degeneration.

178 burden in progressive supranuclear palsy and corticobasal degeneration.

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

180 s a neurodegenerative disease that resembles corticobasal degeneration.

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

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

183 including progressive supranuclear palsy and corticobasal degeneration.

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

185 disease, progressive supranuclear palsy, and corticobasal degeneration.

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

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

188 atrophy, progressive supranuclear palsy, and corticobasal degeneration.

189 lopathy, progressive supranuclear palsy, and corticobasal degeneration.

190 disease, progressive supranuclear palsy and corticobasal degeneration.

191 uals were diagnosed clinically with probable corticobasal degeneration.

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

193 The corticobasal degeneration/progressive supranuclear palsy

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

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

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

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

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

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

200 er's disease (AD), Pick's disease (PiD), and Corticobasal disease (CBD) brains has been shown to diff

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

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

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

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

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

206 inhibition or excess activity of inhibitory corticobasal ganglia loops is unclear.

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

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

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

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

211 rder, a condition linked to abnormalities in corticobasal ganglia networks.

212 Corticobasal ganglia neuronal ensembles bring automatic

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

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

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

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

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

218 Our aim was to test whether cognitive corticobasal ganglia-thalamocortical circuitry is impair

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

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

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

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

223 it for patients with lvPPA, agPPA evolved to corticobasal or progressive supranuclear palsy syndrome

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

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

226 C=92.13%), progressive supranuclear palsy or corticobasal syndrome (AUC=88.47%), and Parkinson's dise

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

228 Cognitive changes are common in corticobasal syndrome (CBS) and significantly impact qua

229 PSP-Richardson syndrome (PSP-RS) or probable corticobasal syndrome (CBS) at MRI.

230 imer disease (AD), is of special interest in corticobasal syndrome (CBS) because autopsy studies have

231 Perirolandic atrophy occurs in corticobasal syndrome (CBS) but is not specific versus p

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

233 ), progressive supranuclear palsy (PSP), and corticobasal syndrome (CBS) have signs and symptoms over

234 Corticobasal syndrome (CBS) is a clinical syndrome chara

235 Corticobasal syndrome (CBS) is associated with asymmetri

236 Progressive supranuclear palsy (PSP) and corticobasal syndrome (CBS) may cause cognitive and beha

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

238 udy of progressive supranuclear palsy (PSP), corticobasal syndrome (CBS), multiple system atrophy (MS

239 disease (AD), frontotemporal dementia (FTD), corticobasal syndrome (CBS), progressive supranuclear pa

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

241 ease with mild cognitive impairment (n = 2), corticobasal syndrome (n = 1), idiopathic rapid-eye-move

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

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

244 D (n = 82), behavioral variant FTD (n = 41), corticobasal syndrome (n = 27), and nonfluent (n = 34) o

245 Patients with corticobasal syndrome also underwent amyloid PET imaging

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

247 al dementia, progressive supranuclear palsy, corticobasal syndrome and controls.

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

249 of behavioural and language variants of FTD, corticobasal syndrome and progressive supranuclear palsy

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

251 51 retention and atrophy in amyloid-negative corticobasal syndrome cases to 32 age-matched healthy co

252 ith the clinical manifestations characterize corticobasal syndrome due to corticobasal degeneration,

253 FTLD and corticobasal syndrome groups performed equally poorly on

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

255 ents with progressive supranuclear palsy and corticobasal syndrome had language impairments consisten

256 Forty-four per cent of patients with corticobasal syndrome had progressive supranuclear palsy

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

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

259 The presence of corticobasal syndrome in patients with 4R-like binding w

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

261 Corticobasal syndrome is the clinical phenotype original

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

263 onounced impairments on social concepts than corticobasal syndrome patients.

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

265 ortical and basal ganglia uptake in a single corticobasal syndrome subject without neuropathological

266 le and three male, median age 72 years) with corticobasal syndrome underwent structural MRI, tau-PET

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

268 sive supranuclear palsy and 12 patients with corticobasal syndrome were recruited from a tertiary ref

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

270 Richardson syndrome or amyloid-beta-negative corticobasal syndrome).

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

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

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

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

275 r rates than progressive supranuclear palsy, corticobasal syndrome, and amyotrophic lateral sclerosis

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

277 chardson syndrome [PSP Richardson syndrome], corticobasal syndrome, and nonfluent-variant primary pro

278 level, only half of PSP Richardson syndrome, corticobasal syndrome, and nonfluent-variant primary pro

279 lzheimer's disease, frontotemporal dementia, corticobasal syndrome, and progressive non-fluent aphasi

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

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

282 ese findings, subjects with amyloid-positive corticobasal syndrome, including two neuropathologically

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

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

285 ecified PPA, progressive supranuclear palsy, corticobasal syndrome, or frontotemporal dementia with a

286 associated clinical syndromes (ie, salience, corticobasal syndrome, progressive supranuclear palsy sy

287 pairment, frontotemporal lobar degeneration, corticobasal syndrome, progressive supranuclear palsy, a

288 posterior cortical atrophy), FTLD syndromes (corticobasal syndrome, progressive supranuclear palsy, b

289 ents with progressive supranuclear palsy had corticobasal syndrome-like features.

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

291 F1R mutation in an individual diagnosed with corticobasal syndrome.

292 ia (PPA), progressive supranuclear palsy and corticobasal syndrome.

293 ared with progressive supranuclear palsy and corticobasal syndrome.

294 ological processes can manifest in life as a corticobasal syndrome.

295 clerosis, progressive supranuclear palsy and corticobasal syndrome.

296 dementia, progressive supranuclear palsy and corticobasal syndrome.

297 against the clinical volitional disorders of corticobasal syndrome.

298 hanism of impairments in voluntary action in corticobasal syndrome.

299 ; n = 35 behavioural variant AD/bvAD; n = 43 corticobasal syndrome/CBS-AD), with a subset of individu

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