ライフサイエンスコーパス: grey matter

1 subpial region-and in spinal cord white and grey matter.

2 erfusion in excess of twice normal appearing grey matter.

3 nd lactate/total creatine ratios in the deep grey matter.

4 ts from structural and functional imaging of grey matter.

5 ole brain (-0.127 +/- 0.037 SD/SD, P<0.001), grey matter (-0.079 +/- 0.038 SD/SD, P = 0.038) and whit

6 versus 33.6 +/- 2.5 mM, P = 0.018) and deep grey matter (38.1 +/- 3.1 mM versus 35.7 +/- 2.4 mM, P =

7 ing-remitting multiple sclerosis in cortical grey matter (41.3 +/- 4.2 mM versus 38.5 +/- 2.8 mM, P =

8 ning (e.g. discordant twins of patients) the grey matter abnormalities in (twin) siblings are progres

9 urrent research it appears that the cortical grey matter abnormalities in siblings are likely to be a

10 We review here the cortical grey matter abnormalities in siblings of patients with s

11 Localized grey matter abnormalities were detected in a topographic

12 disease is considered primarily a disease of grey matter, although the extent of white matter involve

13 not merely a function of disease severity, a grey matter analysis consisting of group level voxel-bas

14 in the frontal lobes, affecting the cortical grey matter and adjacent juxtacortical white matter.

15 re, while combining brain-predicted age with grey matter and cerebrospinal fluid volumes (themselves

16 croglial catalase activity is elevated in MS grey matter and may be an important endogenous anti-oxid

17 nt-responsive patients include reductions in grey matter and perfusion of frontotemporal regions, and

18 1 years, in four we found moderate to severe grey matter and vascular amyloid-beta (Abeta) pathology.

19 entration (both P < 0.001) were higher while grey matter and white matter intracellular sodium volume

20 Global grey matter and white matter total sodium concentration

21 tients and lesions, early neuronal damage in grey matter, and early astrocytic proliferation and acti

22 pite growing evidence of the role that local grey matter architecture plays in a variety of brain dis

23 Imaging measures of the grey matter are necessary, but not sufficient to fully c

24 es overlap with cytoarchitecturally distinct grey matter areas and may serve as the structural basis

25 using a simple ratio method with cerebellar grey matter as reference tissue, taking into account reg

26 , precuneus, and parietotemporal and frontal grey matter, as well as in the basal ganglia.

27 tion (14/14), present in meninges, white and grey matter, associated with variable tissue destruction

28 voxel-based morphometry to identify regional grey matter associations of flavour identification.

29 The segmentation performance for grey matter at C2/C3 level was close to inter-rater vari

30 poE levels were associated with greater deep grey matter atrophy (partial correlation rp=-0.28, p<0.0

31 resent study was therefore to assess whether grey matter atrophy and amyloid pathology contribute to

32 Conversely, increased rates of global grey matter atrophy are significantly associated with fa

33 of white matter hyperintensity expansion and grey matter atrophy are strongly correlated (Pearson's R

34 hometry was used to characterize patterns of grey matter atrophy associated with task performance.

35 ion tomography and the longitudinal rates of grey matter atrophy in a cohort of clinically diagnosed

36 ur identification and this is underpinned by grey matter atrophy in an anteromedial temporal lobe net

37 whereas ApoE levels are associated with deep grey matter atrophy in high risk CIS patients treated wi

38 ciated with characteristic patterns of focal grey matter atrophy in left posterior frontoinsular, ant

39 Grey matter atrophy in patients correlated with both voi

40 alysis aims to assess patterns of cerebellar grey matter atrophy in seven neurodegenerative condition

41 Grey matter atrophy in the hallucinators occurred predom

42 temporal and parietal cortices, subcortical grey matter atrophy including thalamus and cerebellum an

43 al grey matter atrophy, and demonstrate that grey matter atrophy is the major contributor to whole br

44 ls was associated with a 1% increase in deep grey matter atrophy over 2 years.

45 ctural magnetic resonance imaging to examine grey matter atrophy patterns associated with visual hall

46 ion is associated with increases in cortical grey matter atrophy rates, in the medial-frontal, orbito

47 as-based parcellation, and rates of regional grey matter atrophy were assessed using tensor-based mor

48 experienced visual hallucinations, exhibited grey matter atrophy with significant voxel-wise differen

49 ntensities with increasing rates of regional grey matter atrophy, and demonstrate that grey matter at

50 ed categories, and we related performance to grey matter atrophy.

51 y was used to assess and compare patterns of grey matter atrophy.

52 tter hyperintensity progression and cortical grey matter atrophy?

53 ellar parallel fibres, an example of typical grey matter axons, to investigate the effects of K(+) ch

54 White matter connections between 165 grey matter brain regions were defined using tractograph

55 sponders show different alterations in brain grey matter, but the findings are inconsistent.

56 gions of interest were limited to 0.5 cm3 of grey matter centred around sites that had been identifie

57 oups, and availability of coordinate data of grey matter cerebellar atrophy in patients were included

58 erebellum to examine the pattern of regional grey matter change in the male premutation carriers with

59 efault network, correlated with longitudinal grey matter changes in the non-fluent/agrammatic variant

60 ved in both the lesions and normal appearing grey matter compared with control cortex.

61 We measured regional variation in grey matter concentration by using voxel-based morphomet

62 Using probabilistic tractography, a grey matter connection network was defined based upon th

63 Here, we present a new model of intrinsic grey matter connectivity of the human connectome.

64 might help explain histological patterns of grey matter connectivity, highlighting that observed con

65 ding effects of increased cellularity and/or grey matter contamination, allowing successful detection

66 d morphometry in the patient cohort revealed grey matter correlates of auditory motion detection and

67 with the degree of microglial activation and grey matter cortical demyelination.

68 Grey matter cortical thickness and shape analysis reveal

69 This relation between grey matter damage and cognitive impairment has been len

70 In patients with multiple sclerosis (MS), grey matter damage is widespread and might underlie many

71 arch to date has focused largely on studying grey matter damage.

72 Subpial grey matter demyelinated lesions were located both adjac

73 A novel model of subpial cortical grey matter demyelination was set up in Dark Agouti rats

74 cation (in the affected left hemisphere) and grey matter density (in the unaffected right hemisphere)

75 Specifically, we derived grey matter density and standardized uptake value ratios

76 obiological underpinning and correlated with grey matter density in prefrontal and parietal cortex, a

77 ficant negative effect of CGG repeat size on grey matter density in the dorsomedial frontal regions.

78 regression analysis confirmed that increased grey matter density in the right temporo-parietal juncti

79 Significantly less grey matter density was found in multiple brain regions,

80 region of interest, correcting for regional grey matter density, age, education and disease status,

81 MR was used to evaluate differences in brain grey matter density, cerebellar volume, cerebellar neuro

82 xpansion, but also abnormalities of cortical grey matter development involving both greater and lesse

83 t cortical volume and thickness reduction or grey matter diffusion tensor imaging values alterations

84 menter (attention-getting sounds) differs in grey matter distribution compared to chimpanzees that do

85 les of supratentorial and cerebellar damage (grey matter fraction, T2 lesion volume, metrics of cereb

86 heart disease were associated with decreased grey matter (GM) and cortical volumes (p < 0.05), while

87 White matter (WM), grey matter (GM) and thalamic fractions were derived at

88 Grey matter (GM) density and hippocampal volume from the

89 ch neuropsychological measure was related to grey matter (GM) density in each group using voxel-based

90 gesting increased transmission time, whereas grey matter (GM) in auditory cortex partially mediates a

91 Cortical grey matter (GM) lesions are common in multiple sclerosi

92 The extent and clinical relevance of grey matter (GM) pathology in multiple sclerosis (MS) ar

93 Our aim was to investigate the impact of grey matter (GM) volume alterations in lobules VI to VII

94 ALS-FTD) showed reduced motor and extramotor grey matter (GM) volume when compared to neurological co

95 h SCI exhibited decreased cord area, reduced grey matter (GM) volumes in anterior cingulate cortex (A

96 Cross-sectional areas of grey matter (GM), white matter (WM), and posterior colum

97 ination and neuronal loss in the spinal cord grey matter (GM).

98 ogen peroxide-reducing enzyme catalase in MS grey matter (GM).

99 Deep brain electrical stimulation (DBS) of grey matter has been used for MTLE with limited success.

100 dly in injured, but potentially salvageable, grey matter in 50-60% of patients after traumatic brain

101 esonance imaging (MRI) measures of white and grey matter in a large population-derived cohort to inve

102 y speech, whereas non-verbal IQ changed with grey matter in a region that was activated by finger mov

103 l imaging showed that verbal IQ changed with grey matter in a region that was activated by speech, wh

104 in normal appearing white matter (NAWM) and grey matter in all subjects.

105 s published up to January 2015 that compared grey matter in MDD (50 data sets including 4101 individu

106 appearing white matter and cortical and deep grey matter in multiple sclerosis, with higher concentra

107 ciated abnormalities of structure (decreased grey matter in right dorsolateral prefrontal cortex and

108 and right inferior temporal gyrus; increased grey matter in right insula, right putamen, left tempora

109 tter in the cranial corticospinal tracts and grey matter in sensorimotor cortices by tensor-based ana

110 ion (all p<0.010 after correction), and less grey matter in several parietal regions (all p<0.002 unc

111 osocial behaviour, associated with decreased grey matter in the anterior insula, lateral orbitofronta

112 h current depression had bilaterally reduced grey matter in the hippocampus compared with HC and untr

113 veness and depression, and between decreased grey matter in the left inferior frontal cortex and ante

114 ral peduncle (Z score 3.89, p=0.0302) and of grey matter in the left primary motor cortex (Z score 4.

115 tting sounds were characterized by increased grey matter in the ventrolateral prefrontal and dorsal p

116 asking to multiple brain measures, including grey matter in various prefrontal regions and white matt

117 we combine measures of functional activity, grey matter integrity and performance in patients with l

118 Loss of cortical grey matter is a diagnostic marker of many neurodegenera

119 hat the local inflammatory status within the grey matter is importantly linked with tau pathology.

120 spond to injury in the highly interconnected grey matter is poorly understood.

121 We then prepared grey matter lesion maps, based on meta-analyses of publi

122 plays a role in the pathogenesis of cortical grey matter lesions and an increased rate of clinical pr

123 Cortical grey matter lesions are common in multiple sclerosis (MS

124 y of magnetisation transfer ratio values and grey matter lesions withint he same regions, and whole-b

125 requent bilateral, large, brainstem and deep grey matter lesions.

126 t a significantly greater number of cortical grey matter lesions.

127 , in order to discriminate between white and grey matter location of contacts.

128 plain the absence of findings for consistent grey matter loss across studies.

129 Voxel-based morphometry confirmed grey matter loss across the motor and cognitive cerebell

130 ery close association between the pattern of grey matter loss and the regions of interest each scale

131 R = -0.69, P < 1 x 10(-7)), and significant grey matter loss and whole brain atrophy occurs annually

132 arcellation were used to compare patterns of grey matter loss between groups and with age-matched con

133 nd temperature symptoms were associated with grey matter loss in a right-lateralized network includin

134 That grey matter loss in parietal regions is a part of health

135 In this study, we determined whether grey matter loss in the hippocampus in depression (1) is

136 oups showed significant associations between grey matter loss in the left amygdala and increased leve

137 son with healthy controls, we found striking grey matter loss of the patients with fragile X-associat

138 ound B standard unit value ratio and greater grey matter loss over time in the posterior cingulate gy

139 Regional grey matter loss was determined on three-dimensional T1-

140 The other prominent grey matter loss was found in the lateral prefrontal cor

141 echanisms, including, but not restricted to, grey matter loss.

142 by-voxel morphometry revealed no significant grey matter loss.

143 and perform morphometric analyses to assess grey matter loss.

144 ymicrogyria-like cortical dysplasia, but the grey matter malformation was not typical of that seen in

145 A cortical grey matter mask consisting of six predefined regions.wa

146 Mediation analyses revealed both direct and grey matter-mediated effects of 18F-AV-1451 uptake on co

147 tep towards an individual cortex-wide map of grey matter microstructure, The gray/white matter and pi

148 Using grey matter morphometry and probabilistic tractography c

149 alysis protocol, using this disease-specific grey matter network as an input for a dual-regression an

150 tion, on-going inflammation, axonal loss and grey matter neuronal injury are likely pathological proc

151 nal damage occurs preferentially in cortical grey matter next to the outer surface of the brain.

152 network in which signal units flowed between grey matter nodes along white matter paths.

153 ed progressive and widespread changes in the grey matter, notably including the basal ganglia.

154 tigate the normal-appearing white matter and grey matter of subjects with clinically isolated syndrom

155 is with spinal-cord lesions involving mainly grey matter on imaging, or acute cranial nerve dysfuncti

156 s in the frontal lobe affecting the cortical grey matter or the cortical grey and adjacent white matt

157 ased compared with normal-appearing cortical grey matter (P < 10(-10) and P < 10(-7)), and mean corti

158 with higher seizure frequency in whole-brain grey matter (p=0.016) and the hippocampus (p=0.029).

159 ound to project mainly to the periaqueductal grey matter (PAG), predominantly ipsilaterally.

160 contributory role in the underlying subpial grey matter pathology and accelerated clinical course, w

161 ientational complexity (DOC), as an index of grey matter pathology in regions associated with decisio

162 atter pathology was found cross-sectionally, grey matter pathology was dominant longitudinally, and i

163 Grey matter pathology was identified through analysis of

164 16% of white and 14% of mixed cortical and grey matter patient regions showed FA decreases greater

165 sed an expected increase in frontal cortical grey matter perfusion but unexpected perfusion decreases

166 In addition, when confined to the grey matter perfusion deficit, intracellular pH (P < 0.0

167 Central grey matter PK11195 BPND was increased in subjects with

168 rols but no difference was found in cortical grey matter PK11195 BPND.

169 activity, and (iii) a module to compute the Grey Matter Proximity Index, i.e. the distance of each c

170 78, p=0.0087; whole-brain r=0.602, p<0.0001; grey matter r=0.518, p<0.0001; white matter r=0.588, p<0

171 arriers had significantly decreased cortical grey matter rCBF in the occipital lobe (mean difference

172 Grey matter reduction in the hippocampus appears specifi

173 ebral cortex, clusters of highly significant grey matter reduction were found in the extended areas i

174 posterior cingulate deactivations, regional grey matter reductions, CSF Abeta(1-42), total tau and p

175 test two hypotheses: (i) glutamate levels in grey matter regions are abnormal in MS, and (ii) patient

176 d mean diffusivity in all of the subcortical grey matter regions of interest, with increased fraction

177 ch catalyses hydroxymethylation in white and grey matter regions of this animal model.

178 iciently diverse directional variation among grey matter regions to inform parcellation into distinct

179 In the brain, grey matter regions were parcellated with Freesurfer and

180 terms of links (correlations) between nodes (grey matter regions) and to extract information out of t

181 and varying degrees of degeneration of other grey matter regions.

182 eport moderate, widespread expression across grey matter regions.

183 and eight normal-appearing white-matter and grey-matter regions) and from three controls with non-ne

184 minantly affects brain white matter and deep grey matter, resulting in ischaemic damage that ranges f

185 Voxel-based morphometry of grey matter revealed focal atrophy of superior lateral p

186 onal tissue volumes for the subcortical deep grey matter (SDGM) structures were also obtained.

187 s (STEPS) algorithm for segmenting white and grey matter simultaneously.

188 Independent association was seen of deep grey matter sodium concentration with expanded disabilit

189 These findings suggest that the grey matter structure of right hemisphere posterior dors

190 gh the targets of deep brain stimulation are grey matter structures, axonal modulation is known to pl

191 , together with earlier findings on cortical grey matter, suggest that grey and white matter integrit

192 red with patients' normal-appearing cortical grey matter T2* (paired t-test) and with mean cortical T

193 s callosum and corticospinal tract) and deep grey matter (thalamus) structures were significantly red

194 iated with decision-making and also measured grey matter tissue volumes and white matter lesion volum

195 ere taken as a fingerprint of the underlying grey matter tissue, and used to distinguish separate cor

196 In responders across 9 datasets grey matter volume (GMV) was significantly higher in the

197 r sun exposure was associated with increased grey matter volume (GMV, r(p)=0.16, p=0.019) and whole b

198 dy, we tested for differences in subcortical grey matter volume (n = 1157) and white matter integrity

199 ce of a mutation was associated with a lower grey matter volume (P = 0.002), even in presymptomatic s

200 ope of the correlation between education and grey matter volume (P = 0.007).

201 ve to controls and a trend towards increased grey matter volume (VBM) in the same region.

202 ds and left cerebellar peduncle, and smaller grey matter volume and cortical thinning in the leg area

203 We found that impaired cortical grey matter volume and gyrification index in newborns wi

204 a significant negative relationship between grey matter volume and intrinsic cerebellar connectivity

205 s and show that age-related declines in rPPC grey matter volume better account for age-related change

206 First, we obtained a composite measure of grey matter volume by graph-Laplacian principal componen

207 or and posterior parietal cortex, as well as grey matter volume co-localized to these specific region

208 Cortical grey matter volume differences between adolescents with

209 TMEM106B genotype did not influence grey matter volume directly on its own but in mutation c

210 T2 lesion volume, and brain white matter and grey matter volume fractions.

211 .e. TMEM106B polymorphism, rs1990622 T/C) on grey matter volume in a large cohort of presymptomatic s

212 Grey matter volume in a region of right posterior pariet

213 Education directly affected grey matter volume in all the samples (P = 0.02) with lo

214 significant attentional deficits and reduced grey matter volume in fronto-striato-cerebellar and limb

215 have, however, reported reduced hippocampal grey matter volume in MDD and reduced white matter integ

216 an extensive system of abnormally decreased grey matter volume in orbitofrontal, cingulate, insular,

217 bility in patients was related to changes in grey matter volume in pre-supplementary motor area, and

218 nishment; this was associated with decreased grey matter volume in the anterior cingulate, orbitofron

219 ortex, and with a more localized increase in grey matter volume in the basal ganglia.

220 We found that local grey matter volume in the left anterior superior tempora

221 iple comparisons correction) associated with grey matter volume in the left entorhinal cortex, hippoc

222 We identified increased grey matter volume in the right anterior hippocampus/amy

223 muli was significantly associated with lower grey matter volume in the right collateral sulcus, in a

224 hometry, we aimed to determine whether local grey matter volume in the right hemisphere independently

225 for risky rewards in young adults, with less grey matter volume indicating decreased tolerance for ri

226 presumed to be healthy in our sample and its grey matter volume is positively correlated with one's l

227 er's disease exhibited different patterns of grey matter volume loss, with more extensive temporopari

228 between each rating scale and the pattern of grey matter volume loss.

229 healthy aging suggests that diminished rPPC grey matter volume may have a role in modulating risk pr

230 re correlated with individual differences in grey matter volume of the corresponding brain areas.

231 hanged-although less spatially extended-when grey matter volume or 11C-PiB uptake maps were added as

232 There were no significant differences in grey matter volume or structural connectivity between th

233 caine dependence was correlated with greater grey matter volume reduction in orbitofrontal, cingulate

234 Significant grey matter volume reductions appeared in OSA throughout

235 ically investigate whether prefrontal cortex grey matter volume reductions are valid endophenotypes f

236 ubjects show extensive regionally-demarcated grey matter volume reductions in areas that control cogn

237 nd we investigated the relationships between grey matter volume variation, duration of cocaine use, a

238 Results showed that total cerebellar grey matter volume was robustly reduced in SZ relative t

239 ses in basal forebrain and entorhinal cortex grey matter volume were interdependent and sequential.

240 Increased amygdalo-hippocampal grey matter volume with right-sided changes is consisten

241 correlates with neuropsychological measures, grey matter volume, (11)C-Pittsburgh Compound B binding,

242 Compared to controls, posterior thalamic grey matter volume, an area mediating oxygen regulation,

243 onal connectivity were calculated using age, grey matter volume, and mood and anxiety scores as nuisa

244 dividuals, did not show typical increases in grey matter volume, and this relative anatomical immatur

245 ith Mini-Mental State Examination scores and grey matter volume, as well as with Pittsburgh compound

246 nce of neuronal injury, measured as regional grey matter volume, in 16 OSA children (8 male, 8.1 +/-

247 equency was associated with lower cerebellar grey matter volume, while patients with posterior cortic

248 l attainment; and (iii) TMEM106B genotype on grey matter volume.

249 ons withint he same regions, and whole-brain grey matter volume.

250 nt associations with cerebral blood flow and grey matter volume.

251 ticularly for frontal and temporal white and grey matter volume.

252 en cognition and both 18F-AV-1451 uptake and grey matter volume.

253 PBR28 binding also inversely correlated with grey matter volume.

254 en emotion recognition accuracy and regional grey matter volume.

255 Of these, grey-matter volume and inter-tap interval were particula

256 ised by both common and distinct patterns of grey-matter volume changes.

257 Both disorders were associated with lower grey-matter volume relative to healthy individuals in a

258 Here, we examined relative grey matter volumes (rGMVs) between three cortical netwo

259 ouse models of HD, we calculated whole brain grey matter volumes across different age groups with dif

260 ep habits are associated with regional brain grey matter volumes and school grade average in early ad

261 ely, were strongly correlated with white and grey matter volumes at 10 days recovery.

262 lly, the ageing brain atrophies as white and grey matter volumes decrease.

263 ue ratio and longitudinal change in regional grey matter volumes from an in-house modified atlas.

264 sed analysis of T1 volume scans, we compared grey matter volumes in 12 cases of sudden unexpected dea

265 sleeping hours correlate with smaller brain grey matter volumes in frontal, anterior cingulate, and

266 iates with later weekend bedtime and smaller grey matter volumes in medial brain regions.

267 areas, lesion size, and demographic factors, grey matter volumes in parts of the right temporoparieta

268 lated to language outcomes, we then compared grey matter volumes in patients and healthy controls to

269 Grey matter volumes in right temporoparietal clusters we

270 ive brain system, manifested through reduced grey matter volumes in the amygdala bilaterally (but not

271 try was then used to determine whether local grey matter volumes in the right hemisphere explained ad

272 An exploratory analysis demonstrated larger grey matter volumes in the temporal and parietal lobes i

273 Further, grey matter volumes in these areas were greater in strok

274 hips, partial correlations demonstrated that grey matter volumes in these clusters related to verbal

275 In brain areas in which grey matter volumes related to language outcomes, we the

276 For each subject, cortical and subcortical grey matter volumes were generated using a parcellation

277 Mapping toolbox to further control for local grey matter volumes, 11C-PiB uptake, or both.

278 ehavior and suggests that alterations in the grey matter volumes, i.e., brain morphology, of specific

279 inhibition, which manifests through reduced grey matter volumes, this region is presumed to be healt

280 be associated with cingulate and prefrontal grey matter volumes.

281 amyloid burden, but are in part mediated by grey matter volumes.

282 mparisons indicated that findings of smaller grey-matter volumes relative to controls in the right do

283 fractional anisotropy, mean diffusivity, and grey-matter volumes to age and systolic blood pressure,

284 It was also strongly associated with reduced grey-matter volumes, particularly in Brodmann's area 48

285 fractional anisotropy, mean diffusivity, and grey-matter volumes.

286 s also independently associated with reduced grey-matter volumes.

287 Cortical white matter and deep grey matter voxel proton and whole brain (31)P magnetic

288 The cortical grey matter was affected in 15 patients (83.3%) and 13 p

289 myelination and neurite loss in the cortical grey matter was found in cases exhibiting an increased l

290 An increase in grey matter was observed in the hippocampus following tr

291 sclerosis, T2* in normal-appearing cortical grey matter was significantly increased relative to cont

292 The Abeta deposition in the grey matter was typical of that seen in Alzheimer's dise

293 Based on the relative sparing of frontal grey matter, we propose to redefine these clinical syndr

294 ommon type of axons in the mammalian brain's grey matter.We used rat cerebellar parallel fibres, an e

295 maps were calculated for each tissue class (grey matter, white matter, white matter hyperintensities

296 Significantly greater progressive grey-matter, white-matter, whole-brain, and regional atr

297 he contours of strain and strain rate at the grey matter-white matter boundary were mapped.

298 rain injury patients were also mapped at the grey matter-white matter boundary.

299 sed for PML lesion distribution, appearance, grey matter/white matter involvement and possible signs

300 extensive spinal-cord lesions of the central grey matter, with predominant anterior horn-cell involve