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 nd mean diffusivity (MD) in 25 bilateral (10 grey matter; 15 white matter) regions-of-interest (ROIs)

3 athologies to test the prediction that: deep grey matter abnormalities frequently seen in preterm inf

4 uclei on advanced MRI sequences such as fast grey matter acquisition T1 inversion recovery, quantitat

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

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

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

8 ed a negative correlation between prefrontal grey matter and striatal dopamine synthesis capacity, bu

9 shared common associations with whole-brain grey matter and the Monetary Incentive Delay fMRI task,

10 1 years, in four we found moderate to severe grey matter and vascular amyloid-beta (Abeta) pathology.

11 lar risk is associated with reduced cerebral grey matter and white matter integrity within a fronto-p

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

13 Global grey matter and white matter total sodium concentration

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

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

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

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

18 ignificantly decreased cerebral volume in 14 grey matter areas at baseline magnetic resonance imaging

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

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

21 The necrotic lesions were seen in the grey matter at 100 Gy and in white matter at 60 Gy.

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

23 neuropsychological test scores and regional grey matter atrophy (including longitudinal data in a su

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

25 vels were not associated with progression of grey matter atrophy and did not predict survival.

26 Stroked SHRs displayed grey matter atrophy and had a two-fold increase in apopt

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

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

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

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

31 sociated with grey/white matter volume loss; grey matter atrophy in cognitively unimpaired was specif

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

33 inal patterns of flortaucipir PET uptake and grey matter atrophy in the atypical phenotypes, demonstr

34 Grey matter atrophy in the hallucinators occurred predom

35 rks contribute to cognitive dysfunction, and grey matter atrophy is an early sign of potential future

36 Grey matter atrophy is associated with the degree of dis

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

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

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

40 Grey matter atrophy was not predicted by diffuse axonal

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

42 alysis identified a single component for the grey matter atrophy, while two components were found for

43 pathology was associated with the extent of grey matter atrophy.

44 tion (R(2)=0.36) test scores, independent of grey matter atrophy.

45 tter hyperintensity progression and cortical grey matter atrophy?

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

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

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

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

50 ether cerebrovascular function (measured via grey-matter cerebral blood flow (gmCBF)) is altered in y

51 23)Na-MRI and calculated the TSC in cortical grey matter (CGM), deep grey matter, normal-appearing wh

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

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

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

55 litis mouse model of CNS inflammation and in grey matter-containing multiple sclerosis lesions.

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

57 For grey matter cortical analysis, free water fraction was i

58 Grey matter cortical thickness and shape analysis reveal

59 Test and cortical thickness and spinal cord grey matter cross-sectional area of the Timed 25-Foot Wa

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

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

62 Intrathecal inflammation correlates with the grey matter damage since the early stages of multiple sc

63 okines, previously found to be associated to grey matter damage, and the disease activity, among 99 p

64 f amyloid-beta, tau, glucose metabolism, and grey matter degeneration in 15 cognitively normal mutati

65 We derived measures of grey matter degeneration in a priori NbM and the entorhi

66 Relationships between grey matter densities and cognitive scores were analysed

67 In conclusion, reduced grey matter density and elevated NFL concentrations in C

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

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

70 individuals with stroke demonstrated higher grey matter density in secondary motor areas ipsilateral

71 significant association between the reduced grey matter density in the AD-vulnerable regions and inc

72 alidated the association between CSF NFL and grey matter density in the parietotemporal cortex, entor

73 s/posterior cingulate cortex and hippocampal grey matter density were significantly associated with i

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

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

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

77 Rat forebrain grey matter extracts contain a similar activity, and the

78 igate the clinical validity of the different grey matter features, we evaluated whether grey matter v

79 ures and two other common clinical measures (grey matter fraction and MMSE), obtained an accuracy of

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

81 r: total brain (g = -0.96; p < 0.001); total grey matter (g = -0.81, p < 0.001); and total white matt

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

83 d fatigue (SF) associates more strongly with grey matter (GM) changes than reversible fatigue (RF).

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

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

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

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

88 namely (1) higher K(i) in healthy individual grey matter (GM) versus white matter (WM), (2) GM/WM cer

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

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

91 Voxel-based analyses were used to assess grey matter (GM) volume, white matter (WM) microstructur

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

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

94 Grey matter (GM), white matter (WM), density, and GM/WM

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

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

97 correlations between fine motor impairment, grey matter hypoperfusion, and white matter volume loss.

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

99 in the white matter was greater than in the grey matter in all phenotypes (P < 0.001); however when

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

101 on volumes were comparable between white and grey matter in primary progressive patients.

102 e DMN within DLPFC, as well as less cortical grey matter in regions sensitive to these external task

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

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

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

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

107 which is mediated by progressive atrophy of grey matter indicative of increased Alzheimer's disease

108 outcome was defined as death or significant grey matter injury on MRI according to a previously vali

109 Infants with significant grey matter injury on MRI require less active cooling to

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

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

112 de improved contrast for better detection of grey matter lesions.

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

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

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

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

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

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

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

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

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

122 Here, we examine the effect of education on grey matter loss over time.

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

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

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

126 and perform morphometric analyses to assess grey matter loss.

127 a family history of dementia and obesity, on grey matter macro- and microstructure across the whole b

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

129 Cortical gyrification represents a novel grey matter metric distinctive from grey matter thicknes

130 .9), we test for signatures of loneliness in grey matter morphology, intrinsic functional coupling, a

131 Using grey matter morphometry and probabilistic tractography c

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

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

134 the TSC in cortical grey matter (CGM), deep grey matter, normal-appearing white matter (WM) and WM l

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

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

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

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

139 tia, age range 56-88 years), we investigated grey matter organization and volume differences in agein

140 ttainment was associated with slower loss of grey matter over time in mutation carriers.

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

142 partate was reduced in white (p = 0.030) and grey matter (p = 0.038) after HI.

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

144 Grey matter pathology was identified through analysis of

145 16% of white and 14% of mixed cortical and grey matter patient regions showed FA decreases greater

146 morphometric networks and in the whole-brain grey matter pattern characterized individuals with cogni

147 We also derived a measure of whole-brain grey matter pattern organization by correlating grey mat

148 Preservation of the whole-brain grey matter pattern was also related to lower risk of de

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

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

151 Central grey matter PK11195 BPND was increased in subjects with

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

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

154 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

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

156 RI scanning in seven children revealed large grey matter reductions over the left temporoparietal reg

157 Using an inferior cerebellar grey matter reference, 80-100-min 18F-flortaucipir PET s

158 aplacian Principal Component Analysis on 112 grey matter region-of-interest volumes was used to summa

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

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

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

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

163 33.9]; p=0.003) and atrophy rate in several grey matter regions, but not with change in Frontotempor

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

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

166 logical changes in the spinal cord white and grey matter resulting from injury can be observed with M

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

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

169 nce regarding the impact of APOE-epsilon4 on grey matter structure in asymptomatic individuals remain

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

171 the PRS in the relative volumes of four deep grey matter structures (caudate nucleus, thalamus, subth

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

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

174 Between white and grey matter, the absolute lesion volume in the white mat

175 NIH10), we investigated such differences for grey matter thickness (GM(th)), grey matter volume (GM(v

176 a novel grey matter metric distinctive from grey matter thickness or volume and detects differences

177 al dips in WM tracts compared with activated grey matter, thus calling for significant changes to cur

178 ght hemisphere white matter and post-therapy grey matter tissue density changes in bilateral temporal

179 Total grey matter tissue samples were obtained from medial OFC

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

181 ferences for grey matter thickness (GM(th)), grey matter volume (GM(vol)) and white matter surface ar

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

183 f-interest volumes was used to summarise the grey matter volume (GMV).

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

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

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

187 Differences in white matter integrity, grey matter volume and free water fraction between C9+ a

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

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

190 to test the relationship between prefrontal grey matter volume and striatal K(i)(cer).

191 rain atrophy in patients with MS in terms of grey matter volume and white matter volume as well as lo

192 trials to prevent its detrimental effect on grey matter volume and, eventually, cognition.

193 isk subjects had better cognition and higher grey matter volume at baseline; moreover, higher educati

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

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

196 Grey matter volume correlated negatively with illness du

197 Additional analyses using adjusted grey matter volume demonstrated a sequential pattern of

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

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

200 -related neuropathologies on cross-sectional grey matter volume in a cohort of non-FTLD subjects.

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

202 Grey matter volume in a region of right posterior pariet

203 delling strategy that tests whether baseline grey matter volume in a seed region accounts for longitu

204 y matter pattern organization by correlating grey matter volume in all networks across all participan

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

206 characteristic analyses to evaluate how well grey matter volume in each network and whole-brain patte

207 derived morphometric networks and extracted grey matter volume in each network.

208 ole striatal dopamine synthesis capacity and grey matter volume in left (pFWE corr. = 0.017) and righ

209 ted with neurocognitive impairments; smaller grey matter volume in limbic regions such as the amygdal

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

211 used meta-analytic coordinates of decreased grey matter volume in migraineurs as seed regions to gen

212 rphometry showed higher anterior hippocampal grey matter volume in mixed, compared to single supply.

213 Significant changes were found only in grey matter volume in MS subjects.

214 er's disease contributed additive effects on grey matter volume in nearly all networks, except fronta

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

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

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

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

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

220 l dopamine synthesis capacity and prefrontal grey matter volume in treatment-responsive patients with

221 Patients had grey matter volume increases in the temporal and limbic

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

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

224 sed network mapping, we show that regions of grey matter volume loss in migraineurs localize to a com

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

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

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

228 clinical disease severity measures, NfL and grey matter volume of the frontal, temporal and parietal

229 Test (r(s) =-0.32, p=0.002) and with smaller grey matter volume of the parahippocampal gyri (r(s) =-0

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

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

232 t grey matter features, we evaluated whether grey matter volume or whole-brain pattern was related to

233 Significant grey matter volume reductions appeared in OSA throughout

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

235 s more consistent loneliness associations in grey matter volume than other cortical brain networks.

236 Grey matter volume was assessed globally.

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

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

239 the relationships between TDP-43 stages and grey matter volume while controlling for other pathologi

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

241 (i.e. premorbid intelligence and whole brain grey matter volume) had a positive relationship with the

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

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

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

245 These patterns were accompanied by increased grey matter volume, higher mean diffusivity, and enhance

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

247 e best model for SDMT showed that lower deep grey matter volume, reduced efficiency and male gender w

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

249 We assessed grey matter volume, white matter (WM) microstructural me

250 gher education has been related to increased grey matter volume.

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

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

253 eveloping cognitive impairment, more so than grey matter volume.

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

255 Impulsivity was not associated with grey matter volume.

256 o tissue myelin content, as well as quantify grey matter volume.

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

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

259 reward and threat expectancies and regional grey matter volumes (rGMV).

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

261 imer's disease from ageing, heterogeneity in grey matter volumes across morphometric networks and in

262 Grey matter volumes adjusted for pathological and demogr

263 ptake and rates of accumulation and baseline grey matter volumes and rates of atrophy across phenotyp

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

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

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

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

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

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

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

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

272 Grey matter volumes in right temporoparietal clusters we

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

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

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

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

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

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

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

280 Regional grey matter volumes, and regional binding of 18F-AV-1451

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

282 Subtype 1 showed widespread lower grey matter volumes, most prominent in thalamus, nucleus

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

284 be associated with cingulate and prefrontal grey matter volumes.

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

286 Higher grey-matter volumes in the caudate nucleus and the left

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

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

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

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

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

292 frontal lobe networks, where differences in grey matter were more specific to ageing.

293 Regional volumetric measures of grey matter, white matter, and CSF were used to identify

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

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

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

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

298 scored for cortical lesion types I-IV (mixed grey matter/white matter, intracortical, subpial and cor

299 MRI detects focal lesions in the white and grey matter with high sensitivity (with significantly le

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