ライフサイエンスコーパス: gray matter

1 a nonuniform spatial distribution across the gray matter.

2 nal degenerative processes in both white and gray matter.

3 inal cord, targeting the ventral horn of the gray matter.

4 perficial brain white matter and neighboring gray matter.

5 A) exposure has been reported in subcortical gray matter.

6 cting the consequence of HF onto the brain's gray matter.

7 , anterior olfactory nuclei, and spinal cord gray matter.

8 inst radially biased tension in the cortical gray matter.

9 g distinctive connectivity of human temporal gray matter.

10 terminate in different regions of the spinal gray matter.

11 In DLPFC gray matter, 41% of mitochondrial-related genes were dif

12 n a given region relative to the whole-brain gray matter, a pseudotemporal accumulation rate for each

13 ffusional kurtosis imaging (DKI) to describe gray matter abnormalities in ASD in vivo.

14 As a group, relatives exhibited gray matter abnormalities in left supramarginal gyrus, r

15 Subgroup analyses showed disorder-specific gray matter abnormalities in left thalamus and bilateral

16 h shared risk for SCZ, BD, and MDD, regional gray matter abnormalities in neocortex, thalamus, and st

17 iversally as a function of the volume of the gray matter across mammalian species, as would be expect

18 not scale universally with the volume of the gray matter across mammals and is not optimized for wiri

19 class of models emphasises the importance of gray matter: age and risk-related processes cause neurod

20 SIGNIFICANCE STATEMENT: Regional gray matter alterations in chronic pain, as detected wit

21 srupted functional connectivity and abnormal gray matter anatomy in prefrontal areas.

22 whole-brain volumetric analysis on regional gray matter anatomy using voxel-based morphometry.

23 D-only showed volumetric reductions in total gray matter and (mainly) frontal brain areas.

24 n-wide growth in MT trajectories within both gray matter and adjacent juxtacortical white matter.

25 sociated with worse cognition, smaller total gray matter and amygdala volume, larger lateral ventricl

26 hroughout the cervical spinal cord white and gray matter and brain motor centers.

27 g (APD) treatment further decreases cortical gray matter and hippocampus volume, and increases striat

28 d for dorsolateral prefrontal cortex (DLPFC) gray matter and layer 3 and layer 5 pyramidal neurons of

29 Conclusion Iron concentration in the deep gray matter and neocortical regions was higher in patien

30 The relation between regional gray matter and T1 relaxation times suggests decreased t

31 inner plexiform layer (GCIPL), whole-brain, gray matter and thalamic volumes in patients with and wi

32 artments were compared with normal-appearing gray matter and white matter by using Friedman test foll

33 p = .001) even after controlling for global gray matter and white matter volume.

34 participants with glioma, CMRO(2) values in gray matter and white matter volumes were compared by us

35 te (Pi) varied in opposite directions across gray matter and white matter when MDD subjects were comp

36 2LV [T1:T2]), brain atrophy (whole brain and gray matter), and cervical spinal cord lesions (T2LV) an

37 ges, in most brain regions, and in white and gray matter, and leptomeninges.

38 umes of white matter hyperintensities (WMH), gray matter, and regional volumes of amygdala and hippoc

39 potential (BP(ND)) methods, with cerebellar gray matter as a reference region, and were visually ass

40 values were normalized using the cerebellar gray matter as a reference region.

41 lyses revealed reductions of whole brain and gray matter as well as hippocampal and basal ganglia vol

42 synapse degradation, and neuron loss in the gray matter, as well as ongoing axon injury in the white

43 tify an anatomically defined subset of adult gray matter astroglia.

44 architecture shapes cortical and subcortical gray matter atrophy across a spectrum of neurological an

45 d strong evidence for human-like age-related gray matter atrophy in multiple regions of the chimpanze

46 lume of 15.4 cm(3) that did not overlap with gray matter atrophy occupying a volume of 16.9 cm(3).

47 ypotonia, epilepsy, polyneuropathy, cerebral gray matter atrophy), visual impairment, testicular dysg

48 substrate involving cortical demyelination, gray matter atrophy, and meningeal inflammation.

49 ed into three primary meta-analytic classes: gray matter atrophy, increased function, and decreased f

50 ircRNAs expression in 35 postmortem cortical gray matter (BA46) schizophrenia and a non-psychiatric c

51 iated with structural abnormalities in total gray matter, basal ganglia, and cerebellum.

52 rrelations were calculated between white and gray matter before and after partial-volume correction.

53 e brain was segmented according to white and gray matter by using a dual-clustering algorithm.

54 etabolic rates of glucose (CMRGlc) values in gray matter calculated using the AIF and the IDIF.

55 ynapses formed by corticospinal terminals in gray matter caudal to the lesion.

56 ere referenced to a subsection of cerebellar gray matter (cere-crus) as well as a parametrically deri

57 g/kg) using the whole cerebellum, cerebellar gray matter, cerebellar white matter, pons, and subcorti

58 Four RRs (cerebellar gray matter [CGM], whole cerebellum [WCER], pons, and su

59 studies investigating the cellular origin of gray matter changes are lacking.

60 MDD and naMCI did not have the same white or gray matter changes in the frontal-executive and cortico

61 Gray matter changes were prominent in posterior orbitofr

62 Regression analyses were performed between gray matter characteristics and markers of obstructive s

63 s significantly improved the segmentation of gray matter (chi-square x(2), p < 0.05) and demonstrated

64 hin the external capsule and the surrounding gray matter (claustrum and amygdala).

65 The gray matter CMRGlc values determined using these 2 input

66 CMRO(2) was higher in normal-appearing gray matter compared with white matter in both participa

67 umentation of the axonal pathways connecting gray matter components of the human brain has wide-rangi

68 In gray matter, controls had stable (thalamus, cerebellar c

69 d white matter microstructural integrity and gray matter cortical thickness/density differences betwe

70 5 years assessed via MRI (primary outcomes): gray matter (cortical thickness, surface area, hippocamp

71 rmine the relationship between the resulting gray matter covariation components and mutual eye gaze.

72 tic correlations between bout length and two gray matter covariation components.

73 ed source-based morphometry (SBM) to examine gray matter covariation in magnetic resonance imaging sc

74 ite matter glia damage may cause hippocampal gray matter damage during age-dependent limbic decline.

75 However, the importance of gray matter damage has become critical in understanding

76 ent knowledge of the mechanisms that lead to gray matter damage in MS is limited, because the most wi

77 T cell function in the pathogenesis of deep gray matter damage is necessary.

78 cause white matter damage and this leads to gray matter damage.

79 Drinkers exhibited accelerated gray matter decline in anterior lobules and vermis, acce

80 alysis supported white matter damage causing gray matter decline; controlling for fornix glia damage,

81 Few studies show regional gray matter decrease related to HF; however, the underly

82 sed tissue water content underlying regional gray matter decreases.

83 e molecular mechanisms underlying associated gray-matter defects in premature infants remain unknown.

84 as used to estimate cortical and subcortical gray matter deformation from T1-weighted magnetic resona

85 Gray matter deformation was estimated in a sample of 133

86 alongside conventional diagnoses, examining gray matter density (GMD) as an independent validator fo

87 We identified localized patterns of gray matter density (GMD) changes that were largely conc

88 lation between HF biomarkers and the brain's gray matter density (GMD) obtained by magnetic resonance

89 ingle nucleotide polymorphism-based ePRS and gray matter density in areas involved in executive (cort

90 onditions on cognitive flexibility and brain gray matter density in healthy children from two birth c

91 Muller-Lyer illusions, correlated with local gray matter density in the parahippocampal cortex, but n

92 hometry analysis, we found that reduction of gray matter density in ventrolateral prefrontal cortex c

93 Instead, reduction of gray matter density in ventrolateral prefrontal cortex c

94 It is shown for the first time that gray matter density increases from childhood to young ad

95 gional brain volumes, cortical thickness, or gray matter density, and no significant group by age int

96 hite matter volumes, cortical thickness, and gray matter density.

97 Spatial patterns of gray matter differences in CD were significantly associa

98 Novel marker the white-gray matter diffusivity gradient demonstrated the highes

99 Results: The correlation between white and gray matter disappeared after partial-volume correction

100 demonstrated structural similarities to the gray matter distribution on conventional T1-weighted (1)

101 ly increased vascular leak in both white and gray matter during CMH, and this was associated with dis

102 ay important roles in human neurogenesis and gray matter expansion, the mechanisms of human oligodend

103 arily due to a global difference in cortical gray matter (F1,70 = 9.10, p = .004).

104 led equally, and the divisional hierarchy of gray matter follows a topographic arrangement used in BM

105 rrelates of impulsivity (i.e. frontostriatal gray matter, functional connectivity, and dopamine level

106 GSH and both whole-brain and DLPFC-specific gray matter FW in SZ (r = -.48 and -.47, respectively; b

107 sum, internal capsule, anterior commissure), gray matter (globus pallidus, thalamus), and cortices (c

108 Patterns of gray matter (GM) and white matter (WM) atrophy at presen

109 d the relationship of cigarette smoking with gray matter (GM) and white matter (WM) in the UK Biobank

110 measures, including cerebral and cerebellar gray matter (GM) and white matter (WM) volume, surface a

111 Gray matter (GM) anomalies may represent a critical path

112 we compared the results with MRI measures of gray matter (GM) atrophy.

113 We examined gray matter (GM) changes in 34 T2DM and 88 control subje

114 s identified phenotype, cervical spinal cord gray matter (GM) cross-sectional area (CSA), lateral fun

115 rs have demonstrated cerebral white (WM) and gray matter (GM) degeneration before the age of 40 years

116 of sensitivity to both white matter (WM) and gray matter (GM) demyelination.

117 n-induced damage in the lateral funiculi and gray matter (GM) in relapsing-remitting MS and GM atroph

118 the endpoint control of these contractions, gray matter (GM) integrity of the cerebellum, and diseas

119 By contrast, regional gray matter (GM) thickness and volume are not found to m

120 This study aimed to evaluate overall gray matter (GM) volume changes after donepezil treatmen

121 Growth of total cerebral volume, gray matter (GM) volume, and white matter volume as well

122 adversely affected in the in the spinal cord gray matter (GM), and if so, whether it is because of an

123 maps (nlTPMs) of cerebrospinal fluid (CSF), gray matter (GM), and white matter (WM) tissues; 3) deli

124 or predicting brain age based on MRI-derived gray matter (GM).

125 of normal-appearing white matter (NAWM) and gray matter (GM).

126 Single-subject gray matter graphs were extracted from structural MRI sc

127 LTMs had less striatal gray matter, greater cortico-striatal-thalamic functiona

128 Gray matter hypertrophy and thickening were associated w

129 Prominent gray matter hypoplasia was observed in medial frontal re

130 st atlas applied to the spatially normalized gray matter image obtained from segmentation of the base

131 he lipidome composition of prefrontal cortex gray matter in 396 cognitively healthy individuals with

132 her clearing efficiency in white matter than gray matter in accordance with larger proton density inc

133 n performance was driven by parietooccipital gray matter in amyloid-positive patients versus predomin

134 oughout frontal white matter and subcortical gray matter in participants with ASD.

135 While decreased gray matter in right cerebellum might be a common brain

136 ontine micturition center in the lumbosacral gray matter in the anti-Nogo-A antibody-treated animals,

137 asured levels of NAA across white matter and gray matter in the brain using echo planar spectroscopic

138 Thus, the stroke-denervated spinal gray matter, in particular its intermediate laminae, rep

139 In contrast, regional gray matter increases were explained by GABAA receptor c

140 In contrast, regional gray matter increases were partly explained by GABAA rec

141 l for controlling acute-stage poliomyelitis (gray matter inflammation), chronic axonal degeneration,

142 resence nor severity of infarct, subcortical gray matter injury, and microhemorrhage was associated w

143 t groups, mind wandering was associated with gray matter integrity in the hippocampus/parahippocampus

144 wever, there is emerging evidence supporting gray matter involvement and degeneration in MS.

145 er pattern and some subcortical and cortical gray matter involvement.

146 sive retention of [(18)F]AV1451 at the white/gray matter junction in frontal, parietal, and temporal

147 rks of interacting functional modules in the gray-matter, limited research was directed to the functi

148 l connections, is a thin, bilateral sheet of gray matter located between the insular cortex and the s

149 n summary, we found specific visual cortical gray matter loss in Retinitis Pigmentosa patients associ

150 The spatial pattern of gray matter loss is consistent with disuse-driven neuron

151 First, coregistered gray matter masks generated using SPM12 were spatially n

152 The spatially normalized gray matter masks were then visually inspected and quant

153 The frontolateral gray matter matured latest (right, 2.3 years; left, 2.4

154 of autism spectrum disorder (ASD) have shown gray matter microstructural abnormalities, however, in v

155 normalities, however, in vivo examination of gray matter microstructure in ASD has remained scarce du

156 These gray matter networks (GMNs) emerge from the covariation

157 orks correlated with signals from functional gray-matter networks, providing missing knowledge on how

158 cant population, ~2.5% of the total cortical gray matter neurons that would be estimated for a primat

159 intrinsic functional architecture within the gray matter of a single spinal segment, and that rsfMRI

160 t lipid cacostasis occurs in the spinal cord gray matter of ALS patients.

161 ed structural brain alterations in white and gray matter of frontal-executive and corticolimbic circu

162 neuronal cell bodies in areas of the ventral gray matter of the spinal cord where anti-hnRNP A1 antib

163 T1 of the gray matter of the whole brain (P < .001), globus pallid

164 In contrast, no abnormalities of cortical gray matter or white matter were found.

165 tical thickness, such that the volume of the gray matter (or the ratio of gray to total cortical volu

166 22q11DS individuals showed thicker cortical gray matter overall (left/right hemispheres: Cohen's d =

167 min +/- 0.16) compared with normal-appearing gray matter (P < .001) and normal-appearing white matter

168 ith a higher percentage lesion extent in the gray matter (P < .001).

169 In addition, within the MDD group, gray matter Pi, a regulator of oxidative phosphorylation

170 godendrocytes and myelin sheaths in cortical gray matter profoundly alters neural activity and is ass

171 ylaspartate to creatinine levels in parietal gray matter (r = -0.352 and P < .001 at baseline and r =

172 e calculated (t = 80-100 minutes, cerebellum gray matter reference).

173 To achieve this at the gray matter region (macroscale) level, macroscale connec

174 ysis in a mammal (rat) revealed that the 466 gray matter regions composing the right and left sides o

175 The 39 gray matter regions comprising the large dorsal thalamus

176 ible 49,062 macroconnections between the 222 gray matter regions forming the right and left halves of

177 here, the intrinsic connections among all 46 gray matter regions of the rat thalamus on each side of

178 re performed for 12 cortical and subcortical gray matter regions to assess the effect of brain iron o

179 circuitry were examined here at the level of gray matter regions using network analysis tools in a ma

180 In uninjured specimens, spinal gray matter regions were stiffer than white matter regio

181 Our results reveal that there are distinct gray matter regions which are preferentially engaged in

182 3.2% (mean +/- SD across all subjects and 12 gray matter regions) SUV difference for (18)F-FDG (3.7%

183 Within the ARA ontology of gray matter regions, TH-ir neurons localized primarily t

184 We mapped the area of cervical gray matter reinnervation by sprouting contralesional co

185 In ASD participants, decreased kurtosis in gray matter ROIs correlated with increased repetitive an

186 ating that the correlation between white and gray matter signal in (18)F-flortaucipir is not solely d

187 tients with TD also correlated with a higher gray matter signal in deep limbic structures, as well as

188 ive effect of the laser therapy on white and gray matter sparing.

189 ity during reward and emotion processing and gray matter structure in all cortical regions at baselin

190 onsistent markers related to ELT and PTSD on gray matter structure in trauma-exposed individuals.

191 The claustrum is a telencephalic gray matter structure with various proposed functions, i

192 ing hand muscles and extensively sprout into gray matter structures after SCI; therefore, it has been

193 noise ratio, enhanced visualization of white/gray matter structures in microstructural maps, improved

194 Background Deep gray matter structures in patients with Alzheimer diseas

195 ical areas and their layers, 329 subcortical gray matter structures, 81 fiber tracts, and 8 ventricul

196 white matter volume, volumes of subcortical gray matter structures, and regional cortical volumes.

197 us white matter fiber pathways linking these gray matter structures, namely, the uncinate fasciculus,

198 Adults with MDD had thinner cortical gray matter than controls in the orbitofrontal cortex (O

199 ion, U251 cell motility is ~2-fold higher in gray matter than in white matter (91 vs. 43 mum(2)/h), w

200 that connect distant neurons in the cortical gray matter, the relationship between the volumes of the

201 In contrast to the gray matter, these diffusion abnormalities correlated wi

202 utamen and thalamus volumes, and evidence of gray matter thickening compared to the proband group wit

203 The CD group also had significantly less gray matter thickness and density in precuneus, relative

204 group, but no association was found between gray-matter thickness and BPnd for either dopamine recep

205 atively associated with global mean cortical gray-matter thickness in the methamphetamine group, but

206 In the methamphetamine group, mean cortical gray-matter thickness was negatively associated with cum

207 controls with regard to (1) white matter and gray matter total and regional brain volumes, (2) cerebe

208 r marijuana in alcohol effects on cerebellar gray matter trajectories.

209 During CsA infusion, whole-brain gray matter V (T) and K (1) were increased by 29% +/- 17

210 ss the effects of ketamine abuse on cerebral gray matter volume (GMV) and functional connectivity (FC

211 However, the association between gray matter volume (GMV) and HCMV has never been examine

212 ns of interest (ROI) approach indicated that gray matter volume (GMV) and surface area (SA) in dorsol

213 used magnetic resonance imaging to quantify gray matter volume (GMV) and the N-acetylaspartate and N

214 , we used voxel-based morphometry to compare gray matter volume (GMV) in forty-six 14-year-old human

215 n, and direction of sex differences of local gray matter volume (GMV) in the human brain.

216 group and confirmed negative correlations of gray matter volume (GMV) in the left orbitofrontal corte

217 1) highly consistent sex biases in regional gray matter volume (GMV) involving the cortex and classi

218 nal magnetic resonance imaging, and aberrant gray matter volume (GMV) of distributed brain regions, m

219 In analyses of gray matter volume (GMV) using T1-weighted MRI, GMV incr

220 Gray Matter Volume (GMV) was derived from magnetic reson

221 7; P = .003) and was predominantly driven by gray matter volume (mean difference in z score per stand

222 no significant difference in the whole brain gray matter volume (patients: 698.55 cm3; controls: 691.

223 thology was associated with globally reduced gray matter volume across all networks.

224 f inhibitory control was conducted comparing gray matter volume and activation abnormalities between

225 (1) voxel-based morphometry, which measures gray matter volume and concentration; and (2) FreeSurfer

226 tworks (GMNs) emerge from the covariation of gray matter volume and cortical area at the population l

227 architecture emerges from the covariation of gray matter volume and cortical folding.

228 ildhood to young adulthood, in contrast with gray matter volume and cortical thickness, and that fema

229 on was used to model the influence of age on gray matter volume and fractional anisotropy at a whole-

230 The rates of reduction of gray matter volume and fractional anisotropy were signif

231 2 months were associated with smaller total gray matter volume and lower global fractional anisotrop

232 th brain mass, cortical thickness, white and gray matter volume and surface area.

233 from the Childhood Trauma Questionnaire and gray matter volume and tested their generalizability via

234 matter integrity of the pons and cerebellar gray matter volume associated with higher 'p factor' sco

235 mponent differences are mediated by regional gray matter volume changes in both hemispheres of the fr

236 Furthermore, the gray matter volume differences mediated the association

237 ability were each negatively associated with gray matter volume in an overlapping region of the ventr

238 p factor' scores are associated with reduced gray matter volume in the occipital lobe and left cerebe

239 mpter group showed significant reductions in gray matter volume in the orbitofrontal cortex, hippocam

240 e all characterized by significantly greater gray matter volume in the putamen (right: z-score: 5.97,

241 relates with economic irrationality: reduced gray matter volume in this area correlates with the freq

242 The anteromedial pattern of reduced gray matter volume in visual primary and association cor

243 The inferred rate of gray matter volume loss was significantly accelerated in

244 Systematic review of sex differences in gray matter volume of brain regions associated with sexu

245 anticipatory strategies correlated with the gray matter volume of the hippocampus.

246 Furthermore, between-subject variance in gray matter volume of the parahippocampus and dorsal str

247 ween higher p factor scores and both reduced gray matter volume of the visual association cortex and

248 We examined whether gray matter volume of three neural regions supporting fe

249 chronic illness, and the reduction in brain gray matter volume over the course of the illness.

250 ll as emotional trauma, which projected onto gray matter volume patterns in prefronto-cerebellar, lim

251 nd that females, who are known to have lower gray matter volume than males, have higher density throu

252 ures, the replicability of associations with gray matter volume was assessed.

253 Significant loss of gray matter volume was evident in schizophrenia, progres

254 with SNAP, sustained glucose metabolism and gray matter volume were associated with disproportionate

255 up (n = 21), we measured cortical thickness, gray matter volume, and white matter tract integrity (fr

256 : There was no difference in CB(1)R binding, gray matter volume, cognitive function, or psychiatric s

257 results in decreased somatosensory cortical gray matter volume, indicating that the disease process

258 and functional properties of the FPN (i.e., gray matter volume, white matter fractional anisotropy,

259 Regional gray matter volume, white matter integrity, and function

260 Volumetric measures included brain volume, gray matter volume, white matter volume, volumes of subc

261 ributable to degeneration in the whole-brain gray matter volume.

262 most strongly linked to global reductions in gray matter volume.

263 ge cortical projections density, and reduced gray matter volume.

264 release correlated with reduced hippocampal gray matter volume.

265 1, smoking relapse was associated with less gray-matter volume (F1,74 = 28.32; familywise error P th

266 iations between corticothalamic-mediated IC, gray-matter volume, and smoking lapse/relapse.

267 Compared with controls, PLWH had lower gray matter volumes (-13.7 mL; 95% confidence interval,

268 th smaller subcortical and cortical regional gray matter volumes (GMVs).

269 45-78 years), we examined aging of regional gray matter volumes (nodes) and white matter structural

270 s negatively associated with all subcortical gray matter volumes (thalamus, caudate nucleus, putamen,

271 greater ventral diencephalon and cerebellar gray matter volumes and significantly smaller frontal, o

272 These findings suggest that decreased gray matter volumes are not explained by compromised neu

273 Reduced regional gray matter volumes are often interpreted to reflect neu

274 Conclusion Neurodevelopmental scores and gray matter volumes at age 2 years did not differ betwee

275 as used to investigate global differences in gray matter volumes between relatives as a group versus

276 +/- 16 at 2 years, respectively; P = .05) or gray matter volumes between the neonatal SDH group and c

277 her loneliness scores tended to have smaller gray matter volumes in three clusters comprising (i) the

278 ainst the more pronounced changes in CSF and gray matter volumes observed in male rats due to superio

279 derived from no/low drinkers indicated that gray matter volumes of lobules V and VI, crus II, lobule

280 Between groups, white and gray matter volumes were affected differentially during

281 ose To evaluate neurodevelopmental outcomes, gray matter volumes, and MRI findings in asymptomatic ne

282 in data consisted of whole-brain voxel-based gray matter volumes, and the behavioral data included it

283 igher than a random model or models based on gray matter volumes, degree, strength, and clustering co

284 area, cortical thickness and total cortical gray matter volumes.

285 BD, and 3) the normalization effect of Li on gray matter volumes.

286 esity is associated with smaller subcortical gray matter volumes.

287 fined thalamic and hippocampal seeds and all gray matter voxels in the brain.

288 n reversal learning tasks, and its impact on gray matter was measured.

289 Decreased right cerebellar gray matter was the only abnormality common to relatives

290 In BD, cortical gray matter was thinner in frontal, temporal and parieta

291 In all analyses, cerebellar gray matter was used as the reference region.

292 cal MRI optimized for myelin contrast within gray matter, we also observe a stripe pattern.

293 uage-processing network is cortically (i.e., gray matter) well defined.

294 Results T1 values of gray matter were significantly shorter for patients with

295 s a chondroitinase-digested DREZ into spinal gray matter, where the regenerating axons form functiona

296 ted with structural differences in white and gray matter, which was most prominent in precuneus and a

297 ue types (i.e., cerebral spinal fluid (CSF), gray matter, white matter) were greater in old relative

298 isphere affinity structure and ASE capturing gray matter/white matter core-periphery structure.

299 ery in the stroke-denervated cervical spinal gray matter with a focus on promotors of axon growth thr

300 d morphometry, FreeSurfer revealed increased gray matter with obstructive sleep apnea.