ライフサイエンスコーパス: gray matter

1 y projections to the midbrain periaqueductal gray matter.

2 anged, in parvalbumin interneurons and DLPFC gray matter.

3 tem plasticity have primarily focused on the gray matter.

4 parvalbumin interneurons, and in total DLPFC gray matter.

5 connectivity patterns within the spinal cord gray matter.

6 lues in white matter and 1.5 times higher in gray matter.

7 iated with changes in cerebral perfusion and gray matter.

8 showing lesions predominantly restricted to gray matter.

9 horns, dorsal horns, and central spinal cord gray matter.

10 complex and profound than those in cortical gray matter.

11 parvalbumin interneurons, and in total DLPFC gray matter.

12 perficial brain white matter and neighboring gray matter.

13 signal fluctuations similar to those of the gray-matter.

14 Patients showed a global downregulation of gray matter [(11) C]PBR28 binding of 26 +/- 26% (mean +/

15 The main outcome measure was total gray matter [(11)C]PBR28 binding ratio, representing mic

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

17 largely explained by T1 relaxation times in gray matter, a surrogate measure of water content, and n

18 In addition, 10 studies investigating gray matter abnormalities in 263 patients with BPD and 2

19 ed voxel-based morphometry (VBM) to identify gray matter abnormalities in youths with conduct problem

20 ed to investigate the histological origin of gray matter alterations for every distinct clinical enti

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

22 Regional gray matter alterations in chronic pain, as detected wit

23 tion on the histological origins of cerebral gray matter alterations in fibromyalgia, this study adva

24 Chronic pain patients present with cortical gray matter alterations, observed with anatomical magnet

25 healthy individuals (11 women), whether the gray matter anatomy and volume of the hippocampus were r

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

27 numerous complex abnormalities of white and gray matter and a high incidence of long-term neurocogni

28 te MS, fractions of cortical and subcortical gray matter and cerebral white matter, brain lesion volu

29 sociations were found between development of gray matter and family history of depression or experien

30 ted volumes for the number of neurons in the gray matter and for the number of other cells in the whi

31 rolled studies have found regionally greater gray matter and persistence of structural alterations fo

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

33 found with advancing age, the trajectory of gray matter and white matter changes during the disease

34 compounds, Cr, and mI concentrations in the gray matter and white matter of the four cerebral lobes

35 PFC and NAA concentrations in multiple lobar gray matter and white matter regions and subcortical nuc

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

37 ion model that used volumetric predictors of gray matter and white matter was 94.3% accurate.

38 hip did not hold; thus, baseline measures of gray matter and white matter were not significantly rela

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

40 as well as measuring the differences between gray matter and white matter.

41 matter ( WM white matter ), gray matter ( GM gray matter ), and lesions were compared between subject

42 2LV [T1:T2]), brain atrophy (whole brain and gray matter), and cervical spinal cord lesions (T2LV) an

43 is found in neurons, astrocytes, and glia in gray matter, and antisense QAGR proteins accumulate with

44 rease, 2.2%; 95% CI, 0.1%-4.2%; P = .04) and gray matter apparent diffusion coefficient (rate of decr

45 ified reference tissue model with cerebellar gray matter as a reference region) were calculated.

46 also evaluated: whole cerebellum, cerebellar gray matter, atlas-based white matter, and subject-speci

47 pical of the nfvPPA-PSP group, while greater gray matter atrophy and a trend toward greater sentence

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

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

50 but rather formed 1 week later at the white-gray matter border, preferentially including the ventral

51 regulates ErbB4 splicing, were quantified in gray matter by qPCR and in parvalbumin interneurons by m

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

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

54 e tissue model 2 [SRTM2]) of SRTM, all using gray matter cerebellum as the reference region, were app

55 ler neuroanatomical volumes, including total gray matter, cerebral cortex, and putamen.

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

57 or depressive disorder and the trajectory of gray matter change across 3 scan waves.

58 ive sleep apnea severity are associated with gray matter changes among middle-aged and older individu

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

60 ation and axon injury, can lead to secondary gray matter changes, we hypothesized that neurons can un

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

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

63 data from tracer experiments involving only gray matter connections in the primary visual areas of b

64 connectivity patterns within the spinal cord gray matter, consistent with known functional and anatom

65 terations in those processes, showing larger gray matter contraction and decreased white matter expan

66 ices (p < .05, corrected), including greater gray matter contraction and decreased white matter expan

67 Gray matter decreases and white matter increases are typ

68 Regional gray matter decreases were largely explained by T1 relax

69 sed tissue water content underlying regional gray matter decreases.

70 Gray matter degeneration contributes to progressive disa

71 Unraveling gray matter degeneration is critical for developing trea

72 A growing body of evidence suggests that gray matter demyelination, cortical atrophy, and leptome

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

74 Gray matter density (GMD), a measure often assumed to be

75 matter integrity (diffusion tensor imaging); gray matter density (voxel-based morphometry); and hippo

76 s exhibited increased hippocampal volume and gray matter density and decreased cerebrospinal fluid le

77 1 month were also positively correlated with gray matter density change (P < .005).

78 resonance imaging was used to determine the gray matter density changes across groups and their rela

79 n effects with known chemotherapy-associated gray matter density decrease was also assessed to elucid

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

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

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

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

84 hrenia ("schizophrenia score"), based on the gray matter density maps.

85 ith penalized splines, while controlling for gray matter density on a voxelwise basis.

86 Perfusion and gray matter density were assessed using voxel-based puls

87 nders (e.g., neuropsychological measures and gray matter density).

88 The trajectory of cortical gray matter development in childhood has been characteri

89 od depression and the trajectory of cortical gray matter development in late school age and early ado

90 the median signal intensity in basal ganglia gray matter (DGErho = 4.59%) was significantly increased

91 Statistical parametric maps comparing gray matter differences between youths with CP and TD yo

92 isorder or IQ, age range was associated with gray matter differences in the left amygdala.

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

94 are associated with neuron death and loss of gray matter, especially in the frontal cortex and hippoc

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

96 age at onset and the atrophy of subcortical gray matter fraction in women with relapsing-onset MS (s

97 -appearing white matter ( WM white matter ), gray matter ( GM gray matter ), and lesions were compare

98 known metabolic differences between cortical gray matter (GM) and NAWM.

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

100 lied voxel-based morphometry methods to test gray matter (GM) and white matter (WM) volume difference

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

102 ebellar activation was related negatively to gray matter (GM) atrophy (i.e., positively to GM volume)

103 lerosis (MS) is characterized by progressive gray matter (GM) atrophy that strongly correlates with c

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

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

106 ntia (bvFTD) in individual patients by using gray matter (GM) density maps computed from standard T1-

107 ibrary to estimate mean diffusivity (MD) and gray matter (GM) fraction changes.

108 g changes and remission status using pre-ECT gray matter (GM) in 38 MDD patients and validate in two

109 Modeling gray matter (GM) microstructural properties is now possi

110 otal, 71 cerebral areas were mapped onto the gray matter (GM) of an averaged T1-weighted structural M

111 quantified and mapped neuronal damage in the gray matter (GM) of patients with multiple sclerosis (MS

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

113 ata for estimating total brain volume (TBV), gray matter (GM) volume (GMV), and white matter (WM) vol

114 using voxel-based morphometry, we evaluated gray matter (GM) volume changes that may be associated w

115 Gray matter (GM) volume of distribution (VT) derived fro

116 Studies comparing gray matter (GM) volume of schizophrenic patients with o

117 cross-sectional association of rs162008 with gray matter (GM) volume variation in cortices, including

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

119 crophages, in cortex, cortical lesions, deep gray matter (GM), white matter (WM) lesions, and normal-

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

121 Gray matter hypertrophy and thickening were associated w

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

123 can be a primary target of injury within the gray matter in autoimmune neuroinflammatory disease, and

124 velopmental abnormalities, including reduced gray matter in both human patients and rodent models and

125 depression is associated with altered brain gray matter in children, though relations between postpa

126 We found decreased gray matter in fibromyalgia to be associated with T1 rel

127 ciated with paresis linked to involvement of gray matter in the brainstem or spinal cord.

128 nd whole-brain measures of iron, myelin, and gray matter in the participant's individual subspace to

129 tion (F(90)=4.1, P<0.05) as well as expanded gray matter in the posterior cingulate (Pcorrected <0.05

130 ly expressed within the anterior horn of the gray matter, in both cervical and lumbar sections.

131 We previously reported that gray matter increases in these regions were associated w

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

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

134 undergo direct excitatory injury within the gray matter independent of these.

135 ury at their synaptic connections within the gray matter, independent of the white matter pathology,

136 nstrated greater medial orbitofrontal cortex gray matter intensity in controls than maltreated youth

137 s between the maps of Tau, amyloid-beta, and gray matter intensity.

138 IFOF and right SLF's terminals where WM and gray matter intersect, in the absence of a clinically di

139 Gray matter involvement on DWI was assessed among 37 pat

140 ng the first 6 months, the growth pattern of gray matter is anisotropic and spatially inhomogeneous w

141 ordingly, the myelin observed in neocortical gray matter is thought to mostly ensheath excitatory axo

142 acute flaccid limb weakness with spinal cord gray matter lesions on imaging or evidence of spinal cor

143 llar white matter and circumscribed cortical gray matter lesions that developed during the disease co

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

145 vity to syntactic processing demands despite gray matter loss and reduced connectivity to task-relate

146 Widespread cortical gray matter loss has been observed in patients and prodr

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

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

149 and likely cognition and that periadolescent gray matter loss may be less pronounced than previously

150 s characterized by an initial, rapid rate of gray matter loss that slows in middle life, followed by

151 parcellation were used to extract GMD, GMV, gray matter mass (GMM; defined as GMD x GMV), and CT fro

152 ume, thickness, and surface area of cortical gray matter measured using structural magnetic resonance

153 effects and sex differences in four regional gray matter measures in 1189 youths ranging in age from

154 tudy demonstrates that different MRI-derived gray matter measures show distinct age and sex effects a

155 Inspired by this, we test a hypothesis that gray-matter myelin is related to electrophysiological co

156 istics allowed successful differentiation of gray matter (n = 223), white matter (n = 66), gliomas (n

157 works are highly correlated to resting-state gray-matter networks, highlighting their functional role

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

159 roitinase injections into the contralesional gray matter of the cervical spinal cord administered 28

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

161 ring the motor neurons, identified as mature gray matter oligodendrocytes.

162 six patients had T2 hyperintensity of spinal gray matter on magnetic resonance imaging and 43 patient

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

164 d with that in control subjects in the total gray matter (P < .05) and cortex (P = .03).

165 fraction of the leaking brain tissue in the gray matter (P = .004), normal-appearing white matter (P

166 ficantly with increasing leakage in the deep gray matter (P = .007) and cortex (P < .05).

167 ormal-appearing white matter (P < .04), deep gray matter (P = .01), and cortex (P = .004).

168 lateral hypothalamus, and the periaqueductal gray matter (PAG) are involved in these circuits; so, to

169 T1 segmentation and a novel high-resolution gray matter parcellation were used to extract GMD, GMV,

170 However, little is known about their role in gray matter pathology.

171 (18)F-T807 in gray matter peaked quickly (SUV > 2 at approximately 5 m

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

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

174 e brain perfusion relative to the cerebellar gray matter (R1) and binding potentials.

175 psychosis showed a steeper rate of cortical gray matter reduction compared with non-converters and h

176 Gray matter reduction mainly in the anterior cingulate c

177 otes but not A-allele carriers showed strong gray matter reduction with increasing CTQ scores.

178 ated to be transdiagnostically vulnerable to gray matter reduction.

179 We identified gray matter reductions within the insula, amygdala, fron

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

181 n sides) connections between all 77 cortical gray matter regions in each hemisphere of the rat brain.

182 defined axonal connections involving all 45 gray matter regions of the rat cerebral nuclei and revea

183 d by a network of axonal connections between gray matter regions within and between right and left ce

184 high ( approximately 25-55 mL/cm(3)) in all gray matter regions, consistent with the ubiquitous expr

185 levels of analysis: macroconnections between gray matter regions, mesoconnections between neuron type

186 s in TSPO VT (22%-29%) were present in other gray matter regions.

187 an-chance level from the connections between gray-matter regions spared by the lesion.

188 nal while retaining sensitivity in detecting gray matter signal.

189 y and postpartum are associated with altered gray matter structure in children; the observed white ma

190 In this nonrandomized prospective study, gray matter structure was assessed twice at approximatel

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

192 The claustrum is a gray-matter structure that underlies neocortex and recip

193 ves the way for future investigations of the gray-matter structure/function relationship and its brea

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

195 ion with prior GBCA exposure, especially for gray matter structures.

196 min after injection, using either cerebellar gray matter (SUVRCB) or whole subcortical white matter (

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

198 entation, all of which could damage cerebral gray matter that can be indirectly assessed by neuroimag

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

200 formed the largest study to date of cortical gray matter thickness and surface area measures from bra

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

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

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

204 d D2-type receptor availability and cortical gray-matter thickness, respectively.

205 re stable, longer-term changes (for example, gray matter thinning during a depressive episode), they

206 , upper cervical cord area, and the ratio of gray matter to the upper cervical cord area.

207 al gray matter were investigated by means of gray matter VBM.

208 o), was quantitatively investigated in brain gray matter versus white matter of healthy volunteers an

209 per 0.1-m/s slower gait [1.06-1.24]), lower gray matter volume (0.72 per 1-SD increase [0.55-0.95]),

210 s in humans have long described decreases in gray matter volume (GMV) and cortical thickness (CT) dur

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

212 effects of rs1137070 and heroin addiction on gray matter volume (GMV) based on 78 heroin abusers and

213 Regional gray matter volume (GMV) differences in youths with CP c

214 raumatic stress disorder (PTSD) show reduced gray matter volume (GMV) in fear regulatory areas includ

215 ancy and 7 years was calculated for cortical gray matter volume (GMV), white matter volume (WMV), and

216 7; P = .003) and was predominantly driven by gray matter volume (mean difference in z score per stand

217 oup, the PS group had diminished whole-brain gray matter volume (P = 1.8 x 10-10) and expanded white

218 composite SUVR correlated with the composite gray matter volume (r = -0.75, P < 0.001).

219 There was no evidence of regional gray matter volume abnormalities.

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

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

222 es had significantly less growth of cortical gray matter volume and cortical surface area and signifi

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

224 resonance imaging studies have found reduced gray matter volume and cortical thinning in acutely unde

225 pters with bipolar disorder demonstrate less gray matter volume and decreased structural and function

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

227 Gray matter volume and fractional anisotropy were mapped

228 METHOD: Gray matter volume and fractional anisotropy were mapped

229 Between-group differences in gray matter volume and fractional anisotropy were region

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

231 dicted smaller increases in both subcortical gray matter volume and global fractional anisotropy over

232 As expected, we observed a decrease in gray matter volume and myelin, and an increase of iron i

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

234 Gray matter volume at age 8 in distributed brain regions

235 morphometry was applied to study whole brain gray matter volume changes in 27 Retinitis Pigmentosa pa

236 tion of functional hyperactivity and smaller gray matter volume compared with HC.

237 elease were associated with less hippocampal gray matter volume compared with moderate cortisol relea

238 range: 50-75 years) to test whether regional gray matter volume decreases in chronic pain are associa

239 The impact of this retinal loss in cortical gray matter volume has not been addressed before in Reti

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

241 try analysis to determine where reduction of gray matter volume in healthy female and male adults ove

242 es of individual human subjects, we assessed gray matter volume in the frontal polar area, a region t

243 elwise analyses revealed significantly lower gray matter volume in the medial temporal lobe (maximum

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

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

246 the 6 month stage showed a clear decrease in gray matter volume in the right superior and middle temp

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

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

249 demonstrated marked alterations in cortical gray matter volume loss (slope estimate, -0.93 cm(3); 95

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

251 s that cortical thickness of PFC regions and gray matter volume of the hippocampus and amygdala diffe

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

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

254 We found significant reductions in gray matter volume that were restricted to the occipital

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

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

257 sure, whole-brain voxelwise regressions with gray matter volume were calculated.

258 ality, an older age, lower gait speed, lower gray matter volume, and greater global mean diffusivity

259 Cognitive impairment, lower gray matter volume, and white matter microstructural abn

260 l brain volumes, such as total brain volume, gray matter volume, or white matter volume.

261 -related variation in global measurements of gray matter volume, thickness, and surface area.

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

263 eripheral visual loss can lead to changes in gray matter volume.

264 ported in a transdiagnostic meta-analysis of gray matter volume.

265 release correlated with reduced hippocampal gray matter volume.

266 1, smoking relapse was associated with less gray-matter volume (F1,74 = 28.32; familywise error P th

267 Gray-matter volume in the hippocampus, parahippocampus a

268 in D2/D3 BPnd was positively correlated with gray-matter volume in the striatum, prefrontal cortex, i

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

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

271 The total gray matter volumes and cortical thicknesses were signif

272 The presence of lower gray matter volumes and more white matter microstructura

273 epression Rating Scale score by pretreatment gray matter volumes and to investigate ECT-related struc

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

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

276 Scheltens mesial temporal atrophy scale and gray matter volumes by voxel-based morphometry.

277 nal cerebral metabolic rates for glucose and gray matter volumes in cognitively unimpaired mutation c

278 ning our understanding of reduced multifocal gray matter volumes in obesity, our findings show that r

279 ng (F = 17.97, P < .001), and independent of gray matter volumes of the identified brain areas (F = 1

280 , 4697.8 [192.0] vs 5446.0 [159.6]; P = .05) gray matter volumes relative to the putatively preserved

281 In turn, lower ventral striatum gray matter volumes were associated with lower reward de

282 Gray matter volumes were investigated by means of voxel-

283 ank correlation, intraclass correlation, and gray matter volumes.

284 rtical thickness measurement and subcortical gray matter volumetry could provide an early and accurat

285 puted on the whole cortical ribbon, and deep gray matter volumetry was performed after automatic segm

286 of correlations of each voxel with all other gray matter voxels in the brain.

287 [(11)C]PBR28 binding ratio in gray matter was elevated in ultra-high-risk participants

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

289 Cerebellum gray matter was used as the reference region.

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

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

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

293 nts of perfusion values for white matter and gray matter were 0.864-0.917, and all differences were s

294 Alterations in occipital gray matter were investigated by means of gray matter VB

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

296 FA was correlated with astrogliosis in the gray matter, whereas mean diffusivity was correlated wit

297 pholipid-derived signals that differ between gray matter, white matter, gliomas, meningiomas, and pit

298 Volumetric segmentation of global gray matter, white matter, ventricles, and hippocampi wa

299 alcifications were most commonly seen at the gray matter-white matter junction, in 15 of 17 (88%) and

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