ライフサイエンスコーパス: white matter

1 orrelated with diffusion measures of frontal white matter.

2 ding to progressive degeneration of cerebral white matter.

3 have a predilection for the periventricular white matter.

4 or, and from deep to superficial subcortical white matter.

5 ic galactosyl epimers naturally occurring in white matter.

6 most commonly employed metric for assessing white matter.

7 cortices of the hand and the entire cerebral white matter.

8 0.018, 0.091; P = .004) of normal-appearing white matter.

9 ogical diseases that involve the subcortical white matter.

10 ompartment, the late myelinating superficial white matter.

11 rected to the functional organization of the white-matter.

12 al cortex (-7.3%; P = .02), inferior frontal white matter (-11.4%; P < .001), and caudate (-10.6%; P

13 ced the volume of peak OEF found in the deep white matter, a location at high infarct risk in SCA (P

14 White matter abnormalities appear to be a particularly i

15 White matter abnormalities are prevalent in neuropsychia

16 g techniques to characterize microstructural white matter abnormalities for a deeper understanding of

17 n this study, we systematically investigated white matter abnormalities of ASPD using diffusion tenso

18 L2hgdh KO mice exhibit white matter abnormalities, extensive gliosis, microglia

19 by means of diffusion-tensor imaging in the white matter adjacent to the motor and sensory cortices

20 matter lesions relative to normal-appearing white matter (all P < 0.001), accompanied by an increase

21 in diffusion parameters in normal-appearing white matter, although they did not show progressive los

22 oward understanding the relationship between white matter anatomy and the structural connectome.

23 chanisms, including regeneration of cerebral white matter and improvement in neurocognitive function.

24 d with levels of CSF biomarkers across brain white matter and in areas preferentially affected in AD.

25 is accompanied by preservation of myelinated white matter and motor neurons and an increase in axonal

26 spongiform" vacuolation of superficial brain white matter and neighboring gray matter.

27 em targeting bilateral subcallosal cingulate white matter and randomised to 6 months of active or sha

28 amyloid pathologies significantly influence white matter and that these abnormalities may signify an

29 te myelinating brain regions such as frontal white matter and the genu of the corpus callosum.

30 accuracy is not improved when incorporating white matter anisotropy or different skull compartments.

31 ore, increased MD and AD values in different white matter areas was negatively correlated with perfor

32 It also can change white matter as measured by diffusion tensor imaging and

33 impairments in schizophrenia should consider white matter as one of the underlying neural mechanisms.

34 Glial activation in white matter assessed by translocator protein PET signif

35 A multifactorial model of white matter atrophy in focal epilepsy is proposed.

36 d bilaterally small hippocampi, but no focal white matter atrophy was detected, indicating a limited

37 re-crus) as well as a parametrically derived white matter-based reference region (parametric estimate

38 0.08, P = .03) temporal regions, subcortical white matter (beta = -0.13, P = .02), and occipital regi

39 of strain and strain rate at the grey matter-white matter boundary were mapped.

40 patients were also mapped at the grey matter-white matter boundary.

41 imaging, the fimbria-fornix, parahippocampal white matter bundle and uncinate fasciculus were reconst

42 bilaterally, the ipsilateral parahippocampal white matter bundle, and the ipsilateral fimbria-fornix

43 nix and in the contralateral parahippocampal white matter bundle.

44 on on a stereotypic connectome of converging white matter bundles (forceps minor, uncinate fasciculus

45 duplication carriers, presence of decreased white matter, callosal volume, and/or increased ventricl

46 erlying small vessel pathology: those in the white matter centrum semi-ovale have been associated wit

47 Nonacute ischemic white matter changes on T2-weighted imaging, focal tissu

48 Correlations of white matter changes with scores obtained from a detaile

49 repair, indicated by higher TSPO signal and white matter changes, may be associated with NFL play.

50 ad lower FA in a broadly distributed area of white matter compared with those with zero to one concus

51 an three concussions had lower FA in frontal white matter compared with those with zero to one concus

52 ) is the only noninvasive method for mapping white matter connections in the brain.

53 eemingly spared by the stroke due to loss of white matter connectivity and network integrity.

54 g data from 882 youth ages 8-22 to show that white matter connectivity becomes increasingly optimized

55 results demonstrate the importance of strong white matter connectivity between RLPFC and IPL during m

56 in Science transcriptome atlas, and regional white matter connectivity loss at three time points over

57 subjects to show that signals from the human white-matter contain meaningful information.

58 were classified according to their location (white matter, cortex, fiber tracts, basal ganglia).

59 at hypoperfusion results in gliovascular and white matter damage and impaired spatial working memory.

60 tis is associated with extensive superficial white matter damage in patients with incomplete recovery

61 domains highlights the clinical relevance of white matter damage in this disorder and warrants invest

62 However, extensive deep white matter damage wasrecently identifiedin these patie

63 investigate the role of microglia in preterm white matter damage.

64 n the diseased microenvironment can underlie white matter defects.

65 s, indicating a significantly faster rate of white matter deterioration with age.

66 , emphasizing the importance of this axis in white matter development and maintenance.

67 homeostasis, and OPC differentiation during white matter development and repair.

68 uggesting not only a failure of age-expected white matter development but also a progressive loss of

69 ests that early adversity can interfere with white matter development in key brain regions, which may

70 more closely approximating normal-appearing white matter development.

71 gatively impacts subsequent normal-appearing white matter development.

72 demyelinating syndromes on normal-appearing white matter development.

73 than that in contralateral normal-appearing white matter (DGErho = 0.08%) (P < .0001).

74 udies ignored a major part of the brain, the white-matter, discarding signals from it as arising from

75 troke can arise from cortical damage or from white matter disconnection.

76 nes implicated in SCZ form central areas for white matter disconnectivity.

77 t model and determine its relevance to human white matter disease.

78 Moreover, most of the white matter disorders show specific white matter pathol

79 oved regenerative medicine for patients with white matter disorders.

80 Normal-appearing white matter distribution volume ratio at baseline was c

81 odel including the baseline normal-appearing white matter distribution volume ratio, T2 lesion volume

82 Recent studies have demonstrated that the white-matter exhibits blood oxygen level-dependent signa

83 sonance imaging technique that distinguishes white matter fiber arrangement and geometry from changes

84 tients showed decreased FA in multiple major white matter fiber bundles, which connect the fronto-par

85 The deterioration of white matter fiber tracts associated with human brain ag

86 e that the structural integrity of selective white matter fiber tracts, specifically within right pos

87 ains and demonstrate that the quality of the white matter fibers connecting right and left SMA predic

88 yperoxia may benefit peri-lesional brain and white matter following traumatic brain injury (TBI).

89 s greater than that of the healthy volunteer white matter for both radioligands.

90 Oligodendrocytes, which are responsible for white matter formation, are the first targets for treatm

91 We also observed limited change in white matter fractional anisotropy and mean diffusivity

92 r combining them with cortical thickness and white matter fractional anisotropy further improved accu

93 Cerebral white matter from a patient with TUBB4A Asn414Lys mutati

94 es of network diffusion and nexus regions of white matter from edge density imaging, show converging

95 s for statistical inference and to study the white matter geometrical organization.

96 subjects, suggesting accelerated effects of white matter geometry change.

97 imulation (DBS) of the subcallosal cingulate white matter has shown promise as an intervention for pa

98 s12445022) was also associated with cerebral white matter hyperintensities (OR [95% CI] = 1.10 [1.05-

99 on molecule-1: OR, 1.58; 95% CI, 1.28-1.96), white matter hyperintensities (OR, 1.29; 95% CI, 1.19-1.

100 rofound in individuals with higher volume of white matter hyperintensities (P value for interaction=0

101 d patients using imaging biomarkers, such as white matter hyperintensities (WMH) on MRI and amyloid-b

102 Leukoaraiosis or white matter hyperintensities are frequently observed on

103 ts, cerebral microbleeds, and progression of white matter hyperintensities detected on MRI; cognitive

104 hizophrenia cohorts and also associated with white matter hyperintensities in a general population sa

105 al small vessel disease (eg, microbleeds and white matter hyperintensities in strategically important

106 -2.3) or severe (OR = 4.2, 95% CI = 3.0-5.9) white matter hyperintensities on MRI were independently

107 Moreover, higher white matter hyperintensities were associated with poor

108 erebral calcifications, when associated with white matter hyperintensities, are of major importance i

109 cerebrovascular disease, such as lacunes and white matter hyperintensities, as well as dementia.

110 Imaging studies reveal cerebral white matter hyperintensities, with delayed posthypoxic

111 ations were modified by baseline severity of white matter hyperintensities.

112 to determine the cerebrovascular pathology (white-matter hyperintensities and small- and large-vesse

113 cclusion (17.8%), outcomes tended to vary by white matter hyperintensitiy volume (P = 0.10, Cochran-M

114 High white matter hyperintensity (WMH) burden is commonly fou

115 Among SVD markers white matter hyperintensity (WMH) score or volume were a

116 modified Rankin Scale scores differed across white matter hyperintensity quintiles (P < 0.001).

117 n-Mantel-Haenszel test), and the upper three white matter hyperintensity quintiles (versus the first

118 atherosclerosis (39.0%), outcomes varied by white matter hyperintensity volume (P = 0.01, Cochran-Ma

119 .6%), outcomes did not vary significantly by white matter hyperintensity volume (P = 0.19, Cochran-Ma

120 18-1.72) and a greater 5-year progression of white matter hyperintensity volume.

121 We investigated how white matter hyperintensity volumes affect stroke outcom

122 White matter hyperintensity volumes were stratified into

123 and working memory in schizophrenia and (2) white matter impairment in schizophrenia is regional tra

124 nal diffusion properties of normal-appearing white matter in 505 serial scans of 132 paediatric parti

125 and neuroaxonal integrity in the cortex and white matter in early stage multiple sclerosis, their di

126 ophages and the ramified microglia of normal white matter in myelin disease models.

127 ly correlated with damage of the superficial white matter in patients.

128 uced CNP levels correlate with catatonia and white matter inflammation in human subjects.

129 a-induced DWMI.SIGNIFICANCE STATEMENTDiffuse white matter injury (DWMI) caused by hypoxia is a leadin

130 ments exist for preterm infants with diffuse white matter injury (DWMI) caused by hypoxia.

131 Neonatal white matter injury (NWMI) is a lesion found in preterm

132 results indicate that the evolution of grey/white matter injury and blood-brain barrier disruption a

133 n combined with hypothermia attenuates brain white matter injury in comatose survivors of out-of-hosp

134 Subcortical white matter injury is often accompanied by orofacial mo

135 On diffusion tensor imaging, white matter injury was prominent in the corpus callosum

136 HIP rats have brain microhemorrhages, white matter injury, and neurologic deficits.

137 e resistance of SPNs to insults that trigger white matter injury, transient hypoxemia disrupted SPN a

138 ubcortical grey matter volume (n = 1157) and white matter integrity (n = 1089) between depressed indi

139 pecific reductions in cortical thickness and white matter integrity among children raised in deprived

140 al diffusivity delineating extensive loss of white matter integrity and axon demyelination in MAP.

141 ngs from diffusion tensor imaging studies of white matter integrity and connectivity are also inconsi

142 nsity appear fundamental to abnormalities in white matter integrity in early psychosis.

143 hips between epigenetic age acceleration and white matter integrity in humans.

144 maturational changes and progressive loss of white matter integrity in paediatric-onset multiple scle

145 campal grey matter volume in MDD and reduced white matter integrity in several brain regions.

146 Measures of white matter integrity in the brain are also heritable a

147 n improvement, consistent with the increased white matter integrity in the corpus callosum connecting

148 Therefore, white matter integrity in the human brain, more than age

149 an only be detected in the tDCS group, where white matter integrity in the ipsilesional corticospinal

150 frontal cortex, hippocampus, and cerebellum; white matter integrity in the uncinate fasciculus, ventr

151 Whole brain white matter integrity of HD-monkeys was examined longit

152 significant positive correlation between the white matter integrity of the pons and cerebellar gray m

153 plored for diagnosing preclinical changes in white matter integrity or brain microvascular pulsatilit

154 dults was predicted by the degree of reduced white matter integrity throughout multiple white matter

155 tween epigenetic age acceleration and global white matter integrity was investigated with variance de

156 Intact white matter integrity with decreased NAA/Cr levels sugg

157 resonance (MR) spectroscopy and to evaluate white matter integrity with diffusion-tensor imaging in

158 Regional gray matter volume, white matter integrity, and functional connectivity duri

159 ressed individuals versus controls in global white matter integrity, as measured by fractional anisot

160 iNSC therapy demonstrated reduced changes in white matter integrity, cerebral blood perfusion, and br

161 iffusion tensor imaging measures of regional white matter integrity, regional volumes on structural m

162 trol participants, and to report measures of white matter integrity.

163 etween cognitive performance and superficial white matter integrity.

164 patients with autism display impairments in white matter integrity.

165 gnal fluctuations to investigate whether the white-matter is organized as functional networks by appl

166 Conclusion Subcortical white matter ischemic lesion locations and severity of u

167 d right: +10.8%; P = .01), superior temporal white matter (left: +14.6%; P = .003 and right: +9.5%; P

168 in PET significantly improves predictions of white matter lesion enlargement in relapsing remitting p

169 r NT-proBNP level was associated with larger white matter lesion volume (mean difference in z score p

170 White matter lesions (WMLs) were classified as "active"

171 le demyelinating attack-when associated with white matter lesions in the brain-negatively impacts sub

172 Similar findings were observed in white matter lesions relative to normal-appearing white

173 proportion of infants, MRI detects punctate white matter lesions that are not seen on ultrasonograph

174 Punctate white matter lesions without associated cerebral lesions

175 The unique combination of white matter lesions, hypohomocysteinaemia and increased

176 essment to characterize cerebral parameters (white matter lesions, microbleeds), cardiovascular param

177 le sclerosis; (ii) they occur independent of white matter lesions; and (iii) they are associated with

178 frequent occurrence (one-fourth of cases) of white matter magnetic resonance imaging abnormalities, a

179 ratio, T2 lesion volume and normal-appearing white matter magnetization transfer ratio for all of the

180 om them; in optic neuritis, normal-appearing white matter magnetization transfer ratio was lowest adj

181 In normal-appearing white matter, magnetization transfer ratio gradients wer

182 ate the utility of the framework for in vivo white matter mapping and anatomical computing by evaluat

183 Overall, we demonstrate failure of white matter maturational changes and progressive loss o

184 discovery of functional networks within the white-matter may open new avenues of research in cogniti

185 collected from all subjects and superficial white matter mean diffusivity derived from diffusion ten

186 ve impairment, lower gray matter volume, and white matter microstructural abnormalities were evident

187 n tensor imaging (DTI) studies have detected white matter microstructural changes in essential tremor

188 We assessed differences in white matter microstructural integrity, hippocampal volu

189 ymptom ratings and quantitative anatomic and white matter microstructural measures over time.

190 cupuncture using diffusion tensor imaging of white matter microstructure adjacent to the primary soma

191 , the automatic method allowed assessing the white matter microstructure along the tract.

192 White matter microstructure and hippocampal volume were

193 speed contributes to the association between white matter microstructure and working memory in schizo

194 causal relationship, namely that changes in white matter microstructure impact cognition in part by

195 ittle is known about possible impairments of white matter microstructure in ASPD, as well as their re

196 Hence, systematic evaluation of white matter microstructure in the normative brain is cr

197 Associations between white matter microstructure measures and gestation corre

198 Widespread abnormalities in white matter microstructure were also seen, including re

199 ognitive function, brain tissue volumes, and white matter microstructure were assessed in 134 HIV-inf

200 dose dependent relation to abnormalities in white matter microstructure, assessed with tract-based s

201 White matter microstructure, essential for efficient and

202 We suggest that spatial locations of white matter modules overlap with cytoarchitecturally di

203 euroimaging markers while being sensitive to white matter myelin content.

204 areas, that is, in areas of normal-appearing white matter (NAWM) and gray matter (GM).

205 ctivation in lesions and in normal-appearing white matter (NAWM) of multiple sclerosis (MS) patients

206 lated to cross-situational learning; and the white matter near the hippocampus, a structure fundament

207 mporal gyrus, to the fusiform gyrus and to a white matter network including the left posterior tempor

208 Signals in white-matter networks correlated with signals from funct

209 We found microglia activation in normal white matter of controls and that the degree of activati

210 We show that T2 in brain white matter of nondemented volunteers follows a U-shape

211 nt of microglia/macrophage activation in the white matter of the spinal cord.

212 To examine associations between white matter organization and 2 commonly co-occurring ne

213 Connectome white matter organization measured through modularity an

214 en ASD traits and inattention and indexes of white matter organization, particularly in the corpus ca

215 gions, respectively) and in normal-appearing white matter (P < .001 for both contrast-enhancing and n

216 of the white matter disorders show specific white matter pathology caused by different disease mecha

217 explaining the varying effects of localized white matter pathology on cognition and behavior.

218 lso suggest that abnormalities in connecting white matter pathways and functionally connected more po

219 ted to the integrity of the language-related white matter pathways in 40 adults (18 women).

220 t the structural integrity of the connecting white matter pathways influences the level of transfer.S

221 is cortically well defined, the role of the white matter pathways supporting novel word-to-meaning m

222 scores show reduced structural integrity of white matter pathways, as indexed by lower fractional an

223 associations is mainly dependent on temporal white matter pathways.

224 /choline (Cho), and fractional anisotropy of white-matter pathways was assessed.

225 3 weeks of age and located preferentially in white matter, periventricular zones, and meninges.

226 is review focuses on the emerging concept of white matter plasticity.

227 r, MRI-based imaging studies have shown that white matter, primarily composed of myelinated axons, ca

228 iffusivity of non-lesional, normal-appearing white matter progressively increased after clinical pres

229 lator of midline crossing and development of white-matter projections throughout the human CNS.

230 02, p<0.0001; grey matter r=0.518, p<0.0001; white matter r=0.588, p<0.0001; and ventricular expansio

231 lzheimer disease may benefit from the use of white matter reference regions.

232 el-intensity histogram within an atlas-based white matter region and using the center and width of th

233 ealed a steady depletion of sphingomyelin in white matter regions during 28d Li-treatment, particular

234 wever, many studies indicate that failure of white matter repair goes beyond the intrinsic incapacity

235 Findings in the normal-appearing white matter reveal early axonal pathology outside infla

236 tasets, and suggest a new way to explore the white-matter role in cognition and its disturbances in n

237 ance and escape were associated with diffuse white matter signal abnormalities (DWMSAs) on cranial ma

238 However, many other potential causes of white matter signal abnormalities can mimic the changes

239 It manifests itself as white matter signal abnormalities with or without the pr

240 ere estimated and compared across the entire white matter skeleton between groups, and correlated wit

241 modify the effects of concussion history on white matter structure and neural recruitment.

242 Tract-based spatial statistics compared white matter structure between patients and control subj

243 Previous reports of altered grey and white matter structure in Major Depressive Disorder (MDD

244 can reveal dimensional relationships linking white matter structure to neurodevelopmental symptoms.

245 ar gray matter (SUVRCB) or whole subcortical white matter (SUVRWM) as the reference.

246 ole cerebellum [WCER], pons, and subcortical white matter [SWM]) were studied.

247 ion volume ratios (DVR) of [(18) F]Nifene in white matter thalamic radiations were approximately 1.6

248 d after injury, with sustained elevation in white matter through 8 weeks.

249 ignificantly increased compared with that in white matter tissue (DGErho = 0.65%) (P = .028).

250 re calculated in each DTI Studio parcellated white matter tract at 1.25 mm and 1.75 mm isotropic voxe

251 FA in the peritumoral region indicated more white matter tract disruption and independently predicte

252 ble to demonstrate that epigenetic aging and white matter tract integrity also share common genetic i

253 erapy.Significance: These findings show that white matter tract integrity is degraded in areas where

254 defined by diffusion tensor imaging (DTI) of white matter tract microstructure and functional connect

255 y 30 but that this depends on the particular white matter tract.

256 Structural abnormalities across multiple white matter tracts are recognized in people with early

257 nal anisotropy deficits in the corresponding white matter tracts as determined by a meta-analysis (r

258 ed the dynamic relationships over time among white matter tracts connecting frontoparietal cortices (

259 llows performing anatomical manipulations on white matter tracts for statistical inference and to stu

260 striatum receives segregated and integrative white matter tracts from the cortex facilitating informa

261 MRI technique that can detect disruption of white matter tracts in the brain.

262 haracteristics of preoperative temporal lobe white matter tracts known to be important in the generat

263 d white matter integrity throughout multiple white matter tracts known to connect subcortical and cor

264 also found AD/RD deficits in some additional white matter tracts that were not detected by FA.

265 ated to elucidate the relative importance of white matter tracts to the overall network connectivity,

266 this brain-to-cognition pathway in different white matter tracts was strongly associated with the sev

267 g with diffusion-derived metrics of 20 major white matter tracts were extracted for every subject.

268 were variably sized, predominantly affected white matter tracts, and involved the middle cerebral ar

269 f microinfarcts, microhemorrhages, strategic white matter tracts, loss of microstructural tissue inte

270 rative outcome and preoperative pathology of white matter tracts, which constitute crucial components

271 tonic signs is the low-grade inflammation of white matter tracts, which marks a final common pathway

272 d seizures contribute to atrophy in specific white matter tracts.

273 graphy demonstrated broad disorganization of white-matter tracts throughout the human central nervous

274 eoretic analysis showed that highly selected white-matter tracts were consistent across the group and

275 tworks composed of interacting long-distance white-matter tracts.

276 s method is built on (a) relative normalized white matter, ventricular and cortical signal intensitie

277 .003 and P < .001, respectively), decreased white matter volume (22.9%; P < .001, and P < .001, resp

278 mmon genetic variant in NCAN, rs1064395, and white matter volume in the left and right temporoparieta

279 ositively with intracranial volume, gray and white matter volume, and cortical surface area (deletion

280 after controlling for global gray matter and white matter volume.

281 findings in the brain (measured by gray- and white-matter volume, sulcal depth, and gyrification inde

282 ting-state functional MRI (RSfMRI) data from white-matter voxels, in 176 subjects (of both sexes).

283 vity in centromedial amygdala-anterior vmPFC white matter was associated with greater anxiety/depress

284 In contrast, the superficial white matter was intact in recovered patients.

285 no abnormalities of cortical gray matter or white matter were found.

286 n opposite directions across gray matter and white matter when MDD subjects were compared with contro

287 ain-like tau-containing neurites in gray and white matter with heaviest burden in basal ganglia.

288 particular advantage of sensitivity to both white matter (WM) and gray matter (GM) demyelination.

289 Patterns of gray matter (GM) and white matter (WM) atrophy at presentation were assessed

290 e anterior limb of the internal capsule, the white matter (WM) bundle carrying ascending and descendi

291 We investigated focal brain white matter (WM) changes and fluid shifts during 70 day

292 We report that the volume of white matter (WM) is disproportionately reduced in AS mi

293 the connection between amyloid pathology and white matter (WM) macrostructural and microstructural da

294 SCZ, and BP on subcortical brain volumes and white matter (WM) microstructure in a large single sampl

295 euroimaging studies have identified abnormal white matter (WM) microstructure in patients with schizo

296 nly related to immune system dysfunction and white matter (WM) pathology.

297 ases are linked to abnormalities in specific white matter (WM) pathways, and the efficacy of deep-bra

298 brospinal fluid (CSF), gray matter (GM), and white matter (WM) tissues; 3) delineated 25 external and

299 structural brain alterations of the gray and white matter (WM).

300 White-matter (WM) microstructure in the optic radiation