ライフサイエンスコーパス: white matter

1 axonal fiber bundles, collectively termed as white matter.

2 years +/- 0.30; right, 2.03 years +/- 0.28) white matter.

3 L/6 mice by 1-3 d of lesion evolution in the white matter.

4 contributes most of the signals detected in white matter.

5 nied by widespread abnormalities in cerebral white matter.

6 f these systems is underpinned by structural white matter.

7 ared earlier than the abnormal signal in the white matter.

8 ctivated astrocytes predominately located in white matter.

9 e related to the lesion fraction in cerebral white matter.

10 speed was faster in CSF compared to grey and white matter.

11 toward understanding the involvement of CNS white matter.

12 sions compared with that in normal-appearing white matter (0.19 +/- 0.10 vs 0.76 +/- 0.11, respective

13 mean volumes in the brain (28 mL; P < .001), white matter (26 mL; P < .001), mean lateral ventricles

14 0% more iron than the surrounding periplaque white matter (95% CI = 3-64%, p = 0.03).

15 Overall, patients with epilepsy showed white matter abnormalities in the corpus callosum, cingu

16 Previous studies in preterm infants report white matter abnormalities of the corpus callosum (CC) a

17 White matter abnormalities of the human brain are implic

18 r-reflexia, ataxia, dystonia and significant white matter abnormalities, there were differences betwe

19 hypotonia, prenatal-onset ventriculomegaly, white-matter abnormalities, hypoplastic corpus callosum,

20 MRI biomarker-objectively diagnosed diffuse white matter abnormality volume (DWMA; diffuse excessive

21 t were defined in tumor and normal appearing white matter (ADC(NAWM)).

22 tures seen in these nine individuals include white matter alterations (9/9), developmental delay (9/9

23 Premature-born adults exhibit lasting white matter alterations as demonstrated by widespread r

24 Particularly, our findings depict white matter alterations at specific locations on the ri

25 nction of NMDARs in oligodendrocytes and the white matter alterations reported in patients with this

26 impairment observed at later time points of white matter and clinical decline using both internal an

27 characterization of the relationship between white matter and cognitive performance in schizophrenia.

28 ween-group FA differences across whole-brain white matter and fiber tracts at each age; fiber tracts

29 l anisotropy and mean diffusivity within the white matter and performed voxelwise analysis with tract

30 e effectively suppressed water components in white matter and selectively imaged myelin, which had a

31 in the posterior cingulate, consistent with white matter and social-brain theories of ASD.

32 ibility, cognitive tests and MRI measures of white matter and the hippocampus were evaluated as endpo

33 ed reduced levels of multiple metabolites in white matter and the perisylvian cortex and elevated lev

34 ion was particularly prominent in cerebellar white matter and within the deep cerebellar nuclei, wher

35 structure (morphological changes of gray and white matter) and function (functional connectivity and

36 triatum, followed by neocortical regions and white matter, and lowest in the cerebellum.

37 bstantia nigra, putamen, frontal cortex, and white matter, and were all significantly enriched for ge

38 However, it remains unclear how white-matter architecture develops during youth to direc

39 duced deactivation) as well as greater FA in white matter areas near the hippocampus and posterior li

40 value ratios were generated with subcortical white matter as a reference region.

41 ribed; (2) a comprehensive three-dimensional white matter atlas depicting fiber pathways that were ei

42 omparative perspective, the first chimpanzee white matter atlas, constructed from in vivo chimpanzee

43 Comparative white matter atlases provide a useful tool for identifyi

44 own about the neurochemistry of the anterior white matter (AWM) in pediatric BD and how medication st

45 tion and is associated with smaller gray and white matter brain volume.

46 oup differences in specific locations of the white matter bundles.

47 nvestigate underlying local abnormalities in white matter by assessing the tract-specific WMH volumes

48 ral nervous system hypomyelination/vanishing white matter (CACH/VWM), a leukodystrophy characterized

49 mologous to primate subplate or interstitial white matter cells is still debated.

50 cell death, but some remain as interstitial white matter cells.

51 avior to reveal the impact of central neural white matter changes as a function of normal aging on ac

52 Perhaps most strikingly, we show that white matter changes in schizophrenia involve dynamic in

53 ivity in widespread locations, demonstrating white matter changes in the brains of participants with

54 These changes were accompanied by white matter changes in the ventral prefrontal tract, al

55 Here, we show white matter changes in young children exposed to matern

56 l abnormalities, epilepsy, chronic insomnia, white matter changes on brain MRI, dysmorphic features,

57 Although subcortical white matter changes were common, signs of watershed inj

58 gical processing, respectively, the specific white matter components of these networks remain a matte

59 tracts, and not from general differences in white matter condition across the aging brain.SIGNIFICAN

60 ATEMENT Tractography is a unique tool to map white matter connections in the brains of different spec

61 ructural network-based approaches can assess white matter connections revealing topological alteratio

62 nctional territories are not only defined by white matter connections, but also by the highly stereot

63 s across species, especially when applied to white matter connections.

64 is assumed to occur through cortico-cortical white matter connections.

65 nvestigated relationships between structural white matter connectivity and word production in a cross

66 better understand how age-related changes in white matter connectivity at multiple levels of each sen

67 rs with worse depressive symptoms had weaker white matter connectivity between areas related to emoti

68 ghted imaging (DWI) to construct whole-brain white-matter connectomes.

69 er cortical margin as well as tension in the white matter core, together competing against radially b

70 tal lesion such as white matter (subcortical white matter, corpus callosum, internal capsule, anterio

71 nic response to hypoxia, resulting in severe white matter damage.

72 osis type 1 (NF1), a disorder in which brain white matter deficits identified by neuroimaging are com

73 pathway most probably by progressive central white matter degeneration.

74 cally, we explore the ways in which gray and white matter develop throughout adolescence in typically

75 esis that autistic individuals have atypical white matter development across childhood.

76 eterm birth is associated with both impaired white matter development and adverse developmental outco

77 urthermore, the relationship between altered white matter development and longitudinal changes in aut

78 Differences in white matter development between individuals whose autis

79 h overweight/obesity who present a different white matter development.

80 y, we sought to determine whether changes in white matter diffusion parameters were associated with l

81 Vanishing white matter disease (VWM) is a severe leukodystrophy of

82 nction variants in TOMM70 result in variable white matter disease and neurological phenotypes in affe

83 kodystrophies constitute a subset of genetic white matter disorders characterized by a primary lack o

84 as a first-line diagnostic tool for genetic white matter disorders took place between December 1, 20

85 d earlier and greater diagnostic efficacy in white matter disorders.

86 confirm widespread areas of microstructural white matter disruption in Fabry disease, extending beyo

87 The results suggest that white matter disruptions at specific locations of the ci

88 ations, we identified two patterns including white matter-enhancing lesions and basal ganglia abnorma

89 areas, hypothalamus, and cerebellar gray and white matter evolved rapidly in humans.

90 feration, and dispersion important for human white matter expansion and myelination.

91 e mechanisms of human oligodendrogenesis and white matter expansion remain largely unknown.

92 oth the effect-sizes and pattern of lifespan white matter FA differences.

93 ) were also different among groups, although white matter FA showed limited differences.

94 ted MRI data available to date, which reveal white matter features not previously described; (2) a co

95 Contiguous white matter fiber pathways linking these gray matter st

96 of neuropathology emerged when investigating white matter fiber tracts in patients: (1) developmental

97 HRP3 was strongly expressed in the white matter fiber tracts of the peripheral (PNS) and ce

98 otropy (QA; a measure of tract integrity) of white matter fibers correlating with information derived

99 Localized protection was seen in white matter for HT+M versus HT (p = 0.036) and internal

100 rate cortical thickness, subcortical volume, white matter fractional anisotropy (FA), and behavioral

101 sion-weighted imaging (n = 300), we compared white matter fractional anisotropy (FA), mean diffusivit

102 Within patients, average white matter fractional anisotropy and white matter lesi

103 Average white matter fractional anisotropy correlated with the o

104 ompared to healthy controls the mean average white matter fractional anisotropy was lower in [0.423 (

105 at spinal cord lesions involve both grey and white matter from the early multiple sclerosis stages an

106 population, relying on previously-neglected white matter functional signals.

107 rey matter (g = -0.81, p < 0.001); and total white matter (g = -0.81; p < 0.001).

108 disruptions in offspring, including ones in white matter/glia, glucocorticoid receptors, neuroimmune

109 val [CI]: 27%, 59%), nonconfluent multifocal white matter hyperintense lesions seen with fluid-attenu

110 n UK Biobank imaging data and other sources: white matter hyperintensities (N = 42,310), fractional a

111 We divided the group into mild-to-moderate white matter hyperintensities (WMH) and severe WMH group

112 To quantify SVD, we assessed white matter hyperintensities (WMH), enlarged perivascul

113 kers of cerebrovascular pathology, including white matter hyperintensities (WMH), infarcts, cerebral

114 ssel stroke: 11 710 cases, 287 067 controls; white matter hyperintensities (WMH): 10 597 individuals;

115 anifestation of Fabry disease, visualized as white matter hyperintensities on MRI in 42-81% of patien

116 isruption in Fabry disease, extending beyond white matter hyperintensities seen on conventional MRI.

117 d with diabetes mellitus, hyperlipidemia and white matter hyperintensities to predict poorer cognitiv

118 ace area, hippocampal volume), white matter (white matter hyperintensities, fractional anisotropy [th

119 ed on brain magnetic resonance imaging, with white matter hyperintensities, microbleeds, and brain at

120 these associations were modified by cerebral white matter hyperintensity (WMH) burden.

121 (2010-2013) measures of infarct, hemorrhage, white matter hyperintensity (WMH) grade, brain and hippo

122 ral vascular disease (SCeVD) demonstrated by white matter hyperintensity (WMH) on MRI contributes to

123 between blood lead level and log-transformed white matter hyperintensity volume (b = 0.05 log mm3; 95

124 intracerebral hemorrhage, and an increase in white matter hyperintensity volume (beta = 0.11, 95% CI

125 gnitive performance, cortical thickness, and white matter hyperintensity volume at baseline, and the

126 t predicted in vivo beta-amyloid deposition, white matter hyperintensity volume, hippocampal volume o

127 quantified in cerebrospinal fluid (CSF), and white matter hyperintensity volume, lacunar infarcts, an

128 stigation of other brain disorders involving white matter hypoplasia or atrophy.

129 doses, and showed normalization of grey and white matter imaging parameters at the higher dose.

130 n normal-appearing gray matter compared with white matter in both participants with glioma (2.36 mumo

131 of the molecular layer, granular layer, and white matter in chimpanzee and macaque cerebellum slices

132 the frontal lobes, occupy 66% of total brain white matter in humans and 48% in three monkey species:

133 linked to major differences in temporal lobe white matter in humans compared with monkeys.

134 arger frontal cortex and even larger frontal white matter in humans compared with other primates, yet

135 ence between MS lesions and normal-appearing white matter in patients with MS.

136 Our findings strongly suggest that white matter in schizophrenia is affected across entire

137 While the fundamental importance of the white matter in supporting neuronal communication is wel

138 imaging at 7 T was used to segment grey and white matter, including lesions therein.

139 oligodendrocyte dysfunction and repair after white matter injury (WMI) remains undefined.

140 d not fully rescue microglial activation and white matter injury after TBI.

141 These events ultimately attenuated the white matter injury and improved anxiety and depressive-

142 fficient (-0.16) that was similar to that of white matter injury volume (standardized beta = -0.22).

143 in the entire Fontan cohort; the presence of white matter injury was associated with worse paired ass

144 ls and infiltration of Th1 cells resulted in white matter injury, characterized by impaired myelin ba

145 bed in preterm infants affected with diffuse white matter injury, is incompletely understood.

146 on is a promising option in treating diffuse white matter injury, previously called periventricular l

147 mitigate disturbed myelination in premature white matter injury.

148 inical utility of this model to detect focal white matter injury.

149 GCs closer to the white matter (inner-zone GCs) had higher firing threshol

150 H risk variants were associated with altered white matter integrity (p = 2.5x10-7) in brain images fr

151 lationship between executive dysfunction and white matter integrity (r = - 0.74, p < 0.001), than exe

152 Purpose To evaluate white matter integrity before and after thalamotomy and

153 netization transfer (MT) imaging to quantify white matter integrity in 78 subjects with varying level

154 -weighted imaging (DWI) sequence to quantify white matter integrity in both groups.

155 r ALFF, and decreased cortical thickness and white matter integrity in multiple brain regions that we

156 We also assessed white matter integrity measured by fractional anisotropy

157 To test if structural white matter integrity mediates the relationship between

158 -induced effects in microstructural gray and white matter integrity of optic tract, and somatosensory

159 ified tract specific and regional changes in white matter integrity suggesting potential insults to t

160 ciated with reduced cerebral grey matter and white matter integrity within a fronto-parietal brain ne

161 lex relationship between executive function, white matter integrity, stroke characteristics and cereb

162 ormalities in brain structure, function, and white matter integrity, with one of the subtypes showing

163 ects on treatment response through affecting white matter integrity.

164 iffusion tensor imaging metrics of increased white matter integrity.

165 , cerebral neurochemical concentrations, and white matter integrity.

166 hat the tissue property mismatch at the gray-white matter interface places axons crossing this region

167 on of infracortical white matter neurons, or white matter interstitial cells (WMICs), are found withi

168 ortical lesion types I-IV (mixed grey matter/white matter, intracortical, subpial and cortex-spanning

169 ant of the Expanded Disability Status Scale, white matter lesion fractions in the spinal cord and bra

170 the number of objects is unknown, such as in white matter lesion segmentation of multiple sclerosis (

171 erage white matter fractional anisotropy and white matter lesion volume showed statistically signific

172 disease (FD) are at risk for progression of white matter lesions (WMLs) and brain infarctions and wh

173 fractional anisotropy (FA) and diffusivity), white matter lesions (WMLs), and cerebral blood flow (CB

174 ging at 7 T was used to segment cortical and white matter lesions and 3 T imaging for cortical thickn

175 of baseline infratentorial lesions and deep white matter lesions at 1 year.

176 In white matter lesions from MS brain tissue, we noted the

177 e, studies in mouse demyelination models and white matter lesions from patients with multiple scleros

178 In CIS patients, finding typical MS white matter lesions on the patient's MRI scan remains t

179 Similarly, brain white matter lesions were mapped voxel-wise as a functio

180 activity (NEDA; occurrence of relapses, new white matter lesions, and Expanded Disability Status Sca

181 tensities in U-fibers and cortex adjacent to white-matter lesions characteristic of the disease can b

182 Imaging studies show white matter loss and functional connectivity changes wi

183 7, 95% CI = 1.71-7.89, p = 0.001) and severe white matter lucencies (aOR = 2.18, 95% CI = 1.06-4.51,

184 4-4.49, p = 0.001) but not lacunes or severe white matter lucencies, and CT SVD sum score >= 1 (aOR =

185 ndex (r = -0.661, P <= 0.001), while average white matter mean diffusivity showed a strong correlatio

186 46 (SD 0.016), P = 0.002] while mean average white matter mean diffusivity was higher (749 x 10-6 mm2

187 5% CI: 15%, 45%), and extensive and isolated white matter microhemorrhages in nine of 37 patients (24

188 has recently been associated with widespread white matter microstructural abnormalities, but the func

189 White matter microstructural degeneration of the superio

190 Our goal was to rank the most robust white matter microstructural differences across and with

191 Here, we conducted mega-analyses comparing white matter microstructural differences between healthy

192 , and autism spectrum disorder share similar white matter microstructural differences in the body of

193 ed with smaller total brain volume and worse white matter microstructural integrity (all p < 0.001).

194 modelling to investigate whether measures of white matter microstructural integrity (fractional aniso

195 To lend insight into this topic, we examined white matter microstructural integrity and gray matter c

196 ase, smaller brain tissue volumes, and worse white matter microstructural integrity.

197 eline, to elucidate the relationship between white matter microstructure and a measure of general cog

198 Our results indicate that white matter microstructure differences may be a causal

199 nnot conclude physical fitness is related to white matter microstructure in children with overweight/

200 ssociation of cardiorespiratory fitness with white matter microstructure in children, yet little work

201 od exposures to air pollution are related to white matter microstructure in preadolescents.

202 ed us an unprecedented look at the role that white matter microstructure may play in mental illnesses

203 hat the association of muscular fitness with white matter microstructure might be more focal on front

204 sponses during the video task and an altered white matter microstructure of the cingulum).

205 ffusion-tensor-imaging-derived parameters of white matter microstructure to measures of proximal and

206 Measures of white matter microstructure were calculated for the unci

207 HD to hyperactive-impulsive symptoms through white matter microstructure, cortical anatomy, and cogni

208 s mediated across multiple PRS thresholds by white matter microstructure, specifically by axial diffu

209 scular or motor fitness) are associated with white matter microstructure.

210 ncrease in permeability was region specific (white matter, midbrain peduncles, red nucleus, temporal

211 ral and cingulate cortices or the underlying white matter might affect cognitive impairment in patien

212 der and schizophrenia within the putamen and white matter modules, and a significant enrichment of th

213 normalized whole-brain and normal-appearing white matter myelin fractions, which correlated with bas

214 n lesions and with those in normal-appearing white matter (NAWM) in patients with MS and in normal wh

215 A large population of infracortical white matter neurons, or white matter interstitial cells

216 ter (NAWM) in patients with MS and in normal white matter (NWM) in healthy volunteers.

217 activation were observed in the spinal cord white matter of 7-month-old Hri(-/-) mice as compared wi

218 Abnormalities within frontal lobe gray and white matter of bipolar disorder (BD) patients have been

219 re associated with lower FA and higher MD in white matter of preadolescents.

220 ortical FA was significantly reduced only in white matter of the auditory system of aged monkeys, whi

221 Mitochondria in the axon-rich white matter of the brain rely heavily on lactate as a s

222 d a posterior temporal node connected by the white matter of the left arcuate fasciculus.

223 ls (WMICs), are found within the subcortical white matter of the mammalian telencephalon.

224 ated astrocytes located predominately in the white matter of the motor cortex and the spinal cord.

225 ocortical FA was lower only in visual system white matter of the same animals.

226 internal capsule), level of brainstem, grey- white matters on levels of centrum semiovale (CS), high

227 erstanding the anatomical specializations of white matter organization that are unique to the human l

228 Further, as white matter oxygen extraction fraction increased, conne

229 Increased white matter oxygen extraction fraction was associated w

230 gray matter (P < .001) and normal-appearing white matter (P < .001) in accordance with the Warburg t

231 Cerebral white matter pathology is a common CNS manifestation of

232 r leukomalacia (PVL) is a structural loss of white matter pathways that carry visual information from

233 chrotron X-ray nano-holotomography images of white matter samples from the corpus callosum of a monke

234 often with colpocephaly, and periventricular white-matter signal abnormalities (68%).

235 Cranial radiation therapy is associated with white matter-specific brain injury, cortical volume loss

236 of regional gray matter volumes (nodes) and white matter structural connectivity (edges) within 9 we

237 young autistic children have alterations in white matter structure that differ from older autistic i

238 esource that allows detailed descriptions of white matter structures and trajectories of fiber pathwa

239 ynaptic links to the striatal lesion such as white matter (subcortical white matter, corpus callosum,

240 the Wnt pathway targets Apcdd1 and Axin2 in white matter, suggesting paracrine OPC-endothelial signa

241 expanded and more complex occipital-temporal white matter system; additionally, in humans, the invasi

242 indings in 15 of 38 (39.5%) patients, mostly white matter T2/fluid-attenuated inversion recovery hype

243 ve lesions to that of surrounding periplaque white matter, the ratio is significantly higher in immun

244 each epilepsy syndrome and controls for each white matter tract (Bonferroni corrected at P < 0.001).

245 cortical thickness, gray matter volume, and white matter tract integrity (fractional anisotropy, FA)

246 ments, neuroanatomic imaging, and imaging of white matter tract microstructure.

247 After a unilateral section of the dorsal white matter tract of the cervical spinal cord, we found

248 llum (0.17 ug . g(-1) +/- 0.03, P = .01) and white matter tracts (anterior commissure: 0.05 ug . g(-1

249 an participants via plasticity in prefrontal white matter tracts and a colocalized increase in cerebr

250 the heritability of developmental change in white matter tracts and the brain's intrinsic functional

251 changes in microstructural properties along white matter tracts are associated with memory and cogni

252 y, left frontal regions and their underlying white matter tracts corresponding to the frontal aslant

253 lize most critically to a site of converging white matter tracts deep to the left temporo-parietal ju

254 Finally, WMH load was larger in the white matter tracts important for information processing

255 in areas can predict terminations of several white matter tracts in temporo-parietal cortex, includin

256 vity was associated with heritable change in white matter tracts metrics and change in the connectivi

257 ging estimated microstructural properties of white matter tracts on 252 participants.

258 is that differences in the integrity of the white matter tracts that connect these networks should p

259 correlated with diffusion anisotropy in the white matter tracts that connect these structures.

260 We created the white matter tracts using GQI and confirmed the tracts u

261 nal disruption and demyelination in specific white matter tracts within the spinal cord of squirrel m

262 rostructural alterations to specific sensory white matter tracts, and not from general differences in

263 me and water diffusion anisotropy in several white matter tracts, compared to controls.

264 PI5P4Kalpha localizes to white matter tracts, especially the corpus callosum, and

265 e enhanced representations of nervous system white matter tracts, ganglia, and nerves, and an enhance

266 strongest relationships were seen in central white matter tracts, including the body of the corpus ca

267 as a direct anatomical method of identifying white matter tracts, we have characterized these connect

268 s most prominent in precuneus and associated white matter tracts.

269 omically defined brain structures, including white matter tracts.

270 ity, associated with diffusion properties of white matter tracts.

271 ovo myelination in the cortex and associated white matter tracts.

272 For example, several cortical regions and white-matter tracts have been designated as possible ana

273 to comprehensively characterize age-related white matter trajectories, as measured by fractional ani

274 othelial cell interactions regulate neonatal white matter vascular development in a Wnt-dependent man

275 ockout of OPC Wntless resulted in diminished white matter vascular growth in normoxia, whereas loss o

276 ed OPC density results in cognate changes in white matter vascular investment.

277 al cortical growth patterns and larger scale white matter volume and surface measures differed signif

278 erebral volume, gray matter (GM) volume, and white matter volume as well as proportion of GM to total

279 ed that NfL levels were associated with grey/white matter volume loss; grey matter atrophy in cogniti

280 lepsy, developmental regression, and reduced white matter volume with delayed myelination.

281 n male youths than in female youths, whereas white matter volumes in crus I and crus II and lobules V

282 arlier meta-analysis showed reduced grey and white matter volumes in individuals with 22q11.2DS.

283 between plasma NfL and MRI measures of grey/white matter volumes in the Alzheimer's Disease Neuroima

284 th glioma, CMRO(2) values in gray matter and white matter volumes were compared by using Wilcoxon sig

285 on fractions within the spinal cord grey and white matter were related to the lesion fraction in cere

286 ., cerebral spinal fluid (CSF), gray matter, white matter) were greater in old relative to young rats

287 poral cortex) and correlated with changes in white matter, which were confirmed by diffusion tensor i

288 hickness, surface area, hippocampal volume), white matter (white matter hyperintensities, fractional

289 o quantify microstructural damage within the white matter with potential value as a disease biomarker

290 Abnormalities in brain white matter (WM) are reported in youth at-risk for psyc

291 ith research showing a season of RHI produce white matter (WM) changes seen on neuroimaging.

292 e important role of widespread disruption of white matter (WM) connectivity in pathogenesis, cognitiv

293 HD cohorts, showing a centrifugal pattern of white matter (WM) degeneration starting from deep brain

294 ovel approach to generate individual maps of white matter (WM) innate immune cell activation using (1

295 esions, thalamic neuronal loss, and cerebral white matter (WM) lesions to thalamic volume.

296 were used to assess grey matter (GM) volume, white matter (WM) microstructure (fractional anisotropy

297 Alterations in white matter (WM) microstructure have been implicated in

298 imaging (dMRI) studies have reported altered white matter (WM) microstructure in 22q11DS, but small s

299 Grey matter (GM), white matter (WM), density, and GM/WM density ratio of B

300 tinct pipelines were used: (1) regression of white matter (WM)/cerebrospinal fluid (CSF) signals only