ライフサイエンスコーパス: axonal injury

1 nal degeneration, which is known as "diffuse axonal injury".

2 e same pathophysiological process: traumatic axonal injury.

3 epresents the early degenerative response to axonal injury.

4 with severe traumatic brain injury to assess axonal injury.

5 which are most commonly affected by diffuse axonal injury.

6 ns during neuronal development and following axonal injury.

7 s regulated in association with inflammatory axonal injury.

8 n vivo regulators of glial responsiveness to axonal injury.

9 is up-regulated in oligodendroglia following axonal injury.

10 usion tensor imaging as a measure of diffuse axonal injury.

11 for Drosophila glia to sense and respond to axonal injury.

12 nes following a peripheral but not a central axonal injury.

13 oligodendrocytes and its induction following axonal injury.

14 esulting in inflammation, demyelination, and axonal injury.

15 h regenerative and degenerative responses to axonal injury.

16 in axonal regrowth and remodeling following axonal injury.

17 beneficial for central neuron survival after axonal injury.

18 strates of cognitive outcome after traumatic axonal injury.

19 mice, suggesting increased vulnerability to axonal injury.

20 of p-STAT3 and p-cJun in the cell body after axonal injury.

21 generates targeted primary demyelination and axonal injury.

22 e equipped with mechanisms for responding to axonal injury.

23 were performed to examine synaptogenesis and axonal injury.

24 to the limited regeneration of the CNS after axonal injury.

25 engulfment of debris following apoptosis or axonal injury.

26 oading at thresholds that can induce diffuse axonal injury.

27 SCs) and is strongly reactivated in SCs upon axonal injury.

28 h regenerative and degenerative responses to axonal injury.

29 d sensitive way of identifying the impact of axonal injury.

30 structural connectivity produced by diffuse axonal injury.

31 All nerves had an axonal injury.

32 netic resonance imaging that is sensitive to axonal injury.

33 , which are induced in the DRG by peripheral axonal injury.

34 f significant myelin damage due to sustained axonal injury.

35 d cognitive dysfunction seen after traumatic axonal injury.

36 e tool for assessing the pathogenesis of RGC axonal injury.

37 ated mild traumatic brain injury can involve axonal injury.

38 observed from 6 hours to 14 days, reflecting axonal injury.

39 age surveillance mechanism for responding to axonal injury.

40 oxygen species in apoptosis signaling after axonal injury.

41 nd between patients with and without diffuse axonal injury.

42 hies result from retinal ganglion cell (RGC) axonal injury.

43 e prefrontal cortex of patients with diffuse axonal injury.

44 l of MS, were used to evaluate mechanisms of axonal injury.

45 alpain, is a potential candidate for causing axonal injury.

46 eased neuronal excitability after peripheral axonal injury.

47 trauma, corresponding to relatively isolated axonal injury.

48 nded to demyelination, edema, and persistent axonal injury.

49 c deprivation for signaling cell death after axonal injury.

50 anglion cells (RGCs) undergo apoptosis after axonal injury.

51 minated; this can also happen as a result of axonal injury.

52 have previously been considered a marker of axonal injury.

53 he Na(+)/Ca(2+) exchanger is associated with axonal injury.

54 e axon elimination in development and during axonal injury.

55 Unchanged NFL was consistent with no acute axonal injury.

56 te between regenerative and non-regenerative axonal injury.

57 xpression after peripheral, but not central, axonal injury.

58 g diffusion MRI assessment of post-traumatic axonal injury.

59 occur in the mature nervous system following axonal injury.

60 ctivation of transcriptional reporters after axonal injury.

61 zation during neuronal development and after axonal injury.

62 n (NfL) represents a promising biomarker for axonal injury.

63 eton and the subsequent processes that drive axonal injury.

64 s similar to those associated with traumatic axonal injury.

65 causes macrophage-mediated demyelination and axonal injury.

66 e disconnection of network hubs by traumatic axonal injury.

67 both methods for the clinical assessment of axonal injury.

68 ts brain connectivity by producing traumatic axonal injury.

69 sufficient to induce disability or increase axonal injury.

70 Here we provide evidence that axonal injury, a signature characteristic of traumatic b

71 but not yet robustly applied to the study of axonal injury after stroke.

72 s undergo early axonal damage and cumulative axonal injuries along subcortical, limbic, and cortical

73 yses of traumatic brain injury, we show that axonal injury also occurs following subarachnoid haemorr

74 t studies have demonstrated that significant axonal injury also occurs in MS patients and correlates

75 is a cardinal feature in multiple sclerosis, axonal injury also occurs.

76 on of complex IV augments glutamate-mediated axonal injury (amyloid precursor protein and SMI32 react

77 Here we evaluated markers of axonal injury (amyloid precursor protein, Na(v)1.6 chann

78 Axonal injury and apoptotic RGC death induced by 75 mmHg

79 ospinal fluid and positively correlates with axonal injury and clinical outcome.

80 Axonal injury and degeneration are pivotal pathological

81 lination of the CNS axons is associated with axonal injury and degeneration, which is now accepted as

82 n-invasive biomarkers for neuroinflammation, axonal injury and demyelination coexisting in multiple s

83 are consistent with the effects of traumatic axonal injury and exacerbated demyelination.

84 anisotropy that correlate with histological axonal injury and functional outcomes.

85 Axonal injury and histological features of neurons and g

86 BIM expression increased in RGCs after axonal injury and its induction was dependent on JUN.

87 er understanding of the underlying nature of axonal injury and its long-term processes is needed as c

88 hich markedly suppresses the disease course, axonal injury and its progression, is a candidate for th

89 mbination of effects predicted to exacerbate axonal injury and loss in patients.

90 Traumatic brain injury causes diffuse axonal injury and loss of cortical neurons.

91 e investigated the effects of simvastatin on axonal injury and neurite outgrowth after experimental T

92 ain (NfL) is a promising biomarker of active axonal injury and neuronal degeneration.

93 cute inflammatory CNS injury: demyelination, axonal injury and neuronal degeneration.In this article,

94 applicable to in vivo monitoring of diffuse axonal injury and neuronal loss in traumatic brain injur

95 Glasgow Outcome Scale groups between diffuse axonal injury and non-diffuse axonal injury patients wer

96 st time that MAG also promotes resistance to axonal injury and prevents axonal degeneration both in c

97 animals exhibited increased vulnerability to axonal injury and reduced efficiency of remyelination co

98 xpression is regulated by signals related to axonal injury and regeneration, that CNS myelin appears

99 ghtforward, reproducible method to model CNS axonal injury and regeneration.

100 However, in humans the link between diffuse axonal injury and subsequent neurodegeneration has yet t

101 ontrolled signal transduction in response to axonal injury and synaptic activity.

102 ter traumatic brain injury relate to diffuse axonal injury and the consequent widespread disruption o

103 This supports a causal link between axonal injury and the progressive neurodegeneration that

104 mouse, with a wait period of 2 weeks between axonal injury and tracing and 2-8 weeks between tracing

105 rain injury (TBI) often results in traumatic axonal injury and white matter (WM) damage, particularly

106 detection of immunohistochemistry confirmed axonal injury and/or demyelination in middle and rostral

107 arget-derived neurotrophic factors following axonal injury) and glutamate receptor stimulation (to mi

108 of whom had microbleed evidence of traumatic axonal injury, and 25 age-matched controls.

109 egenerative disorder in which neuronal loss, axonal injury, and atrophy of the CNS lead to permanent

110 e more stable following genetic or traumatic axonal injury, and axon loss is delayed in SkpA mutants

111 GEF complex required for glial responses to axonal injury, and demonstrates a critical requirement f

112 vier, resulting in deposition of complement, axonal injury, and disease exacerbation.

113 head (ONH) is the principal site of initial axonal injury, and elevated intraocular pressure (IOP) i

114 ted function for c-Jun in SCs in response to axonal injury, and identify paracrine Ret signaling as a

115 the disease are demyelination, inflammation, axonal injury, and progressive disability.

116 o the loss of immune homeostasis, myelin and axonal injury, and progressive neurological symptoms.

117 iffusion tensor imaging was used to quantify axonal injury, and test whether structural damage correl

118 ears to activate signaling events that mimic axonal injury, and that NgSR released from QHNgSR may be

119 n summary, diffusion MRI measures of diffuse axonal injury are a strong predictor of post-traumatic n

120 erates or undergoes apoptosis in response to axonal injury are not well defined.

121 ration of neurological functions after acute axonal injury are severely limited.

122 visualization of axonal tracts in myelin and axonal injuries as well as human brain and mouse embryon

123 However, mounting evidence indicates diffuse axonal injury as a likely pathological substrate for con

124 These changes were accompanied with acute axonal injury as characterized by structural and biochem

125 cal brain injury, or the amount of traumatic axonal injury as demonstrated by diffusion tensor imagin

126 trics best predict the presence of traumatic axonal injury, as well as which are most highly associat

127 vealed a decrease in retardance in eyes with axonal injury associated with visual field loss, which i

128 DTI detected axonal injury at 6 hours after ONC when SMI-31 did not d

129 matter atrophy was not predicted by diffuse axonal injury at baseline.

130 oncussed players had increased levels of the axonal injury biomarker total tau(median, 10.0 pg/mL; ra

131 lammatory lesions also exhibited evidence of axonal injury but not axonal loss.

132 lter gene expression patterns in response to axonal injury but pathways mediating these responses are

133 ion, glial cell oedema, myelin breakdown and axonal injury, but little intra-parenchymal inflammation

134 Axonal injury by spinal nerve ligation (SNL) elevated SO

135 ralded as the mediators of demyelination and axonal injury by transection.

136 or the focal depolarization that accompanies axonal injury can trigger a local decrease in action pot

137 However, the extent of axonal injury cannot currently be assessed reliably in l

138 t posttraumatic vestibulopathy has a central axonal injury component.

139 After axonal injury, concentrations of BH4 rose in primary sen

140 fy a fibre orientation-dependent gradient of axonal injury consistent with a barotraumatic mechanism.

141 t study of a promising drug to treat diffuse axonal injury (DAI) caused by traumatic brain injury, us

142 It produces diffuse axonal injury (DAI), which contributes to cognitive impa

143 brain injury (TBI) characterized by diffuse axonal injury (DAI).

144 aumatic symptoms, most likely due to diffuse axonal injury (DAI).

145 ral disconnection disorder whereby traumatic axonal injury damages large-scale connectivity, producin

146 levels, a clinically relevant biomarker for axonal injury/degeneration.

147 pinal cord injury (SCI), causing more severe axonal injury, demyelination, and functional impairment

148 Traumatic axonal injury disrupts their white-matter connections, a

149 g diffusion tensor imaging (DTI) to identify axonal injury distant from contusions.

150 link two important mediators of responses to axonal injury, DLK/Wnd and cAMP/PKA, into a unified and

151 Axonal injury due to prostatectomy leads to Wallerian de

152 Mechanisms of ischemic axonal injury during development are not well defined.

153 The increased rate of neuro-axonal injury during the first five years after onset wa

154 thors demonstrated that in vivo DTI detected axonal injury earlier than SMI-31.

155 Axonal injury elicits potent morphological and molecular

156 Our data suggest that simvastatin reduces axonal injury, enhances neurite outgrowth and promotes n

157 growth cones from axons re-emerging from an axonal injury express uPAR and that binding of uPA to th

158 technique previously validated in traumatic axonal injury, from these same specimens demonstrates de

159 Axonal injury further diminished neuronal mTOR activity

160 Axonal injury generates growth inert retraction bulbs wi

161 intrinsically poor regenerative capacity, so axonal injury has permanent consequences.

162 f cerebrospinal fluid (CSF) tau, a marker of axonal injury, have been associated with coma in severe

163 y promotes axonal degeneration shortly after axonal injury, hours before irreversible axon fragmentat

164 arkers of neuronal degeneration, stress, and axonal injury identified additional injured neuronal phe

165 nal ganglion cells (RGCs) die as a result of axonal injury in a variety of optic neuropathies, includ

166 PP and ubiquitin immunostaining as a sign of axonal injury in abusive head trauma.

167 models have shown evidence of a link between axonal injury in active lesions and impaired glutamate m

168 While axonal injury in association with traumatic microbleeds

169 he known predominance of cerebral hemisphere axonal injury in cardiac arrest and chiefly central myel

170 phage density, remyelination impairment, and axonal injury in central nervous system lesions.

171 Acute axonal injury in children with CM is associated with lon

172 model to characterize mechanisms of ischemic axonal injury in developing WM.

173 Axonal injury in Drosophila results in transcriptional u

174 x of sodium and calcium ions, contributes to axonal injury in experimental autoimmune encephalomyelit

175 tifying and monitoring retinal ganglion cell axonal injury in glaucoma.

176 vealed on DTI were consistent with traumatic axonal injury in many of the subjects with traumatic bra

177 time, likely reflecting temporal dynamics of axonal injury in MS.

178 hould be further investigated for monitoring axonal injury in MS.

179 ion, little is known about the mechanisms of axonal injury in MS.

180 ted whether pHERV-W ENV also plays a role in axonal injury in MS.

181 ) titre is likely to be a valid biomarker of axonal injury in multiple sclerosis (MS).

182 idylserine externalization immediately after axonal injury in purified retinal ganglion cells.

183 curs in conjunction with oligodendrocyte and axonal injury in PVL.

184 ndex lens technology with a model of diffuse axonal injury in rodents to enable repeated visualizatio

185 ghlights emerging principles in the study of axonal injury in stroke and the role of the axon in neur

186 te matter structure showed greater traumatic axonal injury in the cerebellum and corpus callosum in t

187 However, the exact pathogenesis of neuronal/axonal injury in the neonatal brain remains unclear.

188 ing primary inflammation, demyelination, and axonal injury in the optic nerve and leads to apoptotic

189 has been shown to be neuroprotective against axonal injury in the peripheral nervous system.

190 rons and retrograde neurodegeneration due to axonal injury in the white matter.

191 resent study explores the extent of neuronal/axonal injury in these infants since this is likely to b

192 rrhage and traumatic brain injury in humans, axonal injury in this model is observed in a multifocal

193 the anti-ganglioside Abs-mediated nodal and axonal injury in this model.

194 on transfer imaging (MTI) can detect diffuse axonal injury in traumatic brain injury (TBI).

195 transcriptional up-regulation in response to axonal injury in vitro and in vivo.

196 immunoglobulins to mediate demyelination and axonal injury in vitro.

197 iffusion tensor imaging measures recovery of axonal injury in white matter (WM) tracts after TBI.

198 quantify the specificity of DTI in detecting axonal injury, in vivo DTI maps from the spinal cords of

199 Regenerative responses to axonal injury involve changes in gene expression; howeve

200 e function following mTBI is associated with axonal injury involving the DLPFC.

201 Axonal injury is a common cause of neurological dysfunct

202 Diffuse axonal injury is a common finding after TBI, and is pres

203 Axonal injury is a major contributor to adverse outcomes

204 immune encephalomyelitis (EAE), inflammatory axonal injury is a major determinant of disability; howe

205 Diffuse axonal injury is a primary neuropathological feature of

206 Axonal injury is a useful pathologic feature that can be

207 er, accumulating evidence has indicated that axonal injury is also a predictor of MS clinical disease

208 r the innate immune system in MS lesions, as axonal injury is associated with macrophage activation.

209 Axonal injury is considered the major cause of disabilit

210 mice, Wallerian degeneration in response to axonal injury is delayed because of a mutation that resu

211 For example, diffuse axonal injury is implicated in disrupting microtubule fu

212 ak vulnerability to PWMI in humans, ischemic axonal injury is not mediated by AMPA/kainate receptors.

213 However, it is unknown whether axonal injury is related to long-term neurologic deficit

214 Axonal injury is the major correlate of permanent disabi

215 inflammation, a treatable feature, on neuro-axonal injury, is paramount to optimize neuroprotective

216 ignature pathology of traumatic brain injury-axonal injury-is also a functionally significant feature

217 ined in a stabilized steady state, yet after axonal injury it can be transformed into a dynamic struc

218 inflammatory demyelination and irreversible axonal injury leading to permanent neurological disabili

219 Because axonal injury leads to acute activation of Wnd, and over

220 age as indicated by co-localization with the axonal injury marker beta amyloid precursor protein.

221 o-accumulation of amyloid precursor protein (axonal injury marker) and calcium was observed in the ip

222 We propose that axonal injury may be an early event in presymptomatic Al

223 The complex IV defect associated with axonal injury may be mediated by soluble products of inn

224 neuritis, corroborating the hypothesis that axonal injury may cause neuronal pathology in multiple s

225 ranscription factors activated by peripheral axonal injury may mediate the conditioning effect by reg

226 esia showed evidence of widespread traumatic axonal injury measured using diffusion magnetic resonanc

227 Diffuse axonal injury, metabolic impairment, alterations in neur

228 o sequences in detecting hemorrhagic diffuse axonal injury, more accurate and objective assessment of

229 diffusion tensor imaging are consistent with axonal injury, myelin injury or both in white matter fib

230 Single mTBI does not cause axonal injury, neuroinflammation, or cell death in the g

231 We found that after axonal injury, Nogo-A is increased in dorsal root gangli

232 A second progressive phase of axonal injury occurs during the subacute period and dama

233 SCs reduced CCI-induced spontaneous pain and axonal injury of dorsal root ganglion (DRG) neurons and

234 -ganglioside Abs induce sequential nodal and axonal injury of intact myelinated nerve fibers, recapit

235 tusions on MRI, and >/=4 foci of hemorrhagic axonal injury on MRI, were each independently associated

236 network hubs, due to the impact of traumatic axonal injury on network connections.

237 ctivity, perhaps secondary to the effects of axonal injury on white matter tracts connecting limbic s

238 In contrast, NMDA injection did not cause axonal injury or behavioral changes in either group.

239 were used to test the hypothesis that either axonal injury or the focal depolarization that accompani

240 l inflammatory activity on the rate of neuro-axonal injury over the MS course.

241 substitute for histology to reveal diffusive axonal injury pathologies in vivo.

242 etween diffuse axonal injury and non-diffuse axonal injury patients were undertaken using effect size

243 Diffuse axonal injury patterns were associated with an increased

244 from the archive were diagnosed with diffuse axonal injury post-mortem.

245 an animal model for multiple sclerosis (MS), axonal injury precedes inflammatory demyelinating lesion

246 Diffuse axonal injury predicted substantially more variability i

247 The location and extent of diffuse axonal injury predicted the degree of brain atrophy: fra

248 is that the severity and location of diffuse axonal injury predicts the degree of progressive post-tr

249 Neurofilament is a biomarker of axonal injury proposed as a useful adjunct in the monito

250 Functional regeneration after axonal injury requires transected axons to regrow and re

251 an evolutionarily conserved component of the axonal injury response pathway.

252 ds our understanding of the genetic basis of axonal injury responses and repair.

253 STAT3 and DLK/JNK pathways are important for axonal injury responses, and we found that ZDHHC5 and ZD

254 tion can be genetically separated from other axonal injury responses: Raw does not modulate JNK-depen

255 Axonal injury results in regenerative success or failure

256 absence of microbleeds (a marker of diffuse axonal injury) revealed diffusion tensor imaging to be m

257 factors were previously known to function in axonal injury signaling and regeneration, Raw's function

258 sponses: Raw does not modulate JNK-dependent axonal injury signaling and regenerative responses, but

259 elayed Wallerian degeneration in response to axonal injury, suggest that axonal degeneration is an ac

260 Traumatic axonal injury (TAI) involves neurofilament compaction (N

261 Traumatic axonal injury (TAI) is a consistent component of traumat

262 Traumatic axonal injury (TAI) is an important component of TBI pat

263 Traumatic axonal injury (TAI) is an important pathoanatomical subg

264 Traumatic axonal injury (TAI) may contribute greatly to neurologic

265 Prior investigations of traumatic axonal injury (TAI), and pharmacological treatments of T

266 mTBI have demonstrated evidence of traumatic axonal injury (TAI), associated with adverse clinical ou

267 al pathology processes involved in traumatic axonal injury (TAI), have been well characterized.

268 r these behavioral deficits may be traumatic axonal injury (TAI), which manifests as impaired axonal

269 rain injury (TBI) often results in traumatic axonal injury (TAI).

270 se spectrin filaments are under tension, any axonal injuries that lacerate spectrin filaments will li

271 oles may constitute a sensitive biomarker of axonal injury that can be identified in mild TBI at acut

272 dentify a novel mechanism of immune-mediated axonal injury that can contribute to axonal pathology in

273 ectivity during development as well as after axonal injury, their role specifically in axonal regener

274 nt degeneration, but also evokes significant axonal injury to DRG cells including those innervating t

275 NCV and amplitude might provide measures of axonal injury to guide clinical practice.Significance: T

276 have previously reported that NO may signal axonal injury to neighboring glial cells.

277 , we used in vitro and in vivo models of CNS axonal injury to test the hypothesis that uPA binding to

278 important role in relaying information about axonal injury to the neuronal cell body.

279 In experimental models, diffuse axonal injury triggers post-traumatic neurodegeneration,

280 ated traumatic brain injury causes traumatic axonal injury, using diffusion tensor imaging (DTI), an

281 However, the pattern of diffuse axonal injury varies between patients and they have a co

282 ed appropriately as the type and severity of axonal injury vary by stroke subtype.

283 Axonal injury was correlated with the inflammatory infil

284 Evidence of axonal injury was not observed in co-localized histopath

285 Axonal injury was reduced at 6 weeks.

286 eurofilament light chain (NFL), a measure of axonal injury, was assessed before and after cART initia

287 ) and elevated excitability after peripheral axonal injury, we examined the contribution of I(h) to e

288 Similarly, markers for axonal injury were barely detectable in the treated mice

289 spinal cords; as a result, demyelination and axonal injury were reduced.

290 gnificance of these assessments of traumatic axonal injury when combined with other clinical and radi

291 TBI frequently results in traumatic axonal injury, which can disconnect brain networks by da

292 ediating the mpz transcriptional response to axonal injury, which is located between -1 and -4 kb.

293 ant recovery, SLP can be an early marker for axonal injury, which may be used to assess recovery pote

294 The assessment of diffuse axonal injury with diffusion MRI is likely to improve pr

295 llowing TBI compared to controls, indicating axonal injury, with longitudinal increases indicating ax

296 tients showed widespread evidence of diffuse axonal injury, with reductions of fractional anisotropy

297 oups have studied the pressure threshold for axonal injury within a nerve, but difficulty accessing t

298 those patients with more evidence of diffuse axonal injury within the adjacent corpus callosum.

299 The extent of traumatic axonal injury within the salience network strongly influ

300 Diffuse axonal injury within the sleep regulation system, disrup

301 at 3 days after retinal ischemia, suggesting axonal injury without myelin damage.