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 esulting in inflammation, demyelination, and axonal injury.

3 h regenerative and degenerative responses to axonal injury.

4 in axonal regrowth and remodeling following axonal injury.

5 beneficial for central neuron survival after axonal injury.

6 strates of cognitive outcome after traumatic axonal injury.

7 mice, suggesting increased vulnerability to axonal injury.

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

9 generates targeted primary demyelination and axonal injury.

10 e equipped with mechanisms for responding to axonal injury.

11 were performed to examine synaptogenesis and axonal injury.

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

13 engulfment of debris following apoptosis or axonal injury.

14 zation during neuronal development and after axonal injury.

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

16 h regenerative and degenerative responses to axonal injury.

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

18 structural connectivity produced by diffuse axonal injury.

19 All nerves had an axonal injury.

20 netic resonance imaging that is sensitive to axonal injury.

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

22 f significant myelin damage due to sustained axonal injury.

23 d cognitive dysfunction seen after traumatic axonal injury.

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

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

26 ated mild traumatic brain injury can involve axonal injury.

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

28 age surveillance mechanism for responding to axonal injury.

29 oxygen species in apoptosis signaling after axonal injury.

30 nd between patients with and without diffuse axonal injury.

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

32 e prefrontal cortex of patients with diffuse axonal injury.

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

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

35 eased neuronal excitability after peripheral axonal injury.

36 trauma, corresponding to relatively isolated axonal injury.

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

38 c deprivation for signaling cell death after axonal injury.

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

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

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

42 e axon elimination in development and during axonal injury.

43 eton and the subsequent processes that drive axonal injury.

44 to protect neurons from the consequences of axonal injury.

45 e role in removing fibrin, which exacerbates axonal injury.

46 ed PKC levels enhance neurite regrowth after axonal injury.

47 gher pathological specificity for myelin and axonal injury.

48 the appearance of demyelination and that of axonal injury.

49 intra-axonal protein synthesis in vivo after axonal injury.

50 s similar to those associated with traumatic axonal injury.

51 causes macrophage-mediated demyelination and axonal injury.

52 occur in the mature nervous system following axonal injury.

53 e disconnection of network hubs by traumatic axonal injury.

54 both methods for the clinical assessment of axonal injury.

55 ts brain connectivity by producing traumatic axonal injury.

56 sufficient to induce disability or increase axonal injury.

57 e same pathophysiological process: traumatic axonal injury.

58 epresents the early degenerative response to axonal injury.

59 ctivation of transcriptional reporters after axonal injury.

60 with severe traumatic brain injury to assess axonal injury.

61 ns during neuronal development and following axonal injury.

62 s regulated in association with inflammatory axonal injury.

63 n vivo regulators of glial responsiveness to axonal injury.

64 is up-regulated in oligodendroglia following axonal injury.

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

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

67 oligodendrocytes and its induction following axonal injury.

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

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

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

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

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

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

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

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

76 Axonal injury and apoptotic RGC death induced by 75 mmHg

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

78 Axonal injury and degeneration are pivotal pathological

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

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

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

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

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

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

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

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

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

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

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

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

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

92 DBI is believed to be comprised by diffuse axonal injury and other forms of diffuse vascular change

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

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

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

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

97 n induces Schwann cell turnover with minimal axonal injury and support the idea that mechanical stimu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

115 Noninvasive surrogate markers for axonal injury are therefore essential to monitor cumulat

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

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

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

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

120 The axonal injury associated with demyelination reflects ela

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

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

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

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

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

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

127 RGCs actively respond to axonal injury by regulating expression of genes that pro

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

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

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

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

132 t posttraumatic vestibulopathy has a central axonal injury component.

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

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

135 Diffuse axonal injury (DAI) is one of the most common and import

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

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

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

139 ther diffuse traumatic brain damage [diffuse axonal injury (DAI)] occurs in such children has not yet

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

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

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

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

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

145 Axonal injury due to prostatectomy leads to Wallerian de

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

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

148 Axonal injury elicits potent morphological and molecular

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

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

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

152 Axonal injury further diminished neuronal mTOR activity

153 Axonal injury generates growth inert retraction bulbs wi

154 Studies of white matter axonal injury have demonstrated that voltage-gated sodiu

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

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

157 Axonal injury in a calcium-free extracellular solution r

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

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

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

161 erapeutically in limiting nerve terminal and axonal injury in autoimmune peripheral neuropathy and in

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

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

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

165 Axonal injury in Drosophila results in transcriptional u

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

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

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

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

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

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

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

173 Renewed interest in axonal injury in multiple sclerosis has significantly sh

174 GDVII virus infection resulted in severe axonal injury in normal appearing white matter at 1 week

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

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

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

178 play a critical supportive role in repairing axonal injury in the adult spinal cord but also can be u

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

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

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

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

183 ssion of Na(v)1.6 and NCX is associated with axonal injury in the spinal cord in EAE.

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

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

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

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

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

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

190 immunoglobulins to mediate demyelination and axonal injury in vitro.

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

192 beta-amyloid precursor protein, a marker of axonal injury, in acute MS lesions.

193 id precursor protein (beta-APP), a marker of axonal injury, in the spinal cord dorsal columns of mice

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

195 ent demonstration of rapid demyelination and axonal injury induced by Mycobacterium leprae provides a

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

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

198 Axonal injury is a common cause of neurological dysfunct

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

200 Axonal injury is a feature of traumatic brain injury (TB

201 Axonal injury is a major contributor to adverse outcomes

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

203 Recent data suggest that axonal injury is a major factor in the long-term disabil

204 Axonal injury is a useful pathologic feature that can be

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

206 Diffuse axonal injury is an uncommon sequel of inflicted head in

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

208 Axonal injury is considered the major cause of disabilit

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

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

211 r subdural haemorrhages, and where traumatic axonal injury is present, show patterns of hemispheric w

212 Axonal injury is the major correlate of permanent disabi

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

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

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

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

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

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

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

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

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

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

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

224 Diffuse axonal injury, metabolic impairment, alterations in neur

225 The results suggest that axonal injury might herald or trigger demyelination.

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

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

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

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

230 The distribution of axonal injury observed during the early phase correspond

231 ls was also required for the majority of the axonal injury observed in these animals.

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 tructures except for 3 patients with diffuse axonal injury of the brain stem.

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

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

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

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

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

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 We show that in response to axonal injury, periaxonal Schwann cells release erythrop

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

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

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

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

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

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

251 We demonstrate that the relevant axonal injury signal that stimulates EPO production from

252 have therapeutic potential for subacute CNS axonal injuries such as spinal cord trauma.

253 nown but differ from those involved in acute axonal injury such as transection, where inflammation an

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

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

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

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

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

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

260 Traumatic axonal injury (TAI), a consequence of traumatic brain in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

275 f them infants, showed evidence of localized axonal injury to the craniocervical junction or the cerv

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

277 After median eminence compression to produce axonal injury, unilateral superfusion of 3 microM TTX in

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

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

280 Axonal injury was correlated with the inflammatory infil

281 Axonal injury was demonstrated by increased amyloid prec

282 resent in 13 cases, but widespread traumatic axonal injury was found in only two children, both of wh

283 und in 21 out of 53 cases, diffuse traumatic axonal injury was present in only three.

284 Axonal injury was reduced at 6 weeks.

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

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

287 while investigating DBI-mediated perisomatic axonal injury, we identified scattered, rapid neuronal s

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

289 2 years; age range, 4-72 years) with diffuse axonal injury were examined with diffusion-weighted MR i

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

291 traumatic brain injury and suspected diffuse axonal injury were studied using a new high-resolution m

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

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

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

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

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

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 These results indicate an asymmetrical focal axonal injury within the language network in PPA.

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