ライフサイエンスコーパス: neuronal death

1 ortem and HD mouse striata, correlating with neuronal death.

2 ation has been previously linked to ischemic neuronal death.

3 rlying cause of the CerS1 deficiency-induced neuronal death.

4 um responses, calcium overload and increased neuronal death.

5 rs attenuated misfolded tau accumulation and neuronal death.

6 f blood-retina barrier breakdown, edema, and neuronal death.

7 phagy, which are known to mediate poststroke neuronal death.

8 avage limit mitochondrial fusion and promote neuronal death.

9 ndent transcriptional activity, and promotes neuronal death.

10 ns did not show any signs of inflammation or neuronal death.

11 equally resistant to proneurotrophin-induced neuronal death.

12 s of photoreceptors was used as a measure of neuronal death.

13 f blood-retina barrier breakdown, edema, and neuronal death.

14 ameliorate symptoms, but not the underlying neuronal death.

15 ytokines may play a direct role in promoting neuronal death.

16 nal superoxide signal, oxidative stress, and neuronal death.

17 eurotransmitter release, and ultimately with neuronal death.

18 cal role for non-NMDA glutamate receptors in neuronal death.

19 in pathological events leading ultimately to neuronal death.

20 inner membrane depolarization, and apoptotic neuronal death.

21 by oligodendrocyte damage, demyelination and neuronal death.

22 tween AEME and mAChRs and how it can lead to neuronal death.

23 ionic homoeostasis, resulting in axonal and neuronal death.

24 at PD is caused by irreversible dopaminergic neuronal death.

25 from synaptic clefts to prevent excitotoxic neuronal death.

26 erminal Set-beta cleavage product can induce neuronal death.

27 ogical hallmark of HD, but did not influence neuronal death.

28 successfully identify new mechanisms driving neuronal death.

29 ("excitotoxicity") induces acute or delayed neuronal death.

30 s, re-entry into the cell-cycle and eventual neuronal death.

31 to ER stress and provides protection against neuronal death.

32 ed to be the main cause for ischemia-induced neuronal death.

33 ial protein import causes mutant Htt-induced neuronal death.

34 (NTR), resulting in axonal fragmentation and neuronal death.

35 , synaptic dysfunction, neuronal injury, and neuronal death.

36 CK1 is causally related to ischemia-induced neuronal death.

37 (d) to identify RNAi knockdowns that enhance neuronal death.

38 vation of extrasynaptic NMDARs, and ischemic neuronal death.

39 er's disease brain, possibly contributing to neuronal death.

40 s, and astrocyte conditioned media triggered neuronal death.

41 t nodose ganglia following capsaicin-induced neuronal death.

42 lin homolog NRA-2 enhances MEC-10(d)-induced neuronal death.

43 d robust protection against ischemia-induced neuronal death.

44 and causes only minimal demyelination and no neuronal death.

45 equently leading to synaptic dysfunction and neuronal death.

46 plasmic reticulum, influencing the extent of neuronal death.

47 tate of neurons, may be critical in ischemic neuronal death.

48 ork function, which contribute to subsequent neuronal death.

49 revents miR-29c down-regulation and ischemic neuronal death.

50 ld lead to early metabolic failure promoting neuronal death.

51 /calpain-2 in CNS function in plasticity and neuronal death.

52 ccompanied by microtubule destabilization or neuronal death.

53 t it played a major role in calpain-mediated neuronal death.

54 n the cells of the brain ultimately provokes neuronal death.

55 particular their role in glutamate-mediated neuronal death.

56 ched protein tyrosine phosphatase (STEP) and neuronal death.

57 in mitochondrial morphology in p53-dependent neuronal death.

58 hen targets the dopaminergic neurons causing neuronal death.

59 changes, such as hyperphosphorylated tau and neuronal death.

60 ta causes neuronal dysfunction and may drive neuronal death.

61 g, activates signaling cascades that lead to neuronal death.

62 o the disruption of cellular homeostasis and neuronal death.

63 egates and the loss of cellular function and neuronal death.

64 rative conditions and a major contributor to neuronal death.

65 -mediated neuroinflammation, thus increasing neuronal death.

66 axonal degeneration in the absence of overt neuronal death.

67 he underlying mechanisms responsible for the neuronal death.

68 rized by increased microglial activation and neuronal death.

69 in this context, it also reduces SE-induced neuronal death.

70 than mere cellular debris produced following neuronal death.

71 icative of axonal dieback that progresses to neuronal death.

72 -methyl-4-phenyl pyrinidium (MPP(+))-induced neuronal death.

73 urons in vivo, strongly enhances excitotoxic neuronal death.

74 known to penetrate into the brain and cause neuronal death.

75 rategy for the treatment of delayed ischemic neuronal death.

76 lain why the former but not the latter cause neuronal death.

77 t compression of the injured spinal cord and neuronal death.

78 dult guts, given previous reports of ongoing neuronal death.

79 dysfunction, tau accumulation, and eventual neuronal death.

80 ns numerous inclusions, there is very little neuronal death.

81 Induction of PH-Tau triggered neuronal death (60% in CA3), astrocytosis, and loss of t

82 300 mg/kg significantly reduced hippocampal neuronal death after brain ischemia, inhibited the ische

83 eimer disease, cleavage of Set-beta leads to neuronal death after stroke, and the full-length Set-bet

84 ignificantly mitigates mHTT accumulation and neuronal death, ameliorating disease-associated phenotyp

85 ws: the cytokine induced caspase-independent neuronal death and accelerated autophagic flux in BDNF-t

86 tinamide salvage, both NAD(+) and NR prevent neuronal death and AxD in a manner that depends on inter

87 to identify specific kinases that regulated neuronal death and axon regeneration.

88 To discover agents that suppress neuronal death and axonal degeneration, we performed dru

89 tosis of NPCs, ZIKV infection causes massive neuronal death and axonal rarefaction, which phenocopy f

90 Massive neuronal death and BBB leakage indicate brain damage, wh

91 Inhibition of cathepsin B prevents neuronal death and behavioural anomalies in ASMko mice.

92 as potential upstream regulators of ischemic neuronal death and Cdk4 activation.

93 t inflammatory response, ultimately leads to neuronal death and cognitive decline.

94 Ischemia-induced brain neuronal death and cognitive deficits also increase in t

95 ural inflammation; these pathologies lead to neuronal death and consequently clinical symptoms, such

96 -associated protein tau, which are linked to neuronal death and disease development and can be caused

97 s normally, which when disrupted may lead to neuronal death and disease.

98 V (MEX1-44), DENV2 grows slower, causes less neuronal death and fails to cause postnatal animal death

99 he formation of a dysfunctional repair cell, neuronal death and failure of functional recovery.

100 CD38 deletion and NAD(+) supplementation on neuronal death and glial activation in the facial nucleu

101 t hypoxia followed by re-oxygenation lead to neuronal death and hallmarks of an injury response, incl

102 Whether axonal p75 signaling contributes to neuronal death and how signaling endosomes contribute to

103 rease in local vascular perfusion as well as neuronal death and impaired function.

104 ated cerebral inflammation, brain edema, and neuronal death and improved neurologic function.

105 nt with lithium reduces solid-stress-induced neuronal death and improves motor coordination.

106 Neuronal death and microgliosis induced by Abeta were re

107 formation, peripheral and CNS inflammation, neuronal death and neurocognitive deficits.

108 ess-induced OPA1 processing by OMA1 promotes neuronal death and neuroinflammatory responses.

109 vivo models of cerebral ischemia, decreasing neuronal death and reducing infarct size, allowing us to

110 epilepticus (SRSE) have been shown to cause neuronal death and reorganization, and visual inspection

111 ides an excellent model for exploring mature neuronal death and replacement by new neurons.

112 Neuronal death and replacement, or neuronal turnover, in

113 nactivation underlies excitotoxicity-induced neuronal death and suggest that PKD1 inactivation may be

114 equirement for DNMTs in mutant Htt-triggered neuronal death and suggesting a neurodegenerative mechan

115 This may be attributed to axon degeneration/neuronal death and sustained neuroinflammation.

116 buffering and temporally preceded apoptotic neuronal death and the generation of spontaneous seizure

117 le for PTPsigma (and LAR) in both retrograde neuronal death and the poor intrinsic regenerative abili

118 mmation may be deleterious and contribute to neuronal death and tissue injury.

119 s also known to contribute to post-ischaemic neuronal death and to physiologically induced LTP.

120 well-established that hyperthermia increases neuronal death and worsens stroke outcome.

121 is a controlled process that may not lead to neuronal death and, thus, we term this phenomenon "neuri

122 ascade that results in synaptic dysfunction, neuronal death, and eventually cognitive deficits.

123 membralin results in beta-amyloid pathology, neuronal death, and exacerbates synaptic/memory deficits

124 contribute to neuronal dysfunction, enhanced neuronal death, and neurodegeneration.

125 OSU-0212320 substantially reduced mortality, neuronal death, and spontaneous recurrent seizures in a

126 Areas of hippocampal neuronal death are associated with the presence of immun

127 r mechanisms whereby HDAC inhibitors prevent neuronal death are currently the focus of intensive rese

128 oss, degeneration of neuronal processes, and neuronal death are hallmarks of neurological diseases an

129 ese results suggest that factors that induce neuronal death are likely to be necessary to initiate th

130 totoxic activation of p38MAPK and subsequent neuronal death are reduced by competing with the nNOS:NO

131 REST-dependent repression of miR-132 in the neuronal death associated with global ischemia and ident

132 involving the proapoptotic protein Trib3 in neuronal death associated with PD.

133 trocytes causes glial activation, tauopathy, neuronal death, brain atrophy, cognitive impairment and

134 ATX reduced neuronal death but did not improve neurologic function i

135 I) at preterm gestation that is unrelated to neuronal death but is associated with decreased dendriti

136 ation causes initial axonal degeneration and neuronal death but subsequent axon outgrowth from surviv

137 eurogenesis is not limited to injury-induced neuronal death, but also can result from normally occurr

138 Tauopathy is accompanied by significant neuronal death, but the relationships between initial ta

139 Suppression of early-stage neuronal death by AAV-YAPdeltaC reduces the later-stage

140 M3 mAChRs, leading to DNA fragmentation and neuronal death by apoptosis.

141 by overactivation of calpains, which induce neuronal death by catalyzing limited proteolysis of spec

142 brains that produce cytokines or counteract neuronal death by clearing myelin debris.

143 pport that temperature increase worsened the neuronal death by depleting intracellular ATP, inducing

144 tress kinases p38 and JNK is instrumental in neuronal death by oxidative stress.

145 Neuronal death can be preceded by progressive dysfunctio

146 Neuronal death caused by excessive excitatory signaling,

147 provide activity-induced protection against neuronal death caused by excitotoxic stimulation.

148 cycle machinery is implicated in a number of neuronal death contexts, including stroke.

149 nd ischemia and that increased apoptosis and neuronal death contribute to the risks to ID in humans.

150 rib3 overexpression is sufficient to promote neuronal death; conversely, Trib3 knockdown protects neu

151 n blood flow is restored, and causes delayed neuronal death (DND) in selective vulnerable regions.

152 Although this focal neuronal death does not impact anxiety/depression-like b

153 in chronic pain and increases ASIC-mediated neuronal death during acidosis.

154 s elicits axon degeneration and nonapoptotic neuronal death even in the absence of injury.

155 ath, E2F4 plays a crucial protective role in neuronal death evoked by DNA damage, hypoxia, and global

156 ia exhibited an increased capacity to induce neuronal death ex vivo and in vivo in the presence of st

157 e pharmacologic inhibition of ASIC1a reduces neuronal death following ischemic stroke in rodents.

158 nsmission, as well as initiation of pain and neuronal death following ischemic stroke.

159 CaN-mediated Drp1 dephosphorylation promotes neuronal death following oxygen-glucose deprivation.

160 neurons, thereby preventing amplification of neuronal death from cytotoxicity.

161 for inflammation, histone modifications, and neuronal death functional classes.

162 ignalling, ion channels, synaptic structure, neuronal death, gliosis, and inflammation.

163 ynuclein (alpha-syn) leading to dopaminergic neuronal death has been recognized as one of the main pa

164 e connection between respiratory defects and neuronal death has never been proven, this hypothesis ha

165 roposed to be a central mechanism leading to neuronal death in a range of neurodegenerative diseases.

166 levels associated with plaque deposition and neuronal death in a transgenic mouse model of cerebral b

167 ate excitotoxicity, which is accountable for neuronal death in acute neurological disorders, includin

168 The timing and characteristics of neuronal death in Alzheimer's disease (AD) remain largel

169 xidative stress and subsequent DNA damage to neuronal death in Alzheimer's disease and related tauopa

170 and have been shown to modulate toxicity and neuronal death in Alzheimer's disease.

171 ributes to long-range toxicity and selective neuronal death in Alzheimer's disease.

172 g promotes relaxation of heterochromatin and neuronal death in an in vivo model of neurodegenerative

173 or Ca(2+) entry blockers to delay pyramidal neuronal death in both regions.

174 Oxidative stress contributes to neuronal death in brain ischemia-reperfusion.

175 n of glutamate receptors is a major cause of neuronal death in cerebral ischemic stroke.

176 l source protected against glutamate-induced neuronal death in control, but not ARALAR-deficient neur

177 re linked to the progressive dysfunction and neuronal death in corticostriatal circuits.

178 thies and identifies a new pathway mediating neuronal death in currently untreatable human neurodegen

179 e and taurursodiol have been found to reduce neuronal death in experimental models.

180 exras1 signaling is a potential mechanism of neuronal death in experimental optic neuritis.

181 forms of tau protein accumulation leading to neuronal death in focal brain areas.

182 hich glia-derived soluble TNFalpha modulates neuronal death in glaucoma.

183 tivity caused by OGD/ischemia contributes to neuronal death in hippocampal neurons via diverse effect

184 key role in a variety of diseases, including neuronal death in ischemia, cancer, cardiac atrial fibri

185 of misfolded proteins that ultimately causes neuronal death in many of these disorders.

186 1 prevented AbetaO-induced synaptic loss and neuronal death in mouse cultured neurons and long-term p

187 utic intervention aimed at the prevention of neuronal death in neurodegenerative diseases.

188 The cause of neuronal death in PD is largely unknown, but several gen

189 hat could be relevant to the mechanism of DA neuronal death in PD.

190 Reduction of Bmal1 expression promoted neuronal death in primary cultures and in mice treated w

191 The mechanisms of neuronal death in protein misfolding neurodegenerative d

192 ally in animals causes selective and delayed neuronal death in pyramidal neurons of the hippocampal C

193 onditional knock-out (CKO) of Cdk5 prevented neuronal death in response to ischemia.

194 75 neurotrophin receptor (p75(NTR)) mediates neuronal death in response to neural insults by activati

195 exhibited reduced anoxic depolarization and neuronal death in response to OGD.

196 (ischemic preconditioning or IPC) can reduce neuronal death in response to subsequent severe ischemic

197 protein kinase Cdk5 is a principal cause of neuronal death in rodents during stroke.

198 r pathways, leading to neuroinflammation and neuronal death in specific brain regions resulting in se

199 Twelve hours of mild hypothermia attenuated neuronal death in subiculum and thalamus but not CA1 and

200 H2AX knockout mice display increased neuronal death in the brain when challenged with 3-nitro

201 ng global cerebral ischemia, exhibit greater neuronal death in the CA1 area of the hippocampus and re

202 ay a role in the regulation of p53-dependent neuronal death in the CNS is currently unknown.

203 rmore, ZIP caused a dose- and time-dependent neuronal death in the dissociated cultures.

204 ult rats, oral treatment with EVT901 reduced neuronal death in the hippocampus and thalamus, reduced

205 air-cell-specific afferent activity prevents neuronal death in the neonatal brain is unknown.

206 rom this protein by MHC-I, which triggers DA neuronal death in the presence of appropriate cytotoxic

207 Here, we examined the role of GJs in neuronal death in the retina, which has arguably the mos

208 and moderate susceptibility to WNV-mediated neuronal death in Tlr8(-/-) mice were attributed to over

209 , neuroinflammation, amyloid deposition, and neuronal death in vitro and in vivo.

210 ficiency did not aggravate glutamate-induced neuronal death in vitro, although glutamate-stimulated r

211 essive mitochondria fission and dopaminergic neuronal death in vitro.

212 tivation of Akt protects against hippocampal neuronal death in vivo following status epilepticus.

213 hil infiltration, ischemic brain damage, and neuronal death in vivo using an adenovirus encoding a re

214 ting that Rhes is critical for mitophagy and neuronal death in vivo.

215 ARM1 ortholog TIR-1 leads to NAD(+) loss and neuronal death, indicating these activities are an evolu

216 In cell cultures, BEZ reduced neuronal death induced by Abeta.

217 Antioxidants abrogated the neuronal death induced by astrocytes exposed to Lys or G

218 hagy plays a significant role in hippocampal neuronal death induced by cerebral I/R following asphyxi

219 rations in overall protein synthesis precede neuronal death induced by deprivation of excitatory affe

220 Finally, expression of LAP2beta rescues neuronal death induced by FMRpolyG.

221 tumor suppressor protein) pathway in delayed neuronal death induced by ischemia.

222 The mechanism of neuronal death induced by ischemic injury remains unknow

223 europrotective profile on in vitro models of neuronal death induced by oxidative stress and energy de

224 We conclude that, both in vitro and in vivo, neuronal death induced by p75(NTR) requires the DD and T

225 In vivo, neuronal death induced by pilocarpine-mediated seizures

226 g by disulfide-linked dimers of p75(NTR) for neuronal death induced by proneurotrophins and epileptic

227 Neuronal death induced by proneurotrophins or epileptic

228 f TrkB-Shc signaling exacerbated hippocampal neuronal death induced by SE.

229 cted the increased neuronal excitability and neuronal death induced by TNFalpha.

230 n particular cyclin D/Cdk4, is implicated in neuronal death induced by various pathologic stresses, i

231 CD47 contributes to neuronal death, inflammation and angiogenesis after brai

232 We examined neuronal death, inflammatory reaction and neurogenesis i

233 Neuritic retraction in the absence of overt neuronal death is a shared feature of normal aging and n

234 At the cellular level, neuronal death is accompanied by the proteolytic cleavag

235 Finally, we find that neuronal death is due to blockage of plasma membrane rec

236 contribution of individual HDAC isoforms to neuronal death is limited.

237 of astrocytes was not toxic, indicating that neuronal death is mediated by astrocytes.

238 Whether HSF1 is protective when neuronal death is not caused by protein misfolding has n

239 However, the mode of neuronal death is not known.

240 However, a role for miR-132 in neuronal death is not, as yet, well-delineated.

241 e that is expressed by Muller glia following neuronal death, is required for Muller glia to progress

242 esults indicate a role for Cdc25A in delayed neuronal death mediated by ischemia.SIGNIFICANCE STATEME

243 ing ischaemia nearly completely prevents the neuronal death, microglial inflammation and sensorimotor

244 -mediated ribosomal stress may contribute to neuronal death, neurodevelopmental disruption and microc

245 the nucleolus may trigger the p53-dependent neuronal death, neurotoxic consequences of a selective i

246 NK) signaling pathway is a critical step for neuronal death occurring in several neurological conditi

247 e exosome is involved in the ethanol-induced neuronal death of the beta-endorphin neuron.

248 een shown to contribute to ethanol-activated neuronal death of the stress regulatory proopiomelanocor

249 alphaPBN and MK801 reduced neuronal death only in 'inactive-phase' neurons.

250 Our results identify a mechanism of neuronal death post-infection and point to a role for ti

251 wborns or P7 rats is enhanced and related to neuronal death processes.

252 gy, XJB-5-131 promotes weight gain, prevents neuronal death, reduces oxidative damage in neurons, sup

253 er, the mechanism by which TNFalpha promotes neuronal death remains poorly defined.

254 of PrP in pathological processes leading to neuronal death remains unclear.

255 n are impaired, and synaptic dysfunction and neuronal death result, with ensuing thinning of key brai

256 abnormal ion channel activity underlies the neuronal death seen in Tg(DeltaCR) mice.

257 characterized by progressive dysfunction and neuronal death, showing specific protein inclusions at a

258 and the further propagation of p75-dependent neuronal death signals.

259 ome-mediated, ethanol-induced beta-endorphin neuronal death.SIGNIFICANCE STATEMENT Neurotoxic action

260 onist activates survival signals and reduces neuronal death significantly better than GDNF, suggestin

261 While strain magnitude affects the time of neuronal death, strain rate influences the pathomorpholo

262 tosis proteins or proteasome function led to neuronal death, suggesting that caspase activation is sp

263 ons (2-4% DMSO) induce caspase-3 independent neuronal death that involves apoptosis-inducing factor (

264 gger death of naive neurons and to propagate neuronal death through activation of naive astrocytes to

265 tivated, causing cyclin B1 stabilization and neuronal death through an unknown mechanism.

266 Hyperactivated DEG/ENaCs induce neuronal death through excessive cation influx and disru

267 rodegeneration, induces oxidative stress and neuronal death through mechanisms largely unknown.

268 ects against stroke-induced brain injury and neuronal death through pharmacological regulation of ion

269 cine protects against excitotoxicity-induced neuronal death through the non-ionotropic activity of Gl

270 , an excessive release of glutamate triggers neuronal death through the overactivation of NMDA recept

271 eases such as multiple sclerosis may lead to neuronal death, thus causing irreversible functional imp

272 ken up by axons and induce axonotoxicity and neuronal death, thus recapitulating key neuropathologica

273 Plp2-deficient mice show increased neuronal death to ER stress and hypoxia in vitro and in

274 with calpain activation and is the result of neuronal death triggered by brain-infiltrating inflammat

275 re significantly increased at D1 and D7, and neuronal death (TUNEL+ / NeuN+ cells) and BBB permeabili

276 rvations have implications for mechanisms of neuronal death under conditions of reduced glucose and m

277 xpression changes induced by AP5, and led to neuronal death under long-term tetrodotoxin or AP5 treat

278 es slightly shorter than those causing acute neuronal death; under these conditions, cytosolic Zn(2+)

279 xamined how temperature increase exacerbates neuronal death using a model of chemical ischemia.

280 This Bcl-xL deficiency-induced neuronal death was a consequence of activation of the ap

281 Rather, neuronal death was associated with activation of the unf

282 Neuronal death was induced by standard doses of thymidin

283 microglia was first detected at 105 dpi, but neuronal death was not detectable until 120 dpi.

284 In the IPC+IR group, neuronal death was reduced and expression of LC3-II sust

285 However, no significant acute or delayed neuronal death was seen in the CN or white matter.

286 owever, how disrupting this process leads to neuronal death was unclear until recently.

287 re the role of the truncated Src fragment in neuronal death, we expressed a recombinant truncated Src

288 d mitochondrial import defect and subsequent neuronal death were attenuated by overexpression of TIM2

289 amyloid precursor protein, synaptic loss and neuronal death were driven by ERK-activated microglia an

290 , the activity of pro-apoptotic caspases and neuronal death were enhanced in prion-infected SARM1 (-/

291 in the facial nucleus, whereas the levels of neuronal death were not significantly different.

292 rons, NMDA-induced superoxide production and neuronal death were prevented by intracellular acidifica

293 /- mouse astrocytes to produce GA and induce neuronal death when challenged with Lys.

294 ated with bim gene activation and subsequent neuronal death, whereas enhanced Hsp27 expression preven

295 d decreased mTORC1 signaling which increased neuronal death, whereas ISR activation was neuroprotecti

296 eramide-1-phosphate or A23187 induced spinal neuronal death, which was substantially reversed by arac

297 ellular release of misfolded tau followed by neuronal death, which we confirmed by correction of the

298 in the absence of hallmark viral budding or neuronal death, with transmission occurring efficiently

299 athways that result in WNV-induced apoptotic neuronal death within the CNS have not been established.

300 We hypothesized that capsaicin-induced neuronal death would increase proliferation of satellite