ライフサイエンスコーパス: neuronal death

1 urons in vivo, strongly enhances excitotoxic neuronal death.

2 in pathological events leading ultimately to neuronal death.

3 inner membrane depolarization, and apoptotic neuronal death.

4 by oligodendrocyte damage, demyelination and neuronal death.

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

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

7 ionic homoeostasis, resulting in axonal and neuronal death.

8 from synaptic clefts to prevent excitotoxic neuronal death.

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

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

11 successfully identify new mechanisms driving neuronal death.

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

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

14 to ER stress and provides protection against neuronal death.

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

16 rategy for the treatment of delayed ischemic neuronal death.

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

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

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

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

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

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

23 vation of extrasynaptic NMDARs, and ischemic neuronal death.

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

25 s, and astrocyte conditioned media triggered neuronal death.

26 t nodose ganglia following capsaicin-induced neuronal death.

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

28 d robust protection against ischemia-induced neuronal death.

29 equently leading to synaptic dysfunction and neuronal death.

30 plasmic reticulum, influencing the extent of neuronal death.

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

32 ork function, which contribute to subsequent neuronal death.

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

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

35 ld lead to early metabolic failure promoting neuronal death.

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

37 ccompanied by microtubule destabilization or neuronal death.

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

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

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

41 particular their role in glutamate-mediated neuronal death.

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

43 in mitochondrial morphology in p53-dependent neuronal death.

44 hen targets the dopaminergic neurons causing neuronal death.

45 changes, such as hyperphosphorylated tau and neuronal death.

46 med to be beneficial and to occur only after neuronal death.

47 in neurons and protects against excitotoxic neuronal death.

48 dysfunction, tau accumulation, and eventual neuronal death.

49 onal regulation of prosurvival signaling and neuronal death.

50 d tau, respectively, have been implicated in neuronal death.

51 ficantly attenuated microglia activation and neuronal death.

52 tylase-3 (HDAC3), a protein known to promote neuronal death.

53 significantly decreased sodium azide-induced neuronal death.

54 and unique domain, was sufficient to induce neuronal death.

55 iptionally responsive targets' implicated in neuronal death.

56 degeneration, suggesting a role in promoting neuronal death.

57 l, whereas interaction with HDAC3 results in neuronal death.

58 , learning and memory impairment and massive neuronal death.

59 f events that cause cellular dysfunction and neuronal death.

60 ide (Abeta) species lead to synapse loss and neuronal death.

61 ed extracellular glutamate levels results in neuronal death.

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

63 tochondrial engagement and directly preceded neuronal death.

64 a critical component of glutamate-dependent neuronal death.

65 late increase in [Ca(2+)](i) coincided with neuronal death.

66 by lipopolysaccharide (LPS), thereby causing neuronal death.

67 eded and strongly correlated with subsequent neuronal death.

68 substantially reduced glial inflammation and neuronal death.

69 )-induced mitochondrial channel activity and neuronal death.

70 ases in rat hippocampus during the period of neuronal death.

71 9, whose expression is down-regulated during neuronal death.

72 d FoxG1 expression frees MecP2-e2 to promote neuronal death.

73 nd reduced vulnerability to ischemia-induced neuronal death.

74 ation has been previously linked to ischemic neuronal death.

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

76 um responses, calcium overload and increased neuronal death.

77 icative of axonal dieback that progresses to neuronal death.

78 rs attenuated misfolded tau accumulation and neuronal death.

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

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

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

82 avage limit mitochondrial fusion and promote neuronal death.

83 ndent transcriptional activity, and promotes neuronal death.

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

85 equally resistant to proneurotrophin-induced neuronal death.

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

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

88 ameliorate symptoms, but not the underlying neuronal death.

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

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

91 eurotransmitter release, and ultimately with neuronal death.

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

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

94 peutic agents that could be used to minimize neuronal death after a stroke or head trauma.

95 300 mg/kg significantly reduced hippocampal neuronal death after brain ischemia, inhibited the ische

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

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

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

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

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

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

102 lacking Hv1 were protected from NOX-mediated neuronal death and brain damage 24 h after stroke.

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

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

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

106 (ADP-ribose) polymer formation, resulting in neuronal death and dysfunction, culminating in neuropath

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

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

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

110 Neuronal death and microgliosis induced by Abeta were re

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

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

113 improved phenotypes including a reduction in neuronal death and prolonged survival.

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

115 immune signaling mechanism for virus-induced neuronal death and reveal potential targets for developm

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

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

118 Our results indicate that Mecp2-e2 promotes neuronal death and that this activity is normally inhibi

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

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

121 are only transient leading to layer-specific neuronal death and the reduction of cortical projections

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

123 unbalance in this concentration can lead to neuronal death and to severe neurodegenerative diseases

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

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

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

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

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

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

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

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

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

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

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

135 also inhibited by IGF-1, which prevents the neuronal death-associated downregulation of FoxG1 expres

136 e brain, achieved a substantial reduction in neuronal death both in vitro and in vivo, and markedly r

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

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

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

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

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

144 Neuronal death can be preceded by progressive dysfunctio

145 minal kinase (JNK) is a central regulator in neuronal death cascades.

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 ng that phagocytosis actively contributes to neuronal death during brain inflammation.

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 are responsible for the secondary (delayed) neuronal death following neuronal injury, including isch

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

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

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

162 unction, neuronal gap junction coupling, and neuronal death has a universal character and operates in

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

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

165 The transcription factor p53 mediates neuronal death in a variety of stress-related and neurod

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

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

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

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

170 s well established that estrogens ameliorate neuronal death in animal models of focal and global isch

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

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

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

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

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

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

177 a promoter of cell survival to a mediator of neuronal death in excitotoxicity.

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

179 Neuronal death in hippocampal CA1 is thought to be an im

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

181 1 prevented AbetaO-induced synaptic loss and neuronal death in mouse cultured neurons and long-term p

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

183 ous clinical strategy to prevent progressive neuronal death in neurological diseases.

184 ltures, but did produce oxidative stress and neuronal death in neurons surrounding the transfected, N

185 Multiple mechanisms likely contribute to neuronal death in Parkinson's disease (PD), including mi

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

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

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

189 alternative routes of calcium entry induced neuronal death in proportion to the degree of calcium lo

190 The mechanisms of neuronal death in protein misfolding neurodegenerative d

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

192 TG1 or TG2 proteins is sufficient to induce neuronal death in Rattus norvegicus cortical neurons in

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 ype glutamate receptors leads to excitotoxic neuronal death in stroke, brain trauma, and neurodegener

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

200 ults may be one of underlying mechanisms for neuronal death in tauopathies.

201 ncreased DNA damage, reduced DNA repair, and neuronal death in the brain.

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

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

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

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

206 animals show that Gal-3 is not required for neuronal death in the hippocampus.

207 umetanide prevents p75(NTR) upregulation and neuronal death in the injured areas with reduced levels

208 vent the requirement for BDNF and consequent neuronal death in the injured areas.

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

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

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

212 de the onset of classical motor symptoms and neuronal death in the striatum and cortex by almost a de

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

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

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

216 essive mitochondria fission and dopaminergic neuronal death in vitro.

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

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

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

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

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

222 ry response, oxidative damage and subsequent neuronal death induced by cerebral ischemia/reperfusion

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

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

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

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

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

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

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

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

231 Neuronal death induced by proneurotrophins or epileptic

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

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

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

235 We examined neuronal death, inflammatory reaction and neurogenesis i

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

237 del of the mechanisms of glutamate-dependent neuronal death is discussed, which includes neuronal gap

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

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

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

241 Excitotoxic neuronal death is mediated in part by NMDA receptor-indu

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

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

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

245 vents have a causal role in ischemia-induced neuronal death is unclear.

246 receptor p75(NTR), best known for regulating neuronal death, is sufficient for its homodimerization.

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

248 tly however, emerging data suggest that many neuronal death mediators may have biphasic properties-de

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

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

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

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

253 Neuronal death occurs at several stages during embryogen

254 isms of how hyperthermia is involved in this neuronal death process.

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

256 The neuronal death produced by prolonged CaMKII inhibition i

257 ist derivative S-memantine prevents ischemic neuronal death, providing a novel therapeutic strategy f

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

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

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

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

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

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

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

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

266 estradiol at physiological doses ameliorates neuronal death, the signaling pathways that mediate the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

282 P-7 enzymatic activity, leading to increased neuronal death via activation of p75(NTR).

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

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

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

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

287 8 (resulting in microglial necroptosis), and neuronal death was restored by rescue of microglia with

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

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

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

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

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 attenuated transmigrated neutrophil-induced neuronal death, whereas the inhibition of key neutrophil

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