ライフサイエンスコーパス: neuronal cell death

1 The Mfsd7c-KO brain exhibited hypoxia and neuronal cell death.

2 stering transported proteins and progressive neuronal cell death.

3 her encephalitic viruses is the induction of neuronal cell death.

4 pase-3 activation and significantly reducing neuronal cell death.

5 ates for blocking pathological axon loss and neuronal cell death.

6 ers for clinical detection and prevention of neuronal cell death.

7 heral immune cells in the CNS, and increased neuronal cell death.

8 tion of a novel "ISG15 proteinopathy" in A-T neuronal cell death.

9 aspase-dependent apoptosis, thus reinforcing neuronal cell death.

10 to the cell cycle, which eventually leads to neuronal cell death.

11 kappaB transcription factor Relish regulates neuronal cell death.

12 d axonal regeneration and severely increased neuronal cell death.

13 d injury and on the role of gap junctions in neuronal cell death.

14 uch as PSP by promoting tau accumulation and neuronal cell death.

15 e vulnerable to glutamate- or stroke-induced neuronal cell death.

16 tested the hypothesis that Dnmts can mediate neuronal cell death.

17 t or exacerbate neuroinflammation and hasten neuronal cell death.

18 proteolytic cleavage to induce dopaminergic neuronal cell death.

19 expression of Myc induces Rattus norvegicus neuronal cell death.

20 phosphate oxidase, followed by predominantly neuronal cell death.

21 fragment that may mediate axonal pruning and neuronal cell death.

22 -Tau and intraneuronal Abeta associated with neuronal cell death.

23 expression, loss of reactive astrocytes and neuronal cell death.

24 oprotective in vitro and in animal models of neuronal cell death.

25 a pathogenic process ultimately resulting in neuronal cell death.

26 pathways correlate with rapidly progressive neuronal cell death.

27 haracterized by progressive synapse loss and neuronal cell death.

28 ylin (rIAPP) reduced oligomer Abeta-mediated neuronal cell death.

29 pecies responsible for neurodegeneration and neuronal cell death.

30 irect target of STAT3 in reperfusion-induced neuronal cell death.

31 eptors and serve as a regulatory protein for neuronal cell death.

32 rough cellular membranes appears to underlie neuronal cell death.

33 tochondrial fission and fusion contribute to neuronal cell death.

34 degradation by AEP, leading to resistance of neuronal cell death.

35 , oxidative stress, and by directly inducing neuronal cell death.

36 n that is associated with brain acidosis and neuronal cell death.

37 pha (TNF) is a leading cause of dopaminergic neuronal cell death.

38 rease in NAPE and FAE levels, which precedes neuronal cell death.

39 sEH activity and protection from OGD-induced neuronal cell death.

40 ) production affects synaptic plasticity and neuronal cell death.

41 d compromised synaptic function that precede neuronal cell death.

42 n 1-independent autophagy is associated with neuronal cell death.

43 onship of Sp1 to Htt protein aggregation and neuronal cell death.

44 and produces reactive oxygen that may cause neuronal cell death.

45 from the virus, is one of the agents causing neuronal cell death.

46 ng to local insulin resistance, resulting in neuronal cell death.

47 ght play a role in HIV-1-mediated widespread neuronal cell death.

48 aumatic brain injury (TBI) causes widespread neuronal cell death.

49 asuring mitochondrial membrane potential and neuronal cell death.

50 tinopathy is characterized by early onset of neuronal cell death.

51 owth, branching, neurite self-avoidance, and neuronal cell death.

52 by NO occurs long before neurite injury and neuronal cell death.

53 nducing a chain of events that culminates in neuronal cell death.

54 glutamate can act synergistically to induce neuronal cell death.

55 on is a common mechanism of amyloid-mediated neuronal cell death.

56 nterfering RNA or HDAC inhibitors suppresses neuronal cell death.

57 lular trafficking is important in regulating neuronal cell death.

58 f aggregate structures in cells destined for neuronal cell death.

59 and long-term potentiation rather than overt neuronal cell death.

60 This volume loss was not the result of neuronal cell death.

61 iated sustained ERK MAPK phosphorylation and neuronal cell death.

62 roxide generation, metabolic dysfunction and neuronal cell death.

63 e release of glutamate, which contributes to neuronal cell death.

64 GDPGP1 in mouse neurons leads to widespread neuronal cell death.

65 he first to find that loss of OGT results in neuronal cell death.

66 xcitotoxic levels of glutamate contribute to neuronal cell death.

67 ed with neurogenesis, synapse formation, and neuronal cell death.

68 s are the main toxic species contributing to neuronal cell death.

69 , synaptic loss, and eventually irreversible neuronal cell death.

70 uli leads to synaptic loss, dysfunction, and neuronal cell death.

71 ted VCP elicits excessive mitophagy, causing neuronal cell death.

72 al ER stress signaling, thus contributing to neuronal cell death.

73 cantly attenuated oxidation-induced striatal neuronal cell death.

74 aspase pathway, ultimately inducing striatal neuronal cell death.

75 sitivity to etoposide-induced DNA damage and neuronal cell death.

76 d memory, as well as in excitotoxic/ischemic neuronal cell death.

77 KCdelta) has been implicated in dopaminergic neuronal cell death.

78 o the accumulation of parkin substrates, and neuronal cell death.

79 on of protein aggregates, tau pathology, and neuronal cell death.

80 CaMKII inhibition protected from NO-induced neuronal cell death.

81 ecretion and is responsible for postischemic neuronal cell death.

82 and indicate its involvement in excitotoxic neuronal cell death.

83 ducing factor release) pathways, and limited neuronal cell death.

84 , together with cytoskeletal proteolysis and neuronal cell death, accompany CAST depletion after intr

85 e as a novel signaling pathway that mediates neuronal cell death after cerebral ischemia.

86 p-regulation of cell cycle proteins, limited neuronal cell death after etoposide-induced DNA damage,

87 To identify miRs that may regulate neuronal cell death after experimental traumatic brain i

88 e, the same splice form selectively promotes neuronal cell death after injury through mechanisms that

89 chanisms and is thought to mediate secondary neuronal cell death after spinal cord injury (SCI).

90 creases in miR-23a and miR-27a contribute to neuronal cell death after TBI by upregulating proapoptot

91 Moreover, excitotoxic neuronal cell death, an underlying process for many neur

92 thetics leads to neurotoxicity manifested by neuronal cell death and abnormal behaviour and cognition

93 These data provide a direct link between neuronal cell death and abnormalities in Trk neurotrophi

94 diated knockdown of KLF6 expression promotes neuronal cell death and also antagonizes the prosurvival

95 Sarm1 functions downstream of ROS to induce neuronal cell death and axon degeneration during oxidati

96 s and the central nervous system and develop neuronal cell death and behavioral deficits.

97 bstantially diminishes kainic acid-triggered neuronal cell death and decreases infarct volume in the

98 the microtubule-associated protein Tau cause neuronal cell death and dementia.

99 demonstrating that Tau misfunction can cause neuronal cell death and dementia.

100 gins with a decline in cognition followed by neuronal cell death and dementia.

101 urodegenerative diseases, often resulting in neuronal cell death and functional impairment.

102 s system (CNS), axonal damage often triggers neuronal cell death and glial activation, with very limi

103 st that birth may be an important trigger of neuronal cell death and identify transient cell groups t

104 ighlighted a role for SARM in stress-induced neuronal cell death and immune responses in the CNS.

105 vates inflammation that leads to progressive neuronal cell death and impairments in cognition (Alzhei

106 es the overexpression of human VPS35 induces neuronal cell death and increases neuronal vulnerability

107 hophysiological effects of cardiac arrest on neuronal cell death and inflammation, and their modulati

108 Dysregulated sphingolipid metabolism causes neuronal cell death and is associated with insulin resis

109 ic endogenous mechanism that interferes with neuronal cell death and ischemic brain injury.

110 Treatment also decreased neuronal cell death and lesion volume, reduced astroglia

111 m degeneration and injury, we show here that neuronal cell death and lesion volumes are significantly

112 ype 3 (T3) reovirus strains induce apoptotic neuronal cell death and lethal encephalitis in infected

113 ure displayed significantly higher levels of neuronal cell death and microglia staining within the hi

114 e useful in studies related to p53-dependent neuronal cell death and neurodegeneration.

115 ure to these compounds may induce widespread neuronal cell death and neurological sequelae, seriously

116 e regulatory networks in nerve regeneration, neuronal cell death and neuropathy in different populati

117 ule misregulation mechanism for Tau-mediated neuronal cell death and provide a novel mechanistic mode

118 ther, it strongly prevents glutamate-induced neuronal cell death and provokes prominent neurite outgr

119 ion of spatial memory characterized by early neuronal cell death and subsequent microglia-dependent p

120 (MTT assay) as a reporter of Abeta-mediated neuronal cell death and suggest that diffusible Abeta pr

121 necrosis factor (TNF)-alpha is a mediator of neuronal cell death and survival in ischemia-reperfusion

122 dehydrogenase in human SH-SHY5Y cells, mouse neuronal cell death and synaptophysin) and long-term pot

123 ke and intracerebral haemorrhage, results in neuronal cell death and the release of factors such as d

124 ented here as new molecules able to decrease neuronal cell death and to increase endogenous neurogene

125 sociation between early anesthetic exposure, neuronal cell death, and adverse neurocognitive and beha

126 ression induced mitochondrial abnormalities, neuronal cell death, and an exacerbation of behavioral h

127 nsheathment of neuron cell bodies, increased neuronal cell death, and defects in animal behavior.

128 ration in the brain, determine the extent of neuronal cell death, and evaluate neurite structural cha

129 hanism for glial-induced non-cell autonomous neuronal cell death, and identify a potential therapeuti

130 t sequestration of specific RBPs, leading to neuronal cell death, and implicate that Pur alpha plays

131 d in the mechanism that exacerbates ischemic neuronal cell death, and inhibiting this enzyme could ha

132 ensory neurons including physiological pain, neuronal cell death, and nerve regeneration.

133 disruption of the blood-spinal-cord barrier, neuronal cell death, and the recruitment of leukocytes.

134 icant increases in oxidative stress, retinal neuronal cell death, and vascular permeability.

135 ntly infected neurons, neither apoptosis nor neuronal cell death appears to occur.

136 e and retrograde mitochondrial transport and neuronal cell death are all rescued by reducing DRP1 GTP

137 CHOP and XBP-1 and their distinct effects on neuronal cell death are also observed in RGCs with other

138 tream transcriptional effects that influence neuronal cell death are less defined.

139 ggests that synapse alterations, rather than neuronal cell death, are the causes of neuronal dysfunct

140 morphous structures and a 3-fold increase in neuronal cell death as compared to Abeta and hIAPP alone

141 otentials, Muller cell reactive gliosis, and neuronal cell death, as assayed by TUNEL staining and re

142 Acute secondary neuronal cell death, as seen in neurodegenerative diseas

143 We focus on the hippocampus neuronal cell death, as well as the potential link betwe

144 Oxidative stress plays an important role in neuronal cell death associated with many different neuro

145 es: the first week, as a critical period for neuronal cell death-associated glial division, and the r

146 ilin-Eosin (H&E) staining was used to assess neuronal cell death at 5 days after surgery.

147 in living zebrafish larvae and to visualize neuronal cell death at single-cell resolution in vivo.

148 d no significant effect on the expression of neuronal cell death, autonomic cardiac control, or behav

149 siology, astrocyte and microglia activation, neuronal cell death, axonal retraction, and development

150 ed that Zn2+ is responsible for the ischemic neuronal cell death, because Zn2+ chelation prevented ce

151 with a normal lifespan, but displayed severe neuronal cell death between E14.5 and three weeks postna

152 neurons and exhibit reduced seizure-induced neuronal cell death, but surprisingly have unaltered pil

153 propagation of the inflammatory response and neuronal cell death by extracellular dysfunctional mitoc

154 dels based in part on its ability to inhibit neuronal cell death by glutamate excitotoxicity.

155 that MST1 mediates oxidative stress-induced neuronal cell death by phosphorylating the transcription

156 The loss of STAT3 activity induced neuronal cell death by reducing Mn-SOD expression.

157 The extent and rate of neuronal cell death can be controlled by conditions that

158 drial fragmentation has been associated with neuronal cell death caused by a variety of experimental

159 nsoluble amyloid fibrils to the debilitating neuronal cell death characteristic of neurodegenerative

160 V and an established ligand of TLR7, induces neuronal cell death dependent on TLR7 and the central ad

161 ings indicate that G-CSF reduces hippocampal neuronal cell death dose-dependently and attenuates sens

162 ere not infected with virus, indicating that neuronal cell death during acute picornavirus infection

163 Neuronal cell death during fatal acute viral encephalomy

164 Neuronal cell death during fatal alphavirus encephalomye

165 e homologs of NADPH oxidase, plays a role in neuronal cell death during retinal ischemia.

166 ns associated with disease state and induces neuronal cell death, establishing this miRNA as a regula

167 Oxidative stress is a major contributor to neuronal cell death following brain injury.

168 LK3-JNK kinase signaling pathway and delayed neuronal cell death following cerebral ischemia.

169 d significantly attenuated apoptotic delayed neuronal cell death following cerebral ischemia.

170 f Rac1 in POSH/MLK/JNK signaling and delayed neuronal cell death following cerebral ischemia.

171 root ganglion sensory neurons and prevented neuronal cell death following cisplatin treatment.

172 gonists block c-Jun upregulation and prevent neuronal cell death following excitotoxic insults.

173 ocampal neurons, and protects the brain from neuronal cell death following transient global ischemia

174 , but not cued memory deficits and increased neuronal cell death following transient global ischemia

175 how that such cell cycle re-entry results in neuronal cell death, gliosis, and cognitive deficits.

176 lecular link between these gene products and neuronal cell death has not been established.

177 excitotoxic glutamate conditions that induce neuronal cell death, HDAC4 rapidly translocates into the

178 Naturally occurring axonal pruning and neuronal cell death help to sculpt neuronal connections

179 n of 20 ng/ml caused little or no detectable neuronal cell death, however, when combined with submaxi

180 s efficiently counteracted mast cell-induced neuronal cell death in a concentration-dependent manner.

181 Neuronal cell death in a number of neurological disorder

182 apoptosis, we examined homocysteine-induced neuronal cell death in a rat cortical neuron tissue cult

183 sis for pathogenic protein accumulations and neuronal cell death in AD and suggests previously uniden

184 ur findings establish apoptosis as a mode of neuronal cell death in aging PS/APP mice and identify th

185 protein kinase signal pathway that mirrored neuronal cell death in Alzheimer disease (AD).

186 (Abeta) may be one of the factors leading to neuronal cell death in Alzheimer's disease (AD).

187 ated with calcium influx that contributes to neuronal cell death in cerebellar neurons.

188 an effective therapeutic modality to reduce neuronal cell death in diabetic retinopathy.

189 igating the functional mechanisms underlying neuronal cell death in early onset Parkinson's Disease.

190 ivation prior to alpha-synuclein-independent neuronal cell death in GBA1 deficiency and suggests upre

191 aminobutyric acid modulator propofol induces neuronal cell death in healthy immature brains by unbala

192 s by which mutant huntingtin (mHTT) leads to neuronal cell death in Huntington's disease (HD) are not

193 ) activated apoptotic pathways and increased neuronal cell death in IL-21 receptor-deficient (IL-21R-

194 Inhibition of c-Jun prevents neuronal cell death in in vivo AD models, highlighting i

195 etic, has been found to be effective against neuronal cell death in in vivo and in vitro models of ne

196 rtant role in protecting against the delayed neuronal cell death in ischemia and stroke.

197 s, reduced brain infarction, and ameliorated neuronal cell death in MCAO rats.

198 y, rather than excessive autophagy, promotes neuronal cell death in most of these disorders.

199 Anesthetics have been linked to widespread neuronal cell death in neonatal animals.

200 Neuronal cell death in neurodegenerative diseases is not

201 onse to stress that has an important role in neuronal cell death in neurodegenerative diseases.

202 stress as a major factor contributing to the neuronal cell death in neurodegenerative disorders, espe

203 hways play an important role in dopaminergic neuronal cell death in Parkinson's disease (PD).

204 may not be the form that is responsible for neuronal cell death in prion diseases.

205 re we show that apoptosis is a major form of neuronal cell death in PS/APP mice modeling AD-like neur

206 molog (PTEN), which plays a critical role in neuronal cell death in response to various insults.

207 GSK3beta by Ser(389) phosphorylation causes neuronal cell death in subregions of the hippocampus and

208 geting energy metabolism can protect against neuronal cell death in such diseases.

209 DARs and that their activation would trigger neuronal cell death in the brain by modulating inflammat

210 g TBI with hypoxia, significant increases in neuronal cell death in the CA1, CA2/3, CA3c, hilus and d

211 (blood ethanol concentration 80 mM) induces neuronal cell death in the cerebellum.

212 approximately 57-70%), and induced selective neuronal cell death in the cerebral cortex and hippocamp

213 At 24 hrs, isoflurane attenuated neuronal cell death in the cortex, associated with an in

214 te-induced seizures; however, the associated neuronal cell death in the hippocampus is attenuated in

215 reduced seizures and minimal seizure-induced neuronal cell death in the hippocampus.

216 at VEGF-A blockade significantly exacerbated neuronal cell death in the hypertensive glaucoma model.

217 Furthermore, neuronal cell death in the lateral septum and the cornu

218 immunohistochemistry was used to investigate neuronal cell death in the nucleus ambiguus.

219 he microglial NMDARs plays a pivotal role in neuronal cell death in the perinatal and adult brain.

220 ssion promotes inflammation and, ultimately, neuronal cell death in this AD mouse model, advocating t

221 s that apoptosis is a contributing factor to neuronal cell death in traumatic brain injury (TBI).

222 ortant cellular protective mechanism against neuronal cell death in various models of neurological di

223 in the signaling cascades that contribute to neuronal cell death in various neurodegenerative disorde

224 key step in the signaling cascade leading to neuronal cell death in various neurological disorders, i

225 and 30 mum) acted synergistically to induce neuronal cell death in vitro, which was prevented by the

226 but not from perforin knock-out mice induced neuronal cell death in vitro.

227 NMDAR subunit NR1 protects from excitotoxic neuronal cell death in vivo and from traumatic brain inj

228 ia have been suggested to be responsible for neuronal cell death in vivo.

229 ecreases paraquat-mediated SNpc dopaminergic neuronal cell death in vivo.

230 m (Ca(2+) ) dysregulation has been linked to neuronal cell death, including in hereditary retinal deg

231 ity is well below threshold for induction of neuronal cell death, indicating that the gamma-H2AX incr

232 HK2 and LDHA during differentiation leads to neuronal cell death, indicating that the shut-off aerobi

233 is an anti-apoptotic peptide that suppresses neuronal cell death induced by Alzheimer's disease, prio

234 Diabetes exacerbates neuronal cell death induced by cerebral ischemia.

235 logical inhibitors of PKR activity abrogated neuronal cell death induced by gp120.

236 coupling Shc signaling from TrkB exacerbates neuronal cell death induced by H(2)O(2).

237 ve mutant of MEK5 is sufficient to attenuate neuronal cell death induced by selective inhibition of R

238 This cell-autonomous neuronal cell death induced by ssRNA40 is amplified in t

239 e but not in TLR7(-/-) mice, confirming that neuronal cell death induced by ssRNA40 through TLR7 occu

240 ive activity of some mammalian TRPs leads to neuronal cell death, interventions that increase Na+/Ca2

241 nsistent with the notion that Abeta-mediated neuronal cell death involves the loss of full-length Tau

242 The hypothesis that rotenone enhancement of neuronal cell death is attributable to oxidative stress

243 itotoxin N-methyl-D-aspartate (NMDA) induced neuronal cell death leading to the appearance of pro-IL-

244 lphaS) is widely regarded as a key factor in neuronal cell death, leading to a wide range of synuclei

245 These findings identify a neuronal cell death mechanism that can be initiated by t

246 microglia play an important role in managing neuronal cell death, neurogenesis, and synaptic interact

247 TOR activation and decreased kainate-induced neuronal cell death, neurogenesis, mossy fiber sprouting

248 sive neurodegeneration, including widespread neuronal cell death, neuroinflammation, increased produc

249 Neuronal cell death occurs during many neurodegenerative

250 kade of TIM-3 markedly reduces infarct size, neuronal cell death, oedema formation and neutrophil inf

251 d neurologic function and markedly decreased neuronal cell death of the hippocampus.

252 whether these structures are contributing to neuronal cell death or protecting against it.

253 s disease is by increasing susceptibility to neuronal cell death, particularly in vulnerable regions

254 k between GSK-3beta and MLK3 activation in a neuronal cell death pathway and identify MLK3 as a direc

255 at elevated levels of cytokines, rather than neuronal cell death, play the dominant role in seizure i

256 ecies (ROS), leading to oxidative damage and neuronal cell death, plays an important role in the path

257 of OPA1 may be a contributing factor in the neuronal cell death processes underlying neurodegenerati

258 Within the cortex, neuronal cell death progressed gradually over the first

259 c species that lead to neurodegeneration and neuronal cell death rather than the later 'mature fibril

260 polyQ-induced neuronal dysfunction preceding neuronal cell death remains largely unknown.

261 Axon guidance errors and increased neuronal cell death result in an absence of P2, I7, and

262 2+) and Ca(2+) accompanies the initiation of neuronal cell death signaling cascades.

263 Neuronal cell death-specific treatment approaches, such

264 ced by sensory activity and that it promotes neuronal cell death, such that inactive olfactory neuron

265 disrupted Pcdh-gamma genes exhibit increased neuronal cell death, suggesting nonconventional roles.

266 ng c.1999G>A leads to dendritic swelling and neuronal cell death, suggestive of excitotoxicity mediat

267 sible for unchecked inflammation that causes neuronal cell death, systemic stress, and lethal immunod

268 ovide greater protection from DNRAb-mediated neuronal cell death than GluN2B antagonists.

269 nce not only seizure phenomena, but also the neuronal cell death that follows.

270 e intracellular calcium and cause subsequent neuronal cell death that is independent of the canonical

271 LS) is a progressive disease associated with neuronal cell death that is thought to involve aberrant

272 rIAPP exhibited reductions in Abeta induced neuronal cell death that was independent of its ability

273 reported whether PrP(C) is required for the neuronal cell death, the most critical element of neurod

274 rP(C) is required for Abeta oligomer-induced neuronal cell death, the pathology essential to cognitiv

275 e Glu or OGD exposure, is able to counteract neuronal cell death through an ADO-dependent chemokine-i

276 er's disease and Parkinson's disease trigger neuronal cell death through endogenous suicide pathways.

277 divisions, and at later stages by promoting neuronal cell death through engulfment.

278 Multiple insults to the brain lead to neuronal cell death, thus raising the question to what e

279 n also abrogates PDI-mediated attenuation of neuronal cell death triggered by ER stress, misfolded pr

280 after axotomy, implicating their actions in neuronal cell death upon nerve injury.

281 mox1) in microglia is necessary to attenuate neuronal cell death, vasospasm, impaired cognitive funct

282 selectively inhibits oligodendrocyte but not neuronal cell death via a receptor-mediated action and m

283 Neuronal cell death via apoptosis or necrosis underlies

284 that oxidative stress in this model induces neuronal cell death via cell cycle-independent pathways

285 mouse brain enhances production of ROSs and neuronal cell death via increased NADPH oxidase activity

286 cally, invading T lymphocytes contributed to neuronal cell death via the Fas/FasL pathway.

287 As a result of SCH treatment, neuronal cell death via up-regulation of Akt-mediated pa

288 Neuronal cell death was examined by terminal deoxynucleo

289 Importantly, NO-induced neuronal cell death was mitigated by Mfn1 and Drp1(K38A)

290 Neuronal cell death was significantly reduced through ph

291 ecular mechanisms involved in Abeta-mediated neuronal cell death, we have treated primary rat hippoca

292 mine if TNFalpha-induced trafficking affects neuronal cell death, we sequestered TNFalpha after SCI u

293 gnificant differences in swallow function or neuronal cell death were found between the two groups.

294 These features and neuronal cell death were markedly reduced by treatment w

295 Aberrant cell cycle activation provokes neuronal cell death, whereas cell cycle inhibition eleva

296 Amyloid protein is well known to induce neuronal cell death, whereas only little is known about

297 enerative disorder with accelerated suicidal neuronal cell death, which could be reversed by lithium.

298 CDK5 contributes to neuronal cell death while beta-catenin enters the neuron

299 ant link survival factor deprivation-induced neuronal cell death with implications for our understand

300 Affected mice exhibited hemorrhage and neuronal cell death within the cerebral cortex and cereb