ライフサイエンスコーパス: neurotoxicity

1 microglial inflammation to fully assess AgNP neurotoxicity.

2 diated increase in epileptic activity led to neurotoxicity.

3 athology plays a causal role in tau-mediated neurotoxicity.

4 g WBRT because of its related risk of severe neurotoxicity.

5 annot by itself account for their associated neurotoxicity.

6 isks of severe cytokine release syndrome and neurotoxicity.

7 red slices markedly aggravated prion-induced neurotoxicity.

8 is indispensable for astrocyte-mediated Tat neurotoxicity.

9 early-onset Alzheimer's disease and enhances neurotoxicity.

10 rotects against mitochondrial stress-induced neurotoxicity.

11 rm treatment with thalidomide is hampered by neurotoxicity.

12 screening, targeted Abeta and attenuated its neurotoxicity.

13 had no symptoms of ototoxicity or peripheral neurotoxicity.

14 acetylcholine receptor signaling leading to neurotoxicity.

15 e oligomers may be primarily responsible for neurotoxicity.

16 der the brain sensitive to propofol-mediated neurotoxicity.

17 lar mechanisms underlying SCA23-mutant Dyn A neurotoxicity.

18 iRNA) inhibition of autophagy aggravated BPA neurotoxicity.

19 ether miRNA dysregulation contributes to tau neurotoxicity.

20 nd LAMP2A overexpression reduces Tat-induced neurotoxicity.

21 ar tangle numbers but were protected against neurotoxicity.

22 -757), and silencing of AMPK exacerbated BPA neurotoxicity.

23 ss may not necessarily be harmful or reflect neurotoxicity.

24 opment, yet excessive exposure can result in neurotoxicity.

25 tis elegans model of mutant ataxin 3-induced neurotoxicity.

26 olding and aggregation that in turn leads to neurotoxicity.

27 ar whether nuclear G4C2 RNA foci also induce neurotoxicity.

28 1(+/-) carriers and alpha-synuclein-mediated neurotoxicity.

29 e binding on alpha-synuclein aggregation and neurotoxicity.

30 t against anticancer drug-induced peripheral neurotoxicity.

31 Abeta production and mediates Abeta-induced neurotoxicity.

32 responsible for the frequent EFV-associated neurotoxicity.

33 cts of MPP(+) on neuronal DA homeostasis and neurotoxicity.

34 lutamate that caused NMDA receptor-dependent neurotoxicity.

35 rization, and perturbing them causes PD-like neurotoxicity.

36 ced DAMB expression and protected against PQ neurotoxicity.

37 rol of inflammatory responses in the CNS and neurotoxicity.

38 he dopaminergic pathway and METH potentiates neurotoxicity.

39 receptor-mediated potentiation of PQ-induced neurotoxicity.

40 stream kinases JNK and p38 influenced TDP-43 neurotoxicity.

41 reducing microglial inflammation and related neurotoxicity.

42 odels of Ass42 and amyloid precursor protein neurotoxicity.

43 s, which places infants at risk of manganese neurotoxicity.

44 that amyloidogenesis is critical for TDP-43 neurotoxicity.

45 mechanism in LRRK2-induced oxidant-mediated neurotoxicity.

46 rophages increased supernatant glutamate and neurotoxicity.

47 ose MTX, 12 did not experience recurrence of neurotoxicity.

48 tients (3.8%) developed MTX-related clinical neurotoxicity.

49 cium/magnesium decreases oxaliplatin-related neurotoxicity.

50 nts, and therapy can be associated with late neurotoxicity.

51 s must therefore be tested for developmental neurotoxicity.

52 the protective effects of NTR1 against Abeta neurotoxicity.

53 otherapy drug oxaliplatin develop peripheral neurotoxicity.

54 t, is associated with both acute and chronic neurotoxicity.

55 e (DMF), decreased supernatant glutamate and neurotoxicity.

56 otein Rhes binding to mHtt and enhancing its neurotoxicity.

57 rotecting APP/PS1 mice against Abeta-induced neurotoxicity.

58 o the generation of transmissible prions and neurotoxicity.

59 esium to protect against oxaliplatin-induced neurotoxicity.

60 uced a more severe, pervasive, and prolonged neurotoxicity.

61 (MT) synergistically potentiate dopaminergic neurotoxicity.

62 d against lithium-induced iron elevation and neurotoxicity.

63 ent, and contributes to oxidopamine-mediated neurotoxicity.

64 ulation from adjacent axons thereby reducing neurotoxicity.

65 ion of the actin cytoskeleton and downstream neurotoxicity.

66 manganese in the blood and brain and develop neurotoxicity.

67 lly cleared over 20 weeks with no detectable neurotoxicity.

68 oxp1 to protect neurons from mut-Htt-induced neurotoxicity.

69 on neuronal cells, leading to suppression of neurotoxicity.

70 peat proteins trigger multiple mechanisms of neurotoxicity.

71 ne release syndrome and/or reversible severe neurotoxicity.

72 possible mechanism(s) by which Se exerts its neurotoxicity.

73 lux and downstream cell signaling events and neurotoxicity.

74 ng astrocytes and for astrocyte-mediated Tat neurotoxicity.

75 of STEP that is involved in Zn(2+)-dependent neurotoxicity.

76 trogliosis-induced microglial activation and neurotoxicity.

77 ion, an altered phosphorylation profile, and neurotoxicity.

78 ticulum (ER) stress in astrocytes and causes neurotoxicity.

79 as tightly coupled to astrocyte-mediated Tat neurotoxicity.

80 en reported to be involved in Zn(2+)-induced neurotoxicity, a potential contribution of tyrosine phos

81 treatment of methamphetamine (METH)-induced neurotoxicity, aerobic exercise is being proposed to imp

82 but no multimer-neutral mutants caused frank neurotoxicity akin to the proapoptotic protein Bax.

83 BPA-mediated neurotoxicity also resulted in mitochondrial loss, bioen

84 ortant environmental contaminant, due to its neurotoxicity and ability to bioaccumulate.

85 olded protein response, are coregulated with neurotoxicity and actin cytoskeletal stabilization in br

86 tracted exposure of neurons to stress led to neurotoxicity and bioenergetics failure after cerebrospi

87 ing neuroblastoma cells, we demonstrated the neurotoxicity and cell-to-cell transmission property of

88 astrocytosis/GFAP up-regulation potentiates neurotoxicity and contributes to neurodegenerative disea

89 e, contributing to hyperammonemia-associated neurotoxicity and encephalopathy in patients with liver

90 ar protein that encode information, generate neurotoxicity and evolve and adapt in vivo.

91 l, most research on NF-kappaB has focused on neurotoxicity and few studies have explored the role of

92 cytes has been shown to be important for Tat neurotoxicity and HIV/neuroAIDS.

93 ers by PD-causing missense mutations and the neurotoxicity and inclusions induced by markedly decreas

94 (EP2) show decreased innate immune-mediated neurotoxicity and increased amyloid beta (Abeta) peptide

95 type 1 and natural killer cells, to unleash neurotoxicity and inflammation-induced neurodegeneration

96 -4 were strong genetic modifiers of ataxin 3 neurotoxicity and necessary for therapeutic efficacy.

97 erapeutic target against carbofuran-mediated neurotoxicity and neurogenesis disruption.

98 etabolite in astrocytes, which could lead to neurotoxicity and neuronal loss.

99 hting the complex tau biology that underlies neurotoxicity and neuroprotection.

100 id cells significantly protects against MPTP neurotoxicity and preserves striatal dopamine levels.

101 ovel regulator of mutant huntingtin-mediated neurotoxicity and provide a new target for developing th

102 sed and small-molecule approaches attenuates neurotoxicity and restores pre-existing striatal dopamin

103 poly-PR and poly-GR peptides plays a role in neurotoxicity and reveal that the pathways altered by th

104 ers, decreases alphaS solubility and induces neurotoxicity and round inclusions.

105 hese fibrillar hydrogel assemblies mitigates neurotoxicity and suggests a potential therapeutic strat

106 y in infants with 2 or more risk factors for neurotoxicity and TSB levels of more than 5 mg/dL above

107 ntial new mechanism contributing to diazinon neurotoxicity and, in particular, its sex-selective effe

108 dividually silenced, protected against Abeta neurotoxicity and/or tau phosphorylation.

109 e Drosophila lifespan by reduction of TDP-43 neurotoxicity, and are predicted to cross the blood-brai

110 Cell-based assays of BBB permeation, neurotoxicity, and neuroprotection supported the potenti

111 formaldehyde (FA) has been linked to cancer, neurotoxicity, and other pathophysiologic effects.

112 n turn contributes to astrocyte-mediated Tat neurotoxicity, and raise the possibility of developing H

113 state(s) of Abeta that mediate the peptides neurotoxicity, and to test ways to prevent the neurotoxi

114 Several strategies to reduce neurotoxicity are being investigated.

115 ytotoxic activities, further activities like neurotoxicity as well as antibiotics resistance genes, a

116 otopolymerization and tested as a cell-based neurotoxicity assay by determining sensitivity to active

117 e impairment, termed chemobrain, is a common neurotoxicity associated with chemotherapy treatment, af

118 vated, synergistically and robustly suppress neurotoxicity associated with misfolded proteins in Caen

119 us (VSV), and tested the hypothesis that the neurotoxicity associated with the virus could be elimina

120 However, the mechanisms of neurotoxicity associated with these poly-dipeptides are

121 amine is involved in methamphetamine-induced neurotoxicity, associations between dopamine receptors a

122 onstration that PCBs can cause developmental neurotoxicity at low levels and alter the genomic charac

123 Neurotoxicity, axon myelination, and advanced oxidized p

124 ochondrial dysfunction as well as microglial neurotoxicity because of glutamate overproduction.

125 ays a protective role in MPTP/MPP(+)-induced neurotoxicity by blocking ASK1-mediated signaling.

126 we have generated a zebrafish model for ACR neurotoxicity by exposing 5 days post-fertilization zebr

127 e holdase activity of secHsp70 masks Abeta42 neurotoxicity by promoting the accumulation of nontoxic

128 est that exercise can attenuate METH-induced neurotoxicity by protecting against the BBB disruption a

129 Cognitive deficits associated with neurotoxicity can be subtle or disabling and frequently

130 the presence of alpha-synuclein-independent neurotoxicity consequent to endolysosomal dysfunction.

131 In Huntington's disease (HD), neurotoxicity correlates with an increased aggregation p

132 y not yet be possible, the identification of neurotoxicity could trigger the conduction of a conventi

133 sphorylation of tau and trigger a cascade of neurotoxicity critically impinging on the integrity of t

134 ating flame retardants causing developmental neurotoxicity (DNT) in humans and rodents.

135 ugh its involvement in prion replication and neurotoxicity during transmissible spongiform encephalop

136 y, VSV-gp160G did not elicit any evidence of neurotoxicity even in severely immunocompromised animals

137 of Cancer Therapy/Gynecologic Oncology Group-Neurotoxicity four-item sensory-specific scale.

138 ake it possible to examine bilirubin-induced neurotoxicity from multiple directions.

139 TDP-43 neurotoxicity has been extensively modeled in mice, zebr

140 eta to trigger its clearance or mitigate its neurotoxicity has so far been unsuccessful.

141 beta peptide (Abeta) monomer aggregation and neurotoxicity have been identified with the ultimate goa

142 assemblies are necessary and sufficient for neurotoxicity in a C. elegans model of FUS-dependent neu

143 lly, we show that Zfp106 potently suppresses neurotoxicity in a Drosophila model of C9orf72 ALS.

144 ligomers in the human brain, which may cause neurotoxicity in a manner similar to other amyloid oligo

145 to the formation of neuronal aggregates and neurotoxicity in a manner similar to that of alpha-syn.

146 form of Hsp70 (secHsp70) suppresses Abeta42 neurotoxicity in adult eyes, reduces cell death, protect

147 onsidered to be a crucial process underlying neurotoxicity in Alzheimer's disease (AD).

148 -associated protein tau is a key mediator of neurotoxicity in Alzheimer's disease and other tauopathi

149 othesized to be the underlying phenomenon of neurotoxicity in Alzheimer's disease.

150 ance phosphorylation of tau and thus promote neurotoxicity in an in vivo setting.

151 ergic neurons from alpha-synuclein-dependent neurotoxicity in C. elegans via a mechanism that is inde

152 ndensed liquids and/or hydrogels, leading to neurotoxicity in C. elegans.

153 ons to improve personalized care in limiting neurotoxicity in cancer survivors.

154 developed as an adjuvant therapy to prevent neurotoxicity in cisplatin-based chemotherapy protocols.

155 derived motor neuron and astrocytic-mediated neurotoxicity in co-culture assays.

156 t has been suggested as a receptor mediating neurotoxicity in common neurodegenerative proteinopathie

157 ed some ability to counteract MPP(+)-induced neurotoxicity in cultured human neuroblastoma SH-SY5Y ce

158 iency of the CIB1 gene enhances MPTP-induced neurotoxicity in dopaminergic neurons in CIB1(-/-) mice.

159 of dipeptide-repeat proteins and alleviates neurotoxicity in Drosophila, patient-derived neurons and

160 atory cytokines, and prevented Abeta-induced neurotoxicity in experimental models of Alzheimer diseas

161 Oxidative stress response and neurotoxicity in exposed fish was greater for nPbO2(s) s

162 human cells and Drosophila while increasing neurotoxicity in flies.

163 y be an underlying mechanism of rCGG-induced neurotoxicity in FXTAS.

164 itochondrial fragmentation, P110, to inhibit neurotoxicity in HD.

165 brains, contributing to non-cell-autonomous neurotoxicity in HD.SIGNIFICANCE STATEMENT Huntington's

166 ociated with excess glutamate production and neurotoxicity in HIV-infected macrophages is a highly co

167 cultural pesticides can induce developmental neurotoxicity in humans, and has been associated with de

168 atory monocytes and enhancing sensitivity to neurotoxicity in inflammatory conditions.

169 The detailed mechanisms of Mn neurotoxicity in nerve cells, especially in dopaminergic

170 In pregnant users, a potential neurotoxicity in offspring has been noted.

171 alpha-synuclein (alpha-Syn) appear to drive neurotoxicity in Parkinson's disease (PD); neuronal accu

172 ched in Lewy bodies and highly implicated in neurotoxicity in Parkinson's disease, is distributed bot

173 played moderate effects against H2O2-induced neurotoxicity in PC12 cells at the concentration of 10 m

174 calpain activity abolished SSC and glutamate neurotoxicity in primary murine neurons.

175 iron-dyshomeostasis is an important cause of neurotoxicity in prion disorders, a group of neurodegene

176 o body burdens associated with developmental neurotoxicity in rodents.

177 omerization and aggregation as a mediator of neurotoxicity in synucleinopathies including MSA.

178 at contributes to hyperbilirubinemia-induced neurotoxicity in the developmental stage.

179 ed tau thus induces extensive but reversible neurotoxicity in the presence of full-length tau through

180 ze multiple markers of neurodegeneration and neurotoxicity in transgenic animals, including analysis

181 hese findings elucidate a basic mechanism of neurotoxicity in vertebrates and might lead to a new the

182 hich reduces Abeta fibrillization as well as neurotoxicity in vitro and in a Drosophila model, but al

183 AR-delta activation also reduced HTT-induced neurotoxicity in vitro and in medium spiny-like neurons

184 nificantly alleviated astrocyte-mediated Tat neurotoxicity in vitro and in the brain of Tat-expressin

185 Abeta aggregation and prevent Abeta-mediated neurotoxicity in vitro.

186 define functional properties of tau driving neurotoxicity in vivo We express wild-type human tau and

187 was demonstrated against paclitaxel-induced neurotoxicity in vivo.

188 the mechanisms of ziram's (a DTC fungicide) neurotoxicity in vivo.

189 membrane binding significantly enhanced its neurotoxicity in vivo.

190 Factors that anticipated their neurotoxicity included aggregation in nucleoli, decrease

191 animals to commonly used anesthetics causes neurotoxicity including impaired neurocognitive function

192 rval zebrafish displayed signs of paclitaxel neurotoxicity, including sensory axon degeneration and t

193 provide evidence that the severity of Abeta neurotoxicity increases with increasing concentration of

194 These findings highlight the mechanisms of neurotoxicity incurred by nanoparticles.

195 atory response and beta-amyloid 42 (Abeta42) neurotoxicity independent of traditional circulating cyt

196 ded prion protein (TPrP) model to understand neurotoxicity induced by prion protein misfolding.

197 tanding the molecular mechanism of EGCG as a neurotoxicity inhibitor.

198 aumatic brain injury (TBI), drives spreading neurotoxicity into surrounding, undamaged, brain areas.

199 Because this neurotoxicity involves ROS production, we investigated t

200 Cumulative neurotoxicity is a prominent toxicity of oxaliplatin-bas

201 Currently, neurotoxicity is attributed to prefibrillar oligomeric s

202 olecular mechanism of astrocyte-mediated Tat neurotoxicity is not defined.

203 growth-permissive microenvironment or cause neurotoxicity is receptor dependent and it may be possib

204 However, the role of microRNAs in ethanol neurotoxicity is still not clear.

205 tive deficits, but the exact mechanism of Mn neurotoxicity is still unclear.

206 MTX-related clinical neurotoxicity is transient, and most patients can receiv

207 Botulinum neurotoxicity is ultimately governed through light chain

208 Although the cause of the clinical neurotoxicity is unknown, it has been postulated, given

209 th therapeutic bioactivity against ACR acute neurotoxicity is urgently needed.

210 Since atropine prevented AEME-induced neurotoxicity, it has been suggested that its toxic effe

211 novel evidence suggesting that METH-induced neurotoxicity leads to a shift from dorsal to ventral st

212 otected in Ca(2+) overload-induced models of neurotoxicity, like glutamate or veratridine exposures.

213 Further in vivo/vitro studies showed neurotoxicity linked with AZA exposure.

214 Neurotoxicity may occur in cancer patients and survivors

215 The primary end point was cumulative neurotoxicity measured by the sensory scale of the Europ

216 These health complications include neurotoxicity, memory loss, infertility in males, and de

217 ying modifiers of mutant huntingtin-mediated neurotoxicity might be a therapeutic strategy for HD.

218 In protecting from alpha-synuclein neurotoxicity, NCEH-1 also stimulates cholesterol-derive

219 , in addition to its role in alcohol-induced neurotoxicity, NF-kappaB mediates the development of alc

220 DRG and SN penetration than paclitaxel, the neurotoxicity observed functionally was consistently mor

221 In histology, the severe neurotoxicity observed in some previous studies with dox

222 BPA-induced neurotoxicity occurs with the generation of oxidative st

223 s, and increasing TGF-beta signaling reduces neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyr

224 The absence of neurotoxicity of a representative analogue may encourage

225 reverse-transcriptase inhibitors rescued the neurotoxicity of AGS neurons and organoids, highlighting

226 Although the neurotoxicity of alpha-synuclein is well established, th

227 ned the efficacy of ethoxyquin in preventing neurotoxicity of cisplatin in rodent models of chemother

228 Ethoxyquin prevented neurotoxicity of cisplatin in vitro in a sensory neurona

229 issue-cultured neurons was effective against neurotoxicity of cisplatin.

230 and we show that, in vitro, it prevents the neurotoxicity of different BoNT serotypes by interfering

231 at dimerization is required for the dominant neurotoxicity of disease-associated GARS mutations and p

232 , and alpha-synuclein accumulation mediating neurotoxicity of dopaminergic (DA) neurons, apoptotic ce

233 ded to elucidate the provenance and putative neurotoxicity of fibrin(ogen), and its potential impact

234 The putative neurotoxicity of IL-6 and TNF-alpha is in agreement with

235 cts have to be balanced against the possible neurotoxicity of infections and immunosuppressive medica

236 Notwithstanding potential neurotoxicity of inhaled titanium dioxide nanoparticles

237 ese findings highlight the importance of the neurotoxicity of mutant AR protein in motor neurons as a

238 nished severing of microtubules, but also by neurotoxicity of mutant spastin proteins, chiefly M1.

239 Acetone may potentiate the neurotoxicity of n-hexane.

240 The acute neurotoxicity of oligomeric forms of amyloid-beta 1-42 (

241 ses from 28 families, studied dose-dependent neurotoxicity of oxysterols in human cortical neurons an

242 growth may be involved in the developmental neurotoxicity of PBDEs.

243 86) as a potential modulator of the distinct neurotoxicity of the caspase-2 fragment mice (N552-Q148)

244 s of chemical mixtures, we found evidence of neurotoxicity of the mixture, as well as potential syner

245 Neurotoxicity of the Parkinson disease-associated pestic

246 In addition, we assessed functional neurotoxicity of tungsten, a common microelectrode mater

247 mutants, supporting a conserved mechanism of neurotoxicity of wild-type tau and FTDP-17 mutant tau in

248 re, none of the compounds exhibited in vitro neurotoxicity or hepatotoxicity and hence they had impro

249 ve function in individuals with METH-induced neurotoxicity or others with striatal dopamine loss, suc

250 ow defects are most common and may be due to neurotoxicity or retinal damage.

251 of therapy experienced more chronic sensory neurotoxicity (P < .0001).

252 lar uncoupling could contribute to cocaine's neurotoxicity, particularly for stimulation conditions w

253 meostasis and oxidative stress but different neurotoxicity pathways.

254 ogy also mitigated this transport defect and neurotoxicity, providing future novel therapy targets.

255 imiting to exponential prion propagation and neurotoxicity relating to critical concentrations of alt

256 n, the molecular mechanisms underlying their neurotoxicity remain poorly understood.

257 However, the mechanism of gp120-mediated neurotoxicity remains unclear.

258 ors on macrophages causes neuroprotection or neurotoxicity, respectively.

259 Methamphetamine (METH)-induced neurotoxicity results in long-lasting depletions of mono

260 des a useful model for validating cell-based neurotoxicity screening approaches, as sensitivity is de

261 m cells (hESC) provide an excellent tool for neurotoxicity screening.

262 ain might result in minor damage, the severe neurotoxicity seen in earlier works does not appear to o

263 The incidences of grade 3 or 4 neurotoxicity, stomatitis, diarrhea, and neutropenia wer

264 usefulness of our approach for environmental neurotoxicity studies.

265 ith the FACT-Cx TOI, items from the FACT-GOG-Neurotoxicity subscale, and a worst pain item from the B

266 bove the ETT and at least 2 risk factors for neurotoxicity, such as prematurity, glucose-6-phosphate

267 it, coupled with its potential for abuse and neurotoxicity, suggest that its use in the clinical sett

268 protection against mutant huntingtin-induced neurotoxicity, suggesting that HSF1 can protect neurons

269 ge site is an important mediator of ataxin-7 neurotoxicity, suggesting that inhibition of caspase-7 c

270 inhibitor, were able to prevent AEME-induced neurotoxicity, suggesting that the toxicity is due to th

271 at disrupts fibril formation also eliminates neurotoxicity, supporting that amyloidogenesis is critic

272 Interestingly, G4C2 transcript-mediated neurotoxicity synergizes with that of PR aggregates, sug

273 to support prioritization for developmental neurotoxicity testing in rodents.

274 or the synapticloss, memory impairments, and neurotoxicity that underlie Alzheimer disease.

275 nction has become an established hallmark of neurotoxicity, the link between Abeta and mitochondrial

276 ve mechanism that attenuates alpha-synuclein neurotoxicity, thereby pointing toward regulation of neu

277 e of endothelial CD36 in enabling neutrophil neurotoxicity through CSF3.

278 phila to explore a strategy to block Abeta42 neurotoxicity through engineering of the Heat shock prot

279 ysosomal exocytosis in astrocytes and causes neurotoxicity through GFAP activation and ER stress indu

280 Aha1 contributes to tau fibril formation and neurotoxicity through Hsp90.

281 trocytes further contributed to the observed neurotoxicity through increased type I interferon secret

282 data indicated that miR-29b mediated ethanol neurotoxicity through the SP1/RAX/PKR cascade.

283 eptable toxicity profile, and no evidence of neurotoxicity thus far.

284 For chronic neurotoxicity, tingling was the most severe symptom, fol

285 um obtained during a window-of-developmental neurotoxicity to draw correlations between early-life ex

286 trongly link alpha-synuclein aggregation and neurotoxicity to the pathogenesis of Parkinson's disease

287 months after chemotherapy cessation, chronic neurotoxicity was assessed with use of the 20-item, Euro

288 e into Rag1 knock-out mice revealed that CTL neurotoxicity was mediated by perforin.

289 to the molecular basis of mutant TG6-induced neurotoxicity, we analyzed all the seven new TG6 mutants

290 ependent induction of Dkk1 by Abeta mediates neurotoxicity, we measured the effects of Abeta and Dkk1

291 To control the pandemic of developmental neurotoxicity, we propose a global prevention strategy.

292 Interestingly, blood biomarkers of neurotoxicity were also altered.

293 fects on microglial inflammation and related neurotoxicity were examined.

294 derlying sensitization of the nerve cells to neurotoxicity when Abeta-target receptors are present.

295 lture and long-lasting neuroinflammation and neurotoxicity when injected into the CNS of mice.

296 ued paclitaxel-induced epithelial damage and neurotoxicity, whereas MMP-13 overexpression in zebrafis

297 release syndrome, and eight (33%) developed neurotoxicity, which was reversible in all but one patie

298 nt arms, with the exception of grades 1 to 2 neurotoxicity, which were reported in 29 patients (38.2%

299 is virus (VSV) that is devoid of its natural neurotoxicity while retaining potent oncolytic activity.

300 ive model encompassing prion replication and neurotoxicity would be indispensable to the pursuit of i