ライフサイエンスコーパス: neurotoxicity

1 t had a grade 4 non-haematological toxicity (neurotoxicity).

2 cal mechanisms underlying Mn homeostasis and neurotoxicity.

3 or subtype and is involved in NMDAR-mediated neurotoxicity.

4 s into pathways of disease susceptibility or neurotoxicity.

5 ether it might protect against prion-induced neurotoxicity.

6 rget sequences prevent inclusions and rescue neurotoxicity.

7 TAAR1 plays a role in regulating MA-induced neurotoxicity.

8 eful for the study of early damage due to HG neurotoxicity.

9 aptic transmission, learning and memory, and neurotoxicity.

10 kinetics, focused specifically on addressing neurotoxicity.

11 genesis of metal-mediated diseases and metal neurotoxicity.

12 ts had 16 dose adjustments, primarily due to neurotoxicity.

13 uld serve as the mechanism of the anesthesia neurotoxicity.

14 ded or misassembled proteins associated with neurotoxicity.

15 include cytokine release syndrome (CRS) and neurotoxicity.

16 e in producing gut microbiota alteration and neurotoxicity.

17 are regulated in drinking water due to their neurotoxicity.

18 after disease onset rescued poly(GR)-induced neurotoxicity.

19 ein aggregates, as well as enhanced cellular neurotoxicity.

20 s and subsequent increased survival, without neurotoxicity.

21 e brain and liver, induce familial manganese neurotoxicity.

22 NMDAR (GluN2B-NMDAR) in homocysteine-induced neurotoxicity.

23 R-mediated signaling in homocysteine-induced neurotoxicity.

24 ensitivity and 72% specificity for grade >=2 neurotoxicity.

25 d 13 patients (52%) presented with grade 3-4 neurotoxicity.

26 al pathway, whereas Abeta-CEL16&28 showed no neurotoxicity.

27 ence that acid extrusion by NBCn1 stimulates neurotoxicity.

28 ce of a copper-iron connection in CZ-induced neurotoxicity.

29 measures for chemotherapy-induced peripheral neurotoxicity.

30 ty of SLC30A10 in the brain protects against neurotoxicity.

31 paraoxon and uncovered a unique mechanism of neurotoxicity.

32 rosophila models of C9orf72 dipeptide repeat neurotoxicity.

33 microglial inflammation to fully assess AgNP neurotoxicity.

34 t against anticancer drug-induced peripheral neurotoxicity.

35 d against lithium-induced iron elevation and neurotoxicity.

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

37 had no symptoms of ototoxicity or peripheral neurotoxicity.

38 Abeta production and mediates Abeta-induced neurotoxicity.

39 rol of inflammatory responses in the CNS and neurotoxicity.

40 reducing microglial inflammation and related neurotoxicity.

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

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

43 tion or in certain instances, antiretroviral neurotoxicity.

44 (MT) synergistically potentiate dopaminergic neurotoxicity.

45 ent, and contributes to oxidopamine-mediated neurotoxicity.

46 ulation from adjacent axons thereby reducing neurotoxicity.

47 ion of the actin cytoskeleton and downstream neurotoxicity.

48 ne if formation of such complexes exacerbate neurotoxicity.

49 manganese in the blood and brain and develop neurotoxicity.

50 lly cleared over 20 weeks with no detectable neurotoxicity.

51 on neuronal cells, leading to suppression of neurotoxicity.

52 peat proteins trigger multiple mechanisms of neurotoxicity.

53 ne release syndrome and/or reversible severe neurotoxicity.

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

55 ctivity to cleave alpha-Syn and promotes its neurotoxicity.

56 lux and downstream cell signaling events and neurotoxicity.

57 essential role in better understanding their neurotoxicity.

58 nhibitor-based approach against GVHD-induced neurotoxicity.

59 y short-lived oligomeric intermediates cause neurotoxicity.

60 such as cytokine release syndrome (CRS) and neurotoxicity.

61 s raised concerns regarding their source and neurotoxicity.

62 aches ameliorates acute and chronic forms of neurotoxicity.

63 chondrial damage, all of which contribute to neurotoxicity.

64 limitations in preclinical animal models of neurotoxicity.

65 to CYP mediated metabolism and PCB mediated neurotoxicity.

66 r paediatric chemotherapy-induced peripheral neurotoxicity.

67 hyperactivity," is required for bcat-1(RNAi) neurotoxicity.

68 es of SHH-activated DMB/MBEN with acceptable neurotoxicity.

69 [PFS] >= 90%) with reduced treatment-related neurotoxicity.

70 6.6-19.2]) of 532 developed grade 3 or worse neurotoxicity.

71 on-durable clinical responses without CRS or neurotoxicity.

72 ing a critical role of NRF2 in air pollution neurotoxicity.

73 ic neuronal amyloid protein and also enhance neurotoxicity.

74 o elucidate mechanisms of DomA developmental neurotoxicity.

75 ignancies but also cause a high incidence of neurotoxicity.

76 tic pathway in the treatment of tau-mediated neurotoxicity.

77 ), asthenia (14% and 16%, respectively), and neurotoxicity (11% and 16%, respectively).

78 ges contribute to the development of CRS and neurotoxicity after CAR-T cell therapy.

79 est neuroprotective effect against oxidative neurotoxicity among 25 endogenous estrogen metabolites t

80 le in late health outcomes except for excess neurotoxicity among LMB survivors.

81 of the 25 patients (48%) developed grade 1-2 neurotoxicity and 13 patients (52%) presented with grade

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

83 , the mechanisms involved in TAAR1's role in neurotoxicity and cell death have not been described in

84 ountered in lymphoma patients with grade 3-4 neurotoxicity and correlated negatively with progression

85 sociated with a high incidence of reversible neurotoxicity and CRS.

86 ted with multiple adverse effects, including neurotoxicity and cytokine release syndrome (CRS).

87 No treatments exist for peripheral neurotoxicity and few assessment measures are specific t

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

89 activation of calpains is required for both neurotoxicity and formation of DNA-platinum adduct forma

90 thways and impairs transcription, triggering neurotoxicity and functional decline in HD.

91 This reduces kynurenine-associated neurotoxicity and generates glutamate as a byproduct.

92 roperties of different paramyxoviruses, like neurotoxicity and immunosuppression, are now understood

93 state but also causes cognitive impairment, neurotoxicity and neurodevelopmental deficits.

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

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

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

97 e 3 or 4) immune-related adverse events like neurotoxicity and pneumonitis.

98 acted pTDP-43 assemblies showed differential neurotoxicity and seeding that were correlated with dise

99 The long delay in neurotoxicity and synaptic dysfunction triggered by Abet

100 erstanding of the mechanisms of MeHg-induced neurotoxicity and the development of effective neuroprot

101 escent tracers has been studied extensively, neurotoxicity and their effect on neural functions remai

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

103 f 15 subjects experienced CAR T-cell-induced neurotoxicity and/or cytokine release syndrome (CRS), wh

104 ensitivity and 33% specificity for grade >=3 neurotoxicity, and 91% sensitivity and 72% specificity f

105 satellite glial cells in oxaliplatin-induced neurotoxicity, and demonstrate that targeting OCT2 using

106 cid metabolism is pivotal for alphaS-induced neurotoxicity, and inhibiting SCD represents a novel PD

107 No patient experienced greater than grade 1 neurotoxicity, and no patient required tocilizumab or st

108 sitive results for endocrine, developmental, neurotoxicity, and obesity were observed for 32, 11, 35,

109 vent the alphaS inclusions, reduce alphaS 3K neurotoxicity, and prevent abnormal phosphorylation and

110 s compared with pathological protein-induced neurotoxicity, and the requirement of a particular glial

111 incidence of grade 3-4 pancreatitis, central neurotoxicity, and thromboses was 12%, 4%, and 6%, respe

112 hanisms for TAAR1 in methamphetamine-induced neurotoxicity are not known.

113 sential key events in acrylamide (ACR) acute neurotoxicity are the formation of adducts with nucleoph

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

115 LTA1-treated mice exhibited no neurotoxicity, as measured by olfactory system testing a

116 ay a substantial reduction in 6-OHDA-induced neurotoxicity, as shown by increased survival of substan

117 proposed as a potential antidote against ACR neurotoxicity, as this chemical is not only a well-known

118 pf, developmental toxicity and developmental neurotoxicity assays were performed, and targeted analyt

119 embrane protein 2B (Bri2) efficiently reduce neurotoxicity associated with Abeta42 fibril formation b

120 ernative strategies that can prevent CRS and neurotoxicity associated with CAR T-cell treatment are u

121 nt of CRS, there is no approved treatment of neurotoxicity associated with CD19-targeted CAR-T (CART1

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

123 s the VSV glycoprotein, thereby reducing the neurotoxicity associated with wild-type VSV.

124 nnels, this mechanism is unlikely to mediate neurotoxicity at lower exposure levels during critical p

125 ized that certain hydroxylated PBDEs mediate neurotoxicity, at least in part, by impairing the MEK-ER

126 1 deletion mitigates Mn-induced dopaminergic neurotoxicity, attenuating Mn-induced reduction in GLAST

127 sion or who had cytokine release syndrome or neurotoxicity between different anti-CD19 CAR T-cell con

128 easing carbon chain length for developmental neurotoxicity, but not developmental toxicity.

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

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

131 nt manganese (Mn(2+)) exposure can stimulate neurotoxicity by increasing inflammation.

132 udy, we hypothesized that TDF contributes to neurotoxicity by modulating mitochondrial biogenesis and

133 usion, these results show a decrease in NMDA neurotoxicity by NBCn1 deletion.

134 whether 4E-BP1 could prevent alpha-synuclein neurotoxicity by treating 4E-BP1-overexpressing primary

135 gy (nanotoxicology), in that low-to-moderate neurotoxicity can be subtle and difficult to measure.

136 interaction, which helps to protect against neurotoxicity carried out by its N terminus.

137 pathway in intestinal mucositis and enteric neurotoxicity caused by 5-FU (450 mg/kg, IP, single dose

138 gene in the NMD pathway, efficiently blocked neurotoxicity caused by arginine-rich dipeptide repeats

139 mising approach for reducing (or preventing) neurotoxicity caused by cancer drugs.

140 Calcineurin inhibitor-induced neurotoxicity (CIIN) is a common and debilitating side e

141 Chemotherapy-induced peripheral neurotoxicity (CIPN) is a common dose-limiting side effe

142 igate the role of HIF-1alpha in MeHg-induced neurotoxicity, cobalt chloride (CoCl2), 2-methoxyestradi

143 Grade 3-4 neurotoxicity correlated negatively with overall surviva

144 Neurotoxicity correlated with severity of cytokine relea

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

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

147 in; however, mechanisms of PCB developmental neurotoxicity (DNT) remain controversial.

148 cusses mechanisms of RNA virus clearance and neurotoxicity during viral encephalitis with a focus on

149 pid membrane-rich inclusions associated with neurotoxicity exceeding that of natural familial PD muta

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

151 d in protection against oxidative stress and neurotoxicity, further supporting our observations.

152 at database closure, whereas none died with neurotoxicity grade 1-2.

153 ferritin levels were associated with higher neurotoxicity grade.

154 alpha-Synuclein (alpha-syn)-induced neurotoxicity has been generally accepted as a key step

155 However, the exact mechanisms of its neurotoxicity have not been fully elucidated.

156 e severe cytokine-release syndrome (CRS) and neurotoxicity, impeding their therapeutic application.

157 release syndrome in 16% (4 of 25) and severe neurotoxicity in 28% (7 of 25) of patients.

158 elease syndrome occurred in 50% and 39%, and neurotoxicity in 50% and 23% of patients with FL and tFL

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

160 ssion of alphaSyn, resulting in dopaminergic neurotoxicity in a mouse model of Mn(2+) exposure.

161 e believed to be principally responsible for neurotoxicity in Alzheimer disease (AD), but it is not k

162 n (TXNIP) activity regulate inflammation and neurotoxicity in Alzheimer disease (AD).

163 3 (Cx43) has increasingly been associated to neurotoxicity in Alzheimer disease (AD).

164 rane of neurons has been proposed to explain neurotoxicity in Alzheimer's disease (AD).

165 isms behind the Amyloid-beta (Abeta) peptide neurotoxicity in Alzheimer's disease are intensely studi

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

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

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

169 hese data suggest an on-target mechanism for neurotoxicity in CD19-directed therapies and highlight t

170 measure for chemotherapy-induced peripheral neurotoxicity in children is needed.

171 es to assess chemotherapy-induced peripheral neurotoxicity in children, two variants of the Total Neu

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

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

174 ents both increased intracellular Ca(2+) and neurotoxicity in Drosophila and cultured primary mouse n

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

176 which T21 could drive immunosuppression and neurotoxicity in DS.

177 Other adverse events were grade 1 or 2 neurotoxicity in eight patients (38%), grade 1 acute ski

178 human cells and Drosophila while increasing neurotoxicity in flies.

179 Bim reduction ameliorates mHTT neurotoxicity in HD cells.

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

181 rmining pathological mechanisms that lead to neurotoxicity in Huntington's disease (HD) and for high

182 How huntingtin (HTT) triggers neurotoxicity in Huntington's disease (HD) remains uncle

183 related gene program, evidenced by increased neurotoxicity in microglia-neuronal co-cultures.

184 Here, we examined NMDA-induced neurotoxicity in NBCn1 knockout mice to determine whethe

185 ng to inhibition of aggregation in vitro and neurotoxicity in neuroblastoma cells.

186 as been shown to induce ER stress and elicit neurotoxicity in Parkinson's disease models.

187 ated by R-DPRs, suggesting that R-DPRs cause neurotoxicity in part by inhibiting cellular RNA surveil

188 o the progressive and selective dopaminergic neurotoxicity in PD.

189 ransporter NBCn1/SLC4A7 can affect glutamate neurotoxicity in primary cultures of rat hippocampal neu

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

191 o body burdens associated with developmental neurotoxicity in rodents.

192 quitination may be linked to pathogenesis or neurotoxicity in schizophrenia, and its manifestation in

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

194 olecular mechanisms underlying Abeta-induced neurotoxicity in the presence of this sensitizing target

195 d species of alpha-Syn and alpha-Syn-induced neurotoxicity in the SNc in two distinct mouse models of

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

197 a role of lipids in alphasyn misfolding and neurotoxicity in various synucleinopathy disorders and p

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

199 enous estrogen metabolites against oxidative neurotoxicity in vitro and in vivo.

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

201 ytic YY1 plays a critical role in Mn-induced neurotoxicity in vivo, at least in part, by reducing ast

202 iposome formulation of paclitaxel (L-PTX) on neurotoxicity in-vitro and in-vivo in comparison to the

203 cessfully developed and demonstrated reduced neurotoxicity in-vitro in neuronal cells and prevented d

204 Likely mechanisms for FUS neurotoxicity include autophagy inhibition and defective

205 ell engager (BiTE) antibodies display severe neurotoxicity, including fatal cerebral edema associated

206 l fibrillary acidic protein increased during neurotoxicity, indicating astrocyte injury.

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

208 Peripheral neurotoxicity is a debilitating condition that afflicts

209 Antibody blocking studies reveal that neurotoxicity is almost entirely attributable to complem

210 These data suggest that developmental neurotoxicity is an important end point to consider for

211 wn that homocysteine-induced, NMDAR-mediated neurotoxicity is facilitated by a sustained increase in

212 mitochondrial transport, and TRPV4-mediated neurotoxicity is modulated by the Ca(2+)-binding mitocho

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

214 , but the structural basis of Abeta-elicited neurotoxicity is unknown.

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

216 rather than pathological tau-induced direct neurotoxicity, is the leading force driving neurodegener

217 e importance of non-cell autonomous-mediated neurotoxicity, it is critical to investigate the contrib

218 ncluding cytokine-release syndrome (CRS) and neurotoxicity, limits broader application.

219 posure to most general anaesthetics leads to neurotoxicity manifested by neuronal cell death and abno

220 eptibility to organophosphate (OP) pesticide neurotoxicity may be greatest during the prenatal period

221 n neurofilament light and that this putative neurotoxicity may contribute to the pathogenesis of deli

222 eurofilament light, as a potential marker of neurotoxicity, may contribute to the pathogenesis of del

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

224 brain processes that restore function; 3) a neurotoxicity model of long-term impairment consequentia

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

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

227 Neurotoxicity occurred in 19 of 43 (44%) subjects.

228 ts, grade >= 3 cytokine release syndrome and neurotoxicity occurred in 7% and 31%, respectively.

229 occurred in one (5%) patient, and grade 3-4 neurotoxicity occurred in three (14%) patients.

230 receive neurotoxic chemotherapy, peripheral neurotoxicity occurs frequently, necessitates dose reduc

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

232 The neurotoxicity of air pollution is undefined for sex and

233 Furthermore, we show that neurotoxicity of cisplatin requires activation of Sarm1,

234 Here we examine the dose-dependent neurotoxicity of dextran-coated iron oxide nanoparticles

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

236 Considering the neurotoxicity of glutamate when present in excess, the s

237 Notwithstanding potential neurotoxicity of inhaled titanium dioxide nanoparticles

238 covers essential mechanistic insights to the neurotoxicity of mutant Htt aggregation and describes th

239 amyloid-like adhesive property underlies the neurotoxicity of mutant Htt aggregation.

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

241 e primarily focused on nanomaterials-induced neurotoxicity of the brain.

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

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

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

245 se the proportion of subjects who experience neurotoxicity or place subjects at risk for infectious s

246 urable antilymphoma response without causing neurotoxicity or severe CRS, representing a safe and pot

247 absence of graft-versus-host disease (GVHD), neurotoxicity, or dose-limiting toxicities.

248 he development of cytokine release syndrome, neurotoxicity, or graft-versus-host disease, and there w

249 nge of secreted signals that protect against neurotoxicity, oxidative stress, and apoptotic cascades.

250 ll infusion were associated with more severe neurotoxicity (P = .030).

251 Ethanol causes developmental neurotoxicity partly by blocking adhesion mediated by th

252 Neurotoxicity profiling of Abeta(M1-42) complexed with 4

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

254 ia including high labeling efficacy, minimal neurotoxicity, rapid labeling, suitable stability in viv

255 grade 3 or 4 neurological symptoms, with no neurotoxicity-related deaths.

256 ular and cellular mechanisms for GAs-induced neurotoxicity remain largely unknown.

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

258 However, treatment-related neurotoxicity remains a significant concern in this vuln

259 e proteins to oxaliplatin-induced peripheral neurotoxicity remains controversial.

260 Neurotoxicity remains frequent in patients on once-daily

261 The mechanism of anesthesia neurotoxicity remains largely to be determined.

262 Neurotoxicity represents a common and potentially life-t

263 Manganese (Mn)-induced neurotoxicity resembles Parkinson's disease (PD), but th

264 therapy agent with significant dose-limiting neurotoxicity resulting in peripheral neuropathy.

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

266 Observed effects were not associated with neurotoxicity, since no dystrophic neuron changes in bra

267 enesis where membralin limited glutamatergic neurotoxicity, suggesting that modulating membralin had

268 nts, such as immune effector cell-associated neurotoxicity syndrome (ICANS), are a clinical challenge

269 me (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS).

270 se syndrome, immune effector cell-associated neurotoxicity syndrome, and acute kidney injury requirin

271 r findings illustrate the continuum of PM2.5 neurotoxicity that contributes to early decline of immed

272 asyn acquires pathogenic properties, such as neurotoxicity, that can contribute to disease developmen

273 nction is a hallmark of amyloid-beta (Abeta) neurotoxicity, the pathogenic protein implicated in AD.

274 e potential role of ER stress for As-induced neurotoxicity, the underlying mechanisms remain poorly u

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

276 V protease NS2B-NS3 heterodimer in mediating neurotoxicity through cleavage of a host protein require

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

278 gions of the brain, nanomaterials may induce neurotoxicity through multiple mechanisms including the

279 eductions in alpha-synuclein aggregation and neurotoxicity, thus validating that 4E-BP1 is a powerful

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

281 otic photoreceptors and increased microglial neurotoxicity to photoreceptors, demonstrating a novel a

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

283 the use of NAC is not indicated in ACR acute neurotoxicity treatment.

284 ICANS is an inflammatory neurotoxicity typically occurring after CRS and characte

285 r weight amyloid beta(1-42) oligomers induce neurotoxicity via plasma membrane damage.

286 Management of CAR T cell-mediated neurotoxicity warrants evaluation in prospective clinica

287 role of GluN2A-NMDAR in homocysteine-induced neurotoxicity was distinctly different from glutamate-NM

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

289 Interestingly, blood biomarkers of neurotoxicity were also altered.

290 Eight patients (32%) with grade 3-4 neurotoxicity were deceased at database closure, whereas

291 fects on microglial inflammation and related neurotoxicity were examined.

292 Symptoms of neurotoxicity were minimal and transient.

293 Toxicities, including neurotoxicity, were acceptable and similar between all f

294 -amyloid oligomers (AbetaO), mediating their neurotoxicity, which contributes to the neurodegeneratio

295 nAChRs, linked to early-stage Abeta-induced neurotoxicity, which may represent novel therapeutic tar

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

297 ities included cytokine release syndrome and neurotoxicity, which were grade 3-4 in 8 (32%) and 3 (12

298 during hyperglycemia because of the risk for neurotoxicity with excessive levels.

299 delicate balance between neuroprotection and neurotoxicity within which these cells operate, extrapol

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