ライフサイエンスコーパス: neurotoxic

1 numerous neuronal functions but in excess is neurotoxic.

2 ligomers) have emerged as being particularly neurotoxic.

3 the amyloid-beta-precursor protein (APP) is neurotoxic.

4 tein forms fibrils, which are believed to be neurotoxic.

5 oids, typically target pest insects by being neurotoxic.

6 -arginine (poly-GR) peptides are known to be neurotoxic.

7 igh-titer infectious prions are not directly neurotoxic.

8 arises from normalizing an imbalance between neurotoxic [3-hydroxykynurenine (3-HK); quinolinic acid

9 TUDCA prevented neurotoxic (A1) polarization of astrocytes and proinflam

10 odies specifically directed against the most neurotoxic Abeta forms are undergoing large-scale trials

11 Deposition of potentially neurotoxic Abeta fragments derived from amyloid precurso

12 itional mechanism of action that neutralizes neurotoxic Abeta oligomer formation through stabilizatio

13 Such nanostructures that target neurotoxic Abeta oligomers are potentially useful for ev

14 s demonstrate the inhibition of the putative neurotoxic Abeta oligomers.

15 tures to avoid the formation of the putative neurotoxic Abeta oligomers.

16 mposed of trimers are thought to be the most neurotoxic Abeta oligomers.

17 on our findings, we propose that glia clear neurotoxic Abeta peptides in the AD model Drosophila bra

18 apeutic strategy to combat overproduction of neurotoxic Abeta.

19 However, previous studies relied heavily on neurotoxic ablation of NK1R spinal neurons, which limite

20 e (Lys) and tryptophan catabolism leading to neurotoxic accumulation of glutaric acid (GA) and relate

21 presence of nAChRs sensitizes neurons to the neurotoxic action of Abeta through the timed activation

22 orphin neuronal death.SIGNIFICANCE STATEMENT Neurotoxic action of alcohol during the developmental pe

23 PrP) seems to exert both neuroprotective and neurotoxic activities.

24 majority of pesticides, are known for their neurotoxic activity in humans.

25 lly, we show that DNT1 pro-domain acquires a neurotoxic activity in the presence of Abeta1-42.

26 However, recent evidence suggests that the neurotoxic activity of BoNT/A is not restricted to the p

27 PBD-C06 was specifically designed to target neurotoxic aggregates and to avoid complement-mediated i

28 the synapse but pathologically misfolds into neurotoxic aggregates that are characteristic for neurod

29 ule-associated protein tau (MAPT, tau) forms neurotoxic aggregates that promote cognitive deficits in

30 lded tau propagating through the brain seeds neurotoxic aggregation of soluble tau in recipient neuro

31 Most studies have focused on accumulation of neurotoxic alpha-synuclein secondary to defects in autop

32 ocomial pneumonia exhibit elevated levels of neurotoxic amyloid and tau proteins in the cerebrospinal

33 Brain accumulation of neurotoxic amyloid beta (Abeta) peptide because of incre

34 the blood-brain barrier (BBB) contributes to neurotoxic amyloid-beta (Abeta) brain accumulation and d

35 modified amyloid-beta (pE-Abeta) is a highly neurotoxic amyloid-beta (Abeta) isoform and is enriched

36 Neurotoxic amyloid-beta peptides (Abeta) are major drive

37 initiates the production and accumulation of neurotoxic amyloid-beta peptides, which is widely consid

38 It is also neurotoxic and broadly cytotoxic, leading to overdose de

39 Excess Abeta is potentially neurotoxic and can lead to atrophy of brain regions such

40 However, Abeta42 is more neurotoxic and essential to the etiology of AD.

41 We found that both PHF6 peptides are neurotoxic and exhibit similar membrane-mediated changes

42 epresents a point of convergence between the neurotoxic and genetic causes of PD.

43 The HIV envelope glycoprotein (gp120) is neurotoxic and has been linked to alterations in mitocho

44 Increased beta-A level is neurotoxic and induces oxidative stress in brain resulti

45 phoramide mustard; and chloroacetaldehyde, a neurotoxic and nephrotoxic compound, arising from the ox

46 However, in many neurotoxic and neurodegenerative disorders, microtubules

47 Anaesthetics have been shown to exert both neurotoxic and neuroprotective effects during developmen

48 ment in ALS and discuss the evidence for the neurotoxic and neuroprotective pathways that have been a

49 number, organization, and expression in both neurotoxic and non-neurotoxic rattlesnakes.

50 angiogenic factors, transitioning to a more neurotoxic and pro-angiogenic phenotype.

51 actor (MIF) was identified and evaluated for neurotoxic and pro-gliotic effects during RD.

52 The means of neurotoxic and respirotoxic compounds were significantly

53 phase transitions of cytoplasmic TDP-43 are neurotoxic and that treatment with oligonucleotides comp

54 tration of or prolonged exposure to Dyn A is neurotoxic and these deleterious effects are very likely

55 Prophylactic therapy is neurotoxic, and a third of the relapses involve the CNS.

56 stress in astrocytes and evoke expression of neurotoxic astrocyte markers.

57 al activation and prevents the generation of neurotoxic astrocytes that induce neuronal and oligodend

58 injure neurons directly or via activation of neurotoxic astrocytes.

59 ors, IL-1alpha, TNFalpha, and C1q, to induce neurotoxic astrocytes.

60 The essential metal manganese becomes neurotoxic at elevated levels.

61 barrier (BBB) in promoting the clearance of neurotoxic beta-amyloid (AB) peptides from the brain int

62 rain barrier (BBB) in promoting clearance of neurotoxic beta-amyloid (Abeta) peptides from the brain

63 n in the hippocampus and increased levels of neurotoxic beta-amyloid.

64 Here, neurotoxic bilateral lesions were placed in the anterior

65 Methamphetamine (MA) is highly addictive and neurotoxic, causing cell death in humans and in rodent m

66 nto potential therapeutic approaches against neurotoxic CEL-glycated Abeta1-42.

67 l phenotypes and pathomechanisms of specific neurotoxic chemotherapeutic agents.

68 Of the 116 patients who started neurotoxic chemotherapy (mean [SD] age was 55.5 [11.9] y

69 onitoring and coaching of patients receiving neurotoxic chemotherapy for new sensory symptoms may fac

70 ropathy (CIPN) is a common adverse effect of neurotoxic chemotherapy resulting in pain, sensory loss,

71 oximately 30 to 40% of patients treated with neurotoxic chemotherapy will develop CIPN, and there is

72 , ovarian, or lung cancer who were beginning neurotoxic chemotherapy with a taxane or platinum agent

73 In children who receive neurotoxic chemotherapy, peripheral neurotoxicity occurs

74 fall-related injuries for patients receiving neurotoxic chemotherapy.

75 amyloid precursor protein and its associated neurotoxic cleavage product amyloid-beta*56.

76 oxidative stress transcriptomics identified neurotoxic CNS innate immune populations and may enable

77 er than 1.0 mmol are associated with serious neurotoxic complications with relative clinical safety a

78 aterials-based formulations to avoid serious neurotoxic complications, which may further lead to deve

79 esis is a potential response to rid cells of neurotoxic components when proteostasis and organelle fu

80 Methylmercury (MeHg) is a neurotoxic compound that threatens wildlife and human he

81 However, neurotoxic compounds could be identified by changes in e

82 comotor activity of diquat dibromide and the neurotoxic compounds in 98 hpf embryos (exposed for 96 h

83 specific responses to injury and potentially neurotoxic compounds leading to development of more effe

84 The EC50s of behavior for neurotoxic compounds were close to the acute fish toxici

85 ect on behavior (embryonic movement) for the neurotoxic compounds.

86 mbryo test (LC50s determination) may exclude neurotoxic compounds.

87 in the nervous system in response to diverse neurotoxic conditions.

88 flanking region alone sufficed to generate a neurotoxic conformation, while the polyQ tract alone exh

89 ay trigger the p53-dependent neuronal death, neurotoxic consequences of a selective impairment of rib

90 neficial mechanism because dysregulation has neurotoxic consequences.

91 ze and respond to self-DNA, with potentially neurotoxic consequences.

92 ific commentary refers to 'Identification of neurotoxic cross-linked amyloid-beta dimers in the Alzhe

93 t the prefibrillar soluble oligomers are the neurotoxic culprits and are associated with the patholog

94 at higher macrophage abundance and increased neurotoxic cytokines have a fundamental role in the phen

95 ll and monocyte signatures and production of neurotoxic cytokines in ALS patients.

96 s response, which triggers the production of neurotoxic cytokines.

97 bition of STING blocks the overproduction of neurotoxic cytokines.

98 Originally used to detect discrete neurotoxic damages, TSPO has generally turned into a bio

99 cytotoxic Abeta(25-35) peptide, exert their neurotoxic effect during Alzheimer's disease by various

100 thermore, Mn(2+)-elicited exosomes exerted a neurotoxic effect in a human dopaminergic neuronal model

101 f 0.3 and 0.75 mM NAC to protect against the neurotoxic effect of 0.75 mM ACR has been tested in vivo

102 hat this interaction could contribute to the neurotoxic effect of Abeta aggregates.

103 ion channel formation with the differential neurotoxic effect of Abeta(1-40) and Abeta(1-42) in Alzh

104 Importantly the neurotoxic effect of CSF treatment could be rescued by e

105 , while efavirenz (EFV) did not contrast the neurotoxic effect of glutamate.

106 to ischemic preconditioning (PC+OGD/RX), the neurotoxic effect of p300 inhibitor C646 was prevented.

107 ecomes down-regulated and propofol loses its neurotoxic effect.

108 way mannose-binding lectin (MBL), and shared neurotoxic effectors C3b and C5b-9 terminal C complex we

109 However, they have also been associated with neurotoxic effects and in particular with the developmen

110 Many MA-induced neurotoxic effects are mediated by inflammation and gut

111 cellular and molecular mechanisms for these neurotoxic effects are not fully understood; however, se

112 deficits) and peripheral (motor dysfunction) neurotoxic effects at concentrations/doses similar to th

113 tion mechanism that may synergize with other neurotoxic effects caused by LRRK2 mutations.

114 endocrine, developmental, reproductive, and neurotoxic effects for 61, 74, 47, and 32 chemicals, res

115 hese compounds together with their potential neurotoxic effects in dolphins are recommended.

116 Exposure to acrylamide may lead to different neurotoxic effects in humans and in experimental animals

117 , modulating neuroplasticity and/or exerting neurotoxic effects in part through their effects on NMDA

118 We hypothesized that the severity of their neurotoxic effects might be explained by the levels at w

119 y help developing new treatments against the neurotoxic effects of acrylamide and of other neurotoxic

120 Neurotoxic effects of brain irradiation include cognitiv

121 h perspective since they could highlight the neurotoxic effects of cannabis use on the central nervou

122 a form of addiction without the confound of neurotoxic effects of drugs, showed impaired goal-direct

123 ltiple neuronal pathways that counteract the neurotoxic effects of early accumulating amyloid-beta ol

124 sed cell models to investigate the potential neurotoxic effects of heavy metals enriched in a highly

125 e of NAC, a potent antioxidant, reversed the neurotoxic effects of HIV and methamphetamine, suggestin

126 plausible driving mechanism of demonstrated neurotoxic effects of MeHg in the organism affected by i

127 viours may be particularly vulnerable to the neurotoxic effects of neonicotinoids.

128 P. gingivalis DNA in brain and mitigates the neurotoxic effects of P. gingivalis infection.

129 f the prion protein, serves to transduce the neurotoxic effects of PrP(Sc), the infectious isoform, b

130 that are diaplacentally transferred, causing neurotoxic effects on neonatal development.

131 ities of mutant PrPs with each other and the neurotoxic effects seen in neurodegenerative diseases, s

132 Abeta may exert its neurotoxic effects via multiple mechanisms and in partic

133 pocampal neurons from knockouts, NMDA had no neurotoxic effects, determined by lactate dehydrogenase

134 perfect storm that explains many acrylamide neurotoxic effects, like the dysregulation of genes rela

135 ted thiram, a DTC pesticide known to display neurotoxic effects, observing that it can react rapidly

136 r remains to be determined but could involve neurotoxic effects.

137 mechanism by which certain DTCs exert their neurotoxic effects.

138 against the mutant HIV-1 strains and reduced neurotoxic effects.

139 luate pharmaceutical compounds for potential neurotoxic effects.

140 Alzheimer's amyloid-beta oligomers, causing neurotoxic effects.

141 but not alcohol consumption, showed lagged (neurotoxic) effects on inhibitory control and working me

142 hin, Dynorphin (Dyn) A and Dyn B, leading to neurotoxic elevated mutant Dyn A levels.

143 matic hydrocarbons (PAHs) are ubiquitous and neurotoxic environmental contaminants.

144 gested that doxorubicin can be significantly neurotoxic, even at small concentrations.

145 he production of longer Abetas, which elicit neurotoxic events underlying pathogenesis.

146 tau dissociates from microtubules and forms neurotoxic extracellular aggregates.

147 igm that GOT enables metabolism of otherwise neurotoxic extracellular Glu through a truncated tricarb

148 HIV-1 gp120 is a neurotoxic factor and is involved in HIV-1-associated ne

149 In this study, we showed that neurotoxic factors other than Tat protein itself were pr

150 Infected non-neuronal cells release neurotoxic factors such as the viral protein transactiva

151 hnique was achieved with only Fluoro-Gold, a neurotoxic fluorescent dye with membrane penetration cha

152 ss is unknown, and therapies to target their neurotoxic functions are not widely available.

153 Here, we test the hypothesis that otherwise neurotoxic glutamate can be productively metabolized by

154 xaloacetate transaminase (GOT) to metabolize neurotoxic glutamate in the stroke-affected brain.

155 ; correction of this HO-1 deficiency reduces neurotoxic glutamate production without an effect on HIV

156 ase of neurotrophic factors and clearance of neurotoxic glutamate.

157 and beta-amyloid (Abeta) peptides coexist as neurotoxic heteromers within the plaques.

158 or the sustained neuronal injury is that the neurotoxic HIV-1 regulatory protein trans-activator of t

159 th their long-standing kidney disease and/or neurotoxic immunosuppressant agents.

160 tation assays, and p.Asp364Tyr is dominantly neurotoxic in a Caenorhabditis elegans model.

161 rons and, unexpectedly, overexpressed SK2 is neurotoxic in a dose-dependent manner.

162 Fibrin(ogen) deposition is neurotoxic in animal models of MS, but has not been eval

163 ent with Cu as an essential nutrient that is neurotoxic in excess.

164 ed form to an amyloid-like aggregate that is neurotoxic in vivo.

165 required for the upregulation of potentially neurotoxic inflammatory factors during cone degeneration

166 d by neonicotinoids, a group of widely used, neurotoxic insecticides, has been joined.

167 structure, but most studies have overlooked neurotoxic insults that impair development, such as lead

168 mRNA levels, nearly normalized levels of the neurotoxic intermediates delta aminolevulinic acid and p

169 ( ALAS1) gene expression and accumulation of neurotoxic intermediates result in neurovisceral attacks

170 r brain injury in vivo is neuroprotective or neurotoxic is not known.

171 ile irinotecan delivery to the brain was not neurotoxic, it did not improve outcomes in the F98 gliom

172 players would have elevated plasma levels of neurotoxic kynurenine metabolites and reduced levels of

173 nto the brain and attenuate the formation of neurotoxic kynurenine metabolites.

174 opathies, resulting in the formation of less neurotoxic larger tau aggregates with decreased hydropho

175 In contrast to the neurotoxic lead(II) acetate, bismuth is used due to its

176 Permanent NAcc dysfunction, via neurotoxic lesion, generally disrupted the ability to sc

177 Using neurotoxic lesions and microdialysis, we examined whethe

178 Following training, they received sham or neurotoxic lesions of BLA or OFC, followed by RDT retest

179 riatum core in rats with sham or ipsilateral neurotoxic lesions of lateral OFC, as they performed an

180 y, the rats underwent either sham surgery or neurotoxic lesions of the hippocampus (HPC), medial dors

181 rvival of Drosophila exposed to either PQ or neurotoxic levels of DA, whereas, conversely, DAMB overe

182 and RNA expression and induces production of neurotoxic levels of glutamate; correction of this HO-1

183 egulation is necessary to maintain Phe below neurotoxic levels.

184 ion of the excitatory neurotransmitter below neurotoxic levels.

185 extracellular glutamate concentrations below neurotoxic levels.

186 he substrate available for the generation of neurotoxic lipid peroxidation products.

187 rtant downstream target of PC(O-16:0/2:0), a neurotoxic lipid species elevated in AD.

188 neurite growth, and neuroprotected RGCs from neurotoxic media conditioned by pro-inflammatory astrocy

189 nt reduction in multiple proinflammatory and neurotoxic mediators with this treatment paradigm.

190 Methylmercury is the environmental form of neurotoxic mercury that is biomagnified in the food chai

191 Prenatal exposure to mercury, a known neurotoxic metal, is associated with lower cognitive per

192 The formation of the potent neurotoxic methylmercury (MeHg) is a microbially mediate

193 II)) is a key step in microbial formation of neurotoxic methylmercury (MeHg), but the mechanisms rema

194 converts inorganic Hg into bioaccumulative, neurotoxic methylmercury (MeHg).

195 As the methylation of inorganic mercury to neurotoxic methylmercury has been attributed to the acti

196 Elevated levels of neurotoxic methylmercury in Arctic food-webs pose health

197 ses also transform reactive ionic mercury to neurotoxic methylmercury.

198 ental mercury and convert the oxidized Hg to neurotoxic methylmercury.

199 es demonstrate that chronic phase removal of neurotoxic microglia after TBI using CSF1R inhibitors ma

200 proteins during development as well as many neurotoxic misfolded proteins during pathogenesis.

201 esfenvalerate) to study toxicokinetics and a neurotoxic mode of action as potential reasons for the d

202 Eleven of these compounds exhibited a neurotoxic mode of action.

203 ne retained in C. atrox was deleted from the neurotoxic Mojave rattlesnake (C. scutulatus; approximat

204 cation for production and bioaccumulation of neurotoxic monomethylmercury (MeHg) is unknown.

205 In two different neurotoxic mouse models of PD, acute MPTP and sub-chroni

206 e spontaneous ionic currents associated with neurotoxic mutants of PrP, and the isolated N-terminal d

207 e Long-Evans rats received bilateral sham or neurotoxic NAcc lesions, recovered, and underwent fear d

208 , we investigated the effect of breaking the neurotoxic neuroinflammatory loop at 1-month after contr

209 rofilament accumulations in animal models of neurotoxic neuropathies and neurodegenerative diseases.

210 epitope character and its propensity to form neurotoxic oligomeric aggregates.

211 PrP(C) may also act as a receptor for neurotoxic, oligomeric species of other proteins that ar

212 structure, leading to its self-assembly into neurotoxic oligomers and aggregates, a process hypothesi

213 e amyloid-beta peptide (Abeta) misfolds into neurotoxic oligomers and assembles into amyloid fibrils.

214 two distinct arrangements leading to either neurotoxic oligomers and fibrils or non-toxic amorphous

215 dverse effects, and is effective at reducing neurotoxic oligomers with a broad spectrum.

216 metal for normal growth and development, is neurotoxic on excessive exposure.

217 is responsible for the growth inhibitory and neurotoxic or anti-adhesion activities of C3.

218 cells in the anterior thalamus after either neurotoxic or electrolytic lesions of the NPH.

219 les following CNS injury that involve either neurotoxic or neuroprotective effects.

220 uman disease and providing insights into the neurotoxic or protective contributions of these cells to

221 are proficient catalysts of the breakdown of neurotoxic organophosphates and have great potential as

222 cy has been shown to lead to accumulation of neurotoxic oxysterols.

223 take lower levels of stress to trigger these neurotoxic pathways, leading to more pronounced brain vo

224 6 play an important role in the oxidation of neurotoxic PCBs to chiral OH-PCBs in humans.

225 Abeta is a neurotoxic peptide excised from the amyloid-beta precurs

226 MCI stage of AD and therapeutic lowering of neurotoxic peptide levels may delay progression of AD an

227 n, it may contribute to efficient removal of neurotoxic peptides from the brain.

228 Conopeptides are neurotoxic peptides in the venom of marine cone snails a

229 al from neurons and transport of APP-derived neurotoxic peptides.

230 mity to agricultural use of five potentially neurotoxic pesticide groups (organophosphates, carbamate

231 s (acephate and oxydemeton-methyl) and three neurotoxic pesticide groups (pyrethroids, neonicotinoids

232 proximity to agricultural use of potentially neurotoxic pesticides and neurodevelopment in 7-year-old

233 residential proximity to agricultural use of neurotoxic pesticides and poorer neurodevelopment in chi

234 SIRT6 in astrocytes by itself abrogates the neurotoxic phenotype of ALS astrocytes.

235 Enhanced SIRT6 activity abrogates the neurotoxic phenotype of astrocytes expressing ALS-linked

236 In turn, astrocytic GA production induces a neurotoxic phenotype that kills striatal and cortical ne

237 polarization of astrocytes and microglia to neurotoxic phenotypes and ameliorated neuropathology in

238 ties, inducing strain-specific pathology and neurotoxic phenotypes.

239 from diffuse into cored plaques, underlying neurotoxic plaque development in AD.

240 The blood-brain barrier (BBB) keeps neurotoxic plasma-derived components, cells, and pathoge

241 ion and the accumulation of locally produced neurotoxic porphyrin precursors within the CNS.

242 Only Abeta-CEL16 and Abeta-CEL28 were neurotoxic, possibly through a nonmitochondrial pathway,

243 the molecular mechanisms responsible for the neurotoxic potential of histone deacetylase 1 (HDAC1) an

244 AEME possesses greater neurotoxic potential than cocaine and an additive effect

245 dust particles prior to investigating their neurotoxic potential.

246 Acrylamide is a carcinogenic and neurotoxic process contaminant that is generated from fo

247 me in youth with PTSD may suggest an ongoing neurotoxic process over development, which further contr

248 esearch also points to other stress-mediated neurotoxic processes, including enhanced inflammation an

249 indicates that misfolded tau aggregates are neurotoxic, producing synaptic loss and neuronal damage.

250 atabolites with potent immunosuppressive and neurotoxic properties, respectively.

251 ged players in neurodegeneration-by clearing neurotoxic protein aggregates, but also providing an opp

252 tent and preferential DDR1 inhibitors reduce neurotoxic protein levels in vitro and in vivo.

253 n's disease (PD), and DDRs knockdown reduces neurotoxic protein levels.

254 We report here that HIV-1 gp120, a neurotoxic protein that is specifically associated with

255 te that DDR1 regulates autophagy and reduces neurotoxic proteins and inflammation and is a therapeuti

256 Here we show that the expression of neurotoxic proteins associated with these diseases in mi

257 Most research has focused on these neurotoxic proteins, but much less is known about the pa

258 eases autophagy and reduces inflammation and neurotoxic proteins.

259 he microglia barrier and the accumulation of neurotoxic protofibrillar Abeta hotspots may constitute

260 metabolism of kynurenine to the potentially neurotoxic quinolinic acid instead of the neuroprotectiv

261 ptophan degradation toward the production of neurotoxic quinolinic acid.

262 O, whose activity promotes the production of neurotoxic quinolinic acid.

263 n, and expression in both neurotoxic and non-neurotoxic rattlesnakes.

264 long been assumed that prions are themselves neurotoxic, recent development of methods to obtain exce

265 ably, ossification of vessels and astrocytic neurotoxic response is associated with specific behaviou

266 PGL-1 confers this neurotoxic response on macrophages: macrophages infected

267 This effect greatly reduced neurotoxic risk associated with VSV infection while stil

268 TS, tetramine) is a formerly used and highly neurotoxic rodenticide.

269 phosphorylation as the signal modulating the neurotoxic role of HDAC1 in response to neurotoxic stimu

270 at TSPO is a key regulator of NOX1-dependent neurotoxic ROS production in the retina.

271 The beta-neurotoxic secreted phospholipases A(2) (sPLA(2)s) block

272 a concise, stereocontrolled synthesis of the neurotoxic sesquiterpenoid (-)-picrotoxinin (1, PXN).

273 hat tau is required to mediate Abeta-induced neurotoxic signals in neurons.

274 ether and how RanBP9 transmits Abeta-induced neurotoxic signals to tau.

275 abilization and aberrant dynamics, promoting neurotoxic SOD1 aggregation.

276 promising way to study such potentially very neurotoxic species and how they could be stabilized or d

277 it has been shown to produce the majority of neurotoxic species during aggregation of Abeta42.

278 vitro and have been implicated as important neurotoxic species in AD.

279 eptide fibrillization interact with the most neurotoxic species is far from being understood.

280 ys to amyloid fibrils, is thought to include neurotoxic species responsible for synaptic loss and neu

281 oid beta-protein (Abeta) oligomers, the main neurotoxic species, are predominantly formed from monome

282 oscopic steps that lead to the production of neurotoxic species.

283 Deoxysphingolipids (1-deoxySLs) are atypical neurotoxic sphingolipids that are formed by the serine-p

284 e tested the involvement of a novel class of neurotoxic sphingolipids, the 1-deoxysphingolipids.

285 Moreover, an atypical and potentially neurotoxic sphingosine isomer was identified in patient

286 al phosphorylation of HDAC1 was decreased by neurotoxic stimuli, which stimulated the phosphatase enz

287 the neurotoxic role of HDAC1 in response to neurotoxic stimuli.

288 ntly diminished axonal damage in response to neurotoxic stimuli.

289 of the disease with respect to environmental neurotoxic stress.

290 n exposure to methylmercury (MeHg), a potent neurotoxic substance.

291 or leukoencephalopathy syndrome (RPLS), is a neurotoxic syndrome of cerebral vasoregulation classical

292 ment of 25 adult patients who presented with neurotoxic syndromes after CAR T-cell therapy at the Mas

293 u oligomers (suggested to be the most likely neurotoxic tau entity) are present in the Huntington's d

294 Chemotherapy with a neurotoxic taxane or platinum agent.

295 h increases in brain and/or plasma levels of neurotoxic TNFalpha and several other proinflammatory cy

296 Some evidence suggests that fluoride may be neurotoxic to children.

297 NK cells are neurotoxic to hSOD1(G93A) MNs which express NKG2D ligand

298 Pyrethroid-treated bed nets are acutely neurotoxic to mosquitoes, inducing symptoms such as loss

299 ensory neurons with resiniferatoxin (RTX), a neurotoxic TRPV1 (transient receptor potential vanilloid

300 ral anesthetics are both neuroprotective and neurotoxic with unclear mechanisms.