ライフサイエンスコーパス: neurotoxic

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

2 rticular Proline-Arginine (PR), are potently neurotoxic.

3 expressed in the same neurons is only mildly neurotoxic.

4 ability to assess whether ethanol itself is neurotoxic.

5 all synaptic disease-related PrP states are neurotoxic.

6 essential nutrient, but overexposure can be neurotoxic.

7 ligomers) have emerged as being particularly neurotoxic.

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

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

10 oids, typically target pest insects by being neurotoxic.

11 ly neuroprotective (kynurenic acid (KA)) and neurotoxic (3-hydroxykynurenine (3HK) and quinolinic aci

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

13 urotoxicity, and to test ways to prevent the neurotoxic Abeta effect.

14 Deposition of potentially neurotoxic Abeta fragments derived from amyloid precurso

15 ive and/or therapeutic approaches to control neurotoxic Abeta levels in the aging brain.

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

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

18 These data reveal the dynamic metabolism of neurotoxic Abeta oligomers in AD brain and could provide

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

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

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

22 er, attempts at targeting the main culprits, neurotoxic Abeta peptides, have thus far proven unsucces

23 f amyloid beta protein (Abeta), particularly neurotoxic Abeta(1-42).

24 apeutic strategy to combat overproduction of neurotoxic Abeta.

25 ive strategy to control the proliferation of neurotoxic Abeta42 oligomers.

26 ere exclusively decreased by the potentially neurotoxic Abeta42 wild-type peptide.

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

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

29 ata show that glucocorticoids potentiate the neurotoxic action of TDP-25 by increasing its levels and

30 ological action of Src, our discovery of the neurotoxic action of the truncated Src fragment suggests

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

32 s may also be involved in microglia-mediated neurotoxic activity in HIV-1-infected brain.

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

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

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

36 with Kv1.3 siRNA, was found to abrogate the neurotoxic activity of microglia resulting from HIV-1 Ta

37 have been shown to be associated with severe neurotoxic activity similar to that observed with Dpl, a

38 rates HDAC3 from Htt, thus de-repressing its neurotoxic activity.

39 The principal neurotoxic agent is an oligomeric form of the amyloid-be

40 oligomeric aggregates that are implicated as neurotoxic agents in Alzheimer's disease.

41 olecular tweezer prevents self-assembly into neurotoxic aggregates by alpha-synuclein and presumably

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

43 , in contrast, alpha-synuclein misfolds into neurotoxic aggregates that mediate neurodegeneration and

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

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

46 including novel synthetic analogs of natural neurotoxic alkaloids, topically applied ex vivo to human

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

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

49 s a therapy to prevent the production of the neurotoxic amyloid beta (Abeta) peptide in Alzheimer's d

50 precursor protein (APP) and accumulation of neurotoxic amyloid beta peptide (Abeta) in the brain is

51 d condition characterized by accumulation of neurotoxic amyloid beta peptides (Abeta) in brain and re

52 nvolved in the proteolytic generation of the neurotoxic amyloid beta-peptide.

53 se plays a pivotal role in the production of neurotoxic amyloid beta-peptides (Abeta) in Alzheimer di

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

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

56 her functions, APOE is proposed to sequester neurotoxic amyloid-beta (Abeta) peptides in the brain, d

57 yloidogenic cleavage of the precursor of the neurotoxic amyloid-beta peptide leads to the secretion o

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

59 ucuronide metabolites, which are known to be neurotoxic and accumulate in CKD; whether insurance type

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

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

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

63 s, although some FMOs metabolites seem to be neurotoxic and hepatotoxic.

64 Thus we sought to determine whether ABri was neurotoxic and if this activity was regulated by oxidati

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

66 Microglial MVs are neurotoxic and myelinotoxic in the presence of Abeta1-42

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

68 However, in many neurotoxic and neurodegenerative disorders, microtubules

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

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

71 he presence of Abeta1-42 in excess, produces neurotoxic and oligodendrotoxic oligomers that, through

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

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

74 The means of neurotoxic and respirotoxic compounds were significantly

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

76 lecule in the CNS: in vitro studies describe neurotoxic and/or antioxidant properties, whereas in viv

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

78 can form beta-strand-rich oligomers that are neurotoxic, and recent observations argue for the existe

79 vealed that beta-synuclein was eventually as neurotoxic as alpha-synuclein for nigral dopaminergic ne

80 injure neurons directly or via activation of neurotoxic astrocytes.

81 Here, neurotoxic bilateral lesions were placed in the anterior

82 ological lesions, suggesting that it was not neurotoxic, but yet transmissible.

83 l phenotypes and pathomechanisms of specific neurotoxic chemotherapeutic agents.

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

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

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

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

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

89 fall-related injuries for patients receiving neurotoxic chemotherapy.

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

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

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

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

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

95 and activity of neurotransmitters, generate neurotoxic compounds, decrease neurotrophic factors, and

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

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

98 Under neurotoxic conditions, p35 undergoes proteolytic cleavag

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

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

101 Indeed, the neurotoxic consequences of HDAC3 depletion could prove r

102 neficial mechanism because dysregulation has neurotoxic consequences.

103 es typically occur in combination with other neurotoxic contaminants.

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

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

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

107 Here we report that neurotoxic damage to adult Area X induced changes in sin

108 duced nitrosative stress and thus ameliorate neurotoxic damage to synapses.

109 sting difference rather than alcohol-induced neurotoxic damage.

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

111 animals and alleviates pathology of distinct neurotoxic disease models.

112 s, 6-week-old Sprague-Dawley rats received a neurotoxic dose of capsaicin, and proliferation was quan

113 enal effects of DA, we administered either a neurotoxic dose of DA or doses below the recognized limi

114 nding (CREB) signaling system, while higher, neurotoxic doses stimulate the p53 cytotoxic system.

115 clinical trial Alliance N08C1 to receive the neurotoxic drug paclitaxel, while undergoing prospective

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

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

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

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

120 To further investigate this neurotoxic effect, we generated lines of transgenic (Tg)

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

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

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

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

125 NO can mediate neurotoxic effects at least in part via protein S-nitros

126 no detectable teratogenic, antiangiogenic or neurotoxic effects at potent anti-inflammatory concentra

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

128 etics and sedatives have been shown to cause neurotoxic effects in laboratory animals.

129 d ionotropic glutamate receptors exert their neurotoxic effects in part by overactivation of calpains

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

131 into question current concepts regarding the neurotoxic effects of ammonia.

132 ed rats was profoundly hypersensitive to the neurotoxic effects of amyloid-beta1-42, the most amyloid

133 Neurotoxic effects of brain irradiation include cognitiv

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

135 ly ways that could avoid the cardiotoxic and neurotoxic effects of current agents such as taxanes.

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

137 subspecialties has examined the potentially neurotoxic effects of general anesthesia on the developi

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

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

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

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

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

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

144 mechanism by which certain DTCs exert their neurotoxic effects.

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

146 luate pharmaceutical compounds for potential neurotoxic effects.

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

148 evels of reactive oxygen species, creating a neurotoxic environment.

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

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

151 More grade 3-4 neurotoxic events (seven [7%] vs one [1%]) and haematoto

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

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

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

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

156 c ALS-derived human adult astrocytes secrete neurotoxic factors that selectively kill motor neurons t

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

158 emonstrated that wild-type beta-synuclein is neurotoxic for cultured primary neurons.

159 erging view that therapies aimed at reducing neurotoxic gene expression hold the potential to halt or

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

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

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

163 ar lesions in SOD1(G93A) mice and eliminated neurotoxic hemoglobin and iron deposits.

164 identify that accumulation of blood-derived neurotoxic hemoglobin and iron in the spinal cord leads

165 AND), likely driven by neuroinflammation and neurotoxic HIV proteins (e.g., envelope and Vpr).

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

167 evidence indicates that rtPA is potentially neurotoxic if it traverses a compromised blood brain bar

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

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

170 cortical cell cultures, we find that LCN2 is neurotoxic in a CCR5-dependent fashion, whereas inhibiti

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

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

173 lutants found to be endocrine disruptive and neurotoxic in animals.

174 mentia with Lewy bodies rendered the protein neurotoxic in transgenic mice, and fibrillation of beta-

175 CR_PrP, a variant that is known to be highly neurotoxic in transgenic mice.

176 s application of aggregated Abeta peptide is neurotoxic in vitro and extracellular Abeta deposits are

177 hibit reduced DNA binding capability and are neurotoxic in vitro and in vivo.

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

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

180 ese mice exhibit significant protection from neurotoxic insult by the dopaminergic toxicant 1-methyl-

181 echanistically, this occurs as a result of a neurotoxic insult that invokes the intracellular elevati

182 nown to increase the brain susceptibility to neurotoxic insults, increase the levels of soluble TDP-2

183 Agents that bind and sequester neurotoxic intermediates of amyloid assembly, inhibit th

184 mechanism by which WT SOD1 is converted to a neurotoxic isoform that has a similar structure, instabi

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

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

187 Using neurotoxic lesions and microdialysis, we examined whethe

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

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

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

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

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

193 ion of the excitatory neurotransmitter below neurotoxic levels.

194 extracellular glutamate concentrations below neurotoxic levels.

195 tamate and maintain its concentrations below neurotoxic levels.

196 egulation is necessary to maintain Phe below neurotoxic levels.

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

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

199 ic neuropathy possibly due to an ischemic or neurotoxic mechanism at the optic nerve head.

200 , suggesting that IL-6 is a major downstream neurotoxic mediator under homeostatic regulation by TAM

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

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

203 o be more a redox modulatory molecule than a neurotoxic metabolite.

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

205 clude excessive nutrient-bound AGEs, such as neurotoxic methyl-glyoxal derivatives (MG).

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

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

208 ses also transform reactive ionic mercury to neurotoxic methylmercury.

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

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

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

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

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

214 pathway, has been largely hypothesized as a neurotoxic molecule contributing to neurodegeneration in

215 y induced by amyloid-beta (Abeta), a primary neurotoxic molecule implicated in AD.

216 Hg) is the transformation of inorganic Hg to neurotoxic monomethylmercury (CH3Hg).

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

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

219 1-42) that is necessary for the formation of neurotoxic oligomeric Abeta species.

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

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

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

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

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

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

226 Microglia exhibit plasticity and can assume neurotoxic or neuroprotective priming states that determ

227 ury in these areas is a concern because this neurotoxic organomercury compound can be highly bioaccum

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

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

230 e regulated by wnt, is part of an Abeta/Dkk1 neurotoxic pathway.

231 w its accumulation may lead to activation of neurotoxic pathways is unclear.

232 vidence suggest that amyloid-beta (Abeta), a neurotoxic peptide, initiates a cascade that results in

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

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

235 amiprid-specific S-18 aptamer to detect this neurotoxic pesticide in a highly rapid, specific, and se

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

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

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

239 eimer disease and confers a proinflammatory, neurotoxic phenotype to microglia.

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

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

242 1 (ALAS1) result in the accumulation of the neurotoxic porphyrin precursors 5-aminolevulinic acid (A

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

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

247 hways activated by NMDAR subtypes during the neurotoxic process.

248 have suggested that reactive astrocytes gain neurotoxic properties, but exactly how reactive astrocyt

249 phoblastic leukemia or lymphoma have various neurotoxic properties.

250 racellular and extracellular accumulation of neurotoxic protein aggregates.

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

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

253 uce spontaneous PrP(C) misfolding leading to neurotoxic PrP-scrapie formation (PrP(SC)).

254 ptophan degradation toward the production of neurotoxic quinolinic acid.

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

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

257 inst protein misfolding, excitotoxicity, and neurotoxic reactive oxygen species.

258 this hypothesis, rats were pretreated with a neurotoxic regimen of METH or with saline.

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

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

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

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

263 the structure of aggregates is important as neurotoxic secondary structures may be specifically targ

264 ins, which are potent neurotoxins that cause neurotoxic shellfish poisoning and respiratory illness i

265 henyl-1,2,3,6-tetrahydropyridine (MPTP) is a neurotoxic side product formed in the chemical synthesis

266 prosurvival kinase Akt is a key step in its neurotoxic signaling pathway.

267 ble amyloid-beta oligomers (AbetaOs) trigger neurotoxic signaling, at least partially, via the cellul

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

269 l activity of PrP(C) is subverted to deliver neurotoxic signals remains uncertain.

270 his interaction controls the transmission of neurotoxic signals to intracellular substrates.

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

272 differing ratios of neuroprotective SirT1 to neurotoxic SirT2; (iii) triggers Tau phosphorylation and

273 gation of other amyloid-forming proteins and neurotoxic soluble peptide aggregates.

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

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

276 ta oligomers (AbetaO), which are the primary neurotoxic species in AD.

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

278 sized that neurotoxicity relates to distinct neurotoxic species produced following a pathway switch w

279 only for identifying the true nature of the neurotoxic species responsible for Huntington's disease

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 more susceptible to cell death from multiple neurotoxic stimuli, including beta-amyloid (Abeta), glut

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 ) or releasing proinflammatory cytokines and neurotoxic substances.

290 Animal models can demonstrate the effects of neurotoxic substances; however, they provide limited ins

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

292 evels and its interaction with Hsp90 promote neurotoxic tau accumulation.

293 neurofibrillary tangles (NFTs), are the true neurotoxic tau entities in neurodegenerative tauopathies

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

295 perphosphorylation, formation of potentially neurotoxic tau fragments by either calpain or caspase-3,

296 Chemotherapy with a neurotoxic taxane or platinum agent.

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

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

299 uence of the enhanced removal of potentially neurotoxic waste products that accumulate in the awake c

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