ライフサイエンスコーパス: Abeta42

1 nucleation of the 42-residue form of Abeta (Abeta42).

2 tibodies binding to the C-terminal region of Abeta42.

3 ly, Abeta burden predicted a decrease in CSF Abeta42.

4 ntibodies targeting the N-terminal region of Abeta42.

5 subsequently convert to having abnormal CSF Abeta42.

6 s of the peptide, Abeta40 and the more toxic Abeta42.

7 dered protein (SOP-IDP) model of Abeta40 and Abeta42.

8 se with their previously reported effects on Abeta42.

9 ereas endothelin-1 was increased by diet and Abeta42.

10 es, but a significant reduction of insoluble Abeta42.

11 of neurotoxic species during aggregation of Abeta42.

12 in the mature Abeta40 aggregates, but not in Abeta42.

13 ms and also to the increased cytotoxicity of Abeta42.

14 eptides could attenuate the toxic effects of Abeta42.

15 ence in the effects of Zn(+2) on Abeta40 and Abeta42.

16 shed day/night amplitude of both Abeta40 and Abeta42.

17 ion of toxic oligomers formed from natural l-Abeta42.

18 istic systems such as the STVIIE peptide and Abeta42.

19 ly high structural similarity with wild-type Abeta42.

20 n vivo in a C. elegans worm model expressing Abeta42.

21 case of MCI (AUC=0.97) even superior to CSF Abeta42.

22 AD mice, PD increased the level of insoluble Abeta42.

23 and increased production of both Abeta40 and Abeta42.

24 001), P-tau (1.88, 1.79-1.97, p<0.0001), and Abeta42 (0.56, 0.55-0.58, p<0.0001).

25 under the current solution conditions (14 uM Abeta42, 20 mM sodium phosphate, 200 uM EDTA, pH 6.8).

26 D of residuals: Abeta40, -7.42 pM; P < .001; Abeta42, -3.72 pM; P < .001).

27 -causing mutations in presenilin altered the Abeta42/40 peptide ratio generated by the HMW beta/gamma

28 lts emphasize the importance of reducing the Abeta42/40 ratio in AD therapy.

29 s of total and phosphorylated tau as well as Abeta42/40 ratio in CSF.

30 Roles of Abeta42/40 ratio on tau pathology are also confirmed wit

31 Here, we provide direct evidence that Abeta42/40 ratio, not total Abeta level, plays a critica

32 conformation, and resulting increase in the Abeta42/40 ratio.

33 and aggregation are tightly correlated with Abeta42/40 ratio.

34 MD) mutant hNPCs, which display differential Abeta42/40 ratios without mutant PS1.

35 array of Abeta peptides, with physiological Abeta42/40 ratios.

36 ve hNPCs co-cultured with APP TMD I45F (high Abeta42/40) cells, not with I47F cells (low Abeta42/40),

37 Abeta42/40) cells, not with I47F cells (low Abeta42/40), develop robust tau pathology in a 3D non-ce

38 blood Abeta1-42 levels (P = 0.01) and higher Abeta42:40 ratio (P = 0.06) were observed in participant

39 phospho-tau, but resulted in an elevation in Abeta42:40 ratio and no reduction in phospho-tau in fAD

40 ingly, FERMT2 reduction had no effect on the Abeta42:40 ratio in corrected neurons and a reduction of

41 fAD mutation lines demonstrated an increased Abeta42:40 ratio relative to controls, yet displayed var

42 litatively distinct mechanisms behind raised Abeta42:40.

43 these peptides, we expressed Abeta36-40 and Abeta42-43 in Drosophila melanogaster to evaluate inhere

44 des (Abeta37-39), and longer Abeta peptides (Abeta42-43).

45 performed with the full-size Abeta protein (Abeta42), a decapeptide Abeta(14-23) and alpha-synuclein

46 42-residue form of the amyloid beta peptide (Abeta42), a protein fragment whose aggregation into amyl

47 ion, as suggested by a significantly reduced Abeta42/Abeta40 ratio in the hippocampus, improved basal

48 the brain parenchyma, and an increase in the Abeta42/Abeta40 ratio is correlated with early-onset AD.

49 rains and reduced in KI/+ brains, though the Abeta42/Abeta40 ratio is slightly increased in KI/+ brai

50 ides produced by proteolysis, as well as the Abeta42/Abeta40 ratio, both of which are linked to the p

51 decrease Abeta40 formation and increase the Abeta42/Abeta40 ratio.

52 the newer assays improved significantly when Abeta42:Abeta40 (AUCs, 0.93-0.95; P </= .01), Abeta42 to

53 The concordance of CSF Abeta42 levels and Abeta42:Abeta40 and Abeta42:tau ratios with visual [18F]

54 suggest the benefit of implementing the CSF Abeta42:Abeta40 or Abeta42:tau ratios as a biomarker of

55 F]flutemetamol PET assessment when using the Abeta42:Abeta40 or Abeta42:tau ratios.

56 impaired, plaques were more diffuse, and the Abeta42:Abeta40 ratio and amount of soluble, fibrillar A

57 A combination of the Abeta42:Abeta40 ratio and T-tau or P-tau level did not i

58 diffuse in PS2APP;Trem2(ko) brains, and the Abeta42:Abeta40 ratio was elevated.

59 asma P-tau181, plasma NfL, CSF P-tau181, CSF Abeta42:Abeta40 ratio, and MRI measures (AUC range, 0.67

60 light levels significantly reduced cortical Abeta42 accumulation and activity levels during the ligh

61 , 228 proteins were significantly altered by Abeta42 accumulation and were enriched for AD-associated

62 se findings by showing different patterns of Abeta42 accumulation following HSV-1 infection of 2D com

63 t stem cells (hiPSCs) to compare patterns of Abeta42 accumulation in HSV-1 infected 2D (neuronal mono

64 es-that underline the heterogeneity of these Abeta42 aggregates and represent the progression of Abet

65 a qualitative difference between Abeta40 and Abeta42 aggregates in the brain tissue of patients with

66 in catalyses the heterogeneous nucleation of Abeta42 aggregates.

67 al basis of the progression of Arctic mutant Abeta42 aggregation in the cell.

68 For the first time, the acceleration in Abeta42 aggregation induced by the Arctic mutation was m

69 Soluble Abeta42 aggregation intermediates (oligomers) have emerg

70 amylin aggregation and, to a lesser extent, Abeta42 aggregation into amyloid fibrils.

71 Y5Y human neuroblastoma cell cultures, where Abeta42 aggregation into large insoluble deposits is rep

72 synuclein that determines the outcome of the Abeta42 aggregation reaction.

73 p a rational drug discovery strategy against Abeta42 aggregation that uses as a read-out the changes

74 tant from infected cells to induce amylin or Abeta42 aggregation was quantitated.

75 aggregates and represent the progression of Abeta42 aggregation within the cell.

76 embled into fibrils and catalyzed amylin and Abeta42 aggregation.

77 l molecules on specific microscopic steps in Abeta42 aggregation.

78 ds that target specific microscopic steps in Abeta42 aggregation.

79 il-catalyzed secondary nucleation process in Abeta42 aggregation.

80 echanisms are involved in amyloid-beta 1-42 (Abeta42) aggregation.

81 r species in Alzheimer's disease (AD) is the Abeta42 alloform of Abeta peptide, which is dominant in

82 ously reported effects of age and amyloid on Abeta42 amplitude at least partially affect each other.

83 as a possible mechanism of cell toxicity of Abeta42 amyloids.

84 stic insight into the aggregation pathway of Abeta42 and a putative toxic mechanism in the pathogenes

85 In symptomatic Alzheimer's disease, CSF Abeta42 and Abeta deposition predicted each other; howev

86 Abeta42 and Abeta40 differ only near the C-terminus, whe

87 binant adeno-associated virus (AAV) encoding Abeta42 and Abeta40 peptides fused to BRI2 protein by in

88 d to as C99) increases the ratio between the Abeta42 and Abeta40 peptides largely due to a decrease i

89 h constructs leads to production of secreted Abeta42 and Abeta40 respectively.

90 nd cerebrospinal fluid (CSF) levels for both Abeta42 and Abeta40, and negative correlations between p

91 eins from flies that were induced to express Abeta42 and age-matched healthy controls using label-fre

92 Furthermore, this peptide bound fibrillar Abeta42 and also stained plaques ex vivo in brain tissue

93 particles are able to inhibit aggregation of Abeta42 and cross the blood-brain barrier (BBB) followin

94 show an independent association between CSF Abeta42 and delirium incidence in an elective surgical p

95 We synthesized l- and D-Abeta42 and found their equimolar mixing to lead to acce

96 D3.3 possesses a larger binding affinity to Abeta42 and higher brain biodistribution compared with i

97 40, and negative correlations between plasma Abeta42 and neocortical amyloid deposition (measured wit

98 mission tomography and CSF concentrations of Abeta42 and phosphorylated tau (p-tau).

99 ratio, and p-tau appeared more accurate than Abeta42 and t-tau alone.

100 rotein (APP) cleaving enzyme-1 (BACE-1), and Abeta42 and tau aggregation inhibition).

101 cognitive impairment (age, UPSIT, RBDSQ, CSF Abeta42, and caudate uptake on DAT imaging) allowed pred

102 Due to their consistency, T-tau, P-tau, Abeta42, and NFL in CSF should be used in clinical pract

103 High EDE levels of Abeta40, Abeta42, and phospho-181T-tau in patients with WMH sugge

104 lirium risk, particularly when combined with Abeta42, and this requires further investigation.

105 demonstrated to have high affinity to serum Abeta42, and to be able to identify AD sera with high se

106 Engineered anti-Abeta42 antibodies are a promising strategy to stall the

107 downstream of Draper in glia in response to Abeta42(arc) exposure.

108 Neuronal expression of human Abeta42(arc) in adult flies results in robust Abeta accu

109 ction and steady-state levels of Abeta40 and Abeta42 are undetectable in KI/KI brains and reduced in

110 2-residue amyloid-beta peptides (Abeta40 and Abeta42) are polymorphic, with variations in molecular s

111 fibrillization of beta-amyloid peptide 1-42 (Abeta42) as a function of time and by comparing to the r

112 ed with familial amyloid polyneuropathy, and Abeta42 associated with Alzheimer's disease by stabilizi

113 e protection of cells from the toxicity of l-Abeta42 at concentrations up to 50 mum.

114 -ray crystallographic analysis revealed that Abeta42 binding to fragment D of fibrinogen induced a st

115 la to investigate the protective activity of Abeta42-binding agents in an AD-relevant functional assa

116 peutics, reduce production of the pathogenic Abeta42 but increase the relative abundance of short Abe

117 d day/night amplitude and linear increase of Abeta42 but not of Abeta40.

118 bolites (secreted APPbeta, C99, Abeta40, and Abeta42) but has no effect on presenilin 1 and presenili

119 studies indicate that treatments that lower Abeta42 by raising the levels of short Abeta peptides co

120 can only assume U-shaped conformations while Abeta42 can also arrange as S-shaped three-stranded chai

121 We found that Abeta42 caused the accumulation of presynaptic vesicular

122 and Abeta burden reciprocally predicted CSF Abeta42 changes; however, in contrast to healthy elderly

123 f so, could the enhanced aggregation rate of Abeta42 compared to Abeta40 be rationalized from the spa

124 can be a powerful tool to trap and stabilize Abeta42 conformers that might otherwise be too transient

125 In humans, increased plasma Abeta42 correlated with diabetes and endothelial dysfunc

126 is associated with premature loss of normal Abeta42 day/night patterns in older adults, suggesting t

127 The Abeta42-dependent synapse decay does not involve transcr

128 ransgenic mice at levels sufficient to drive Abeta42 deposition, Abeta38 and Abeta40 did not deposit

129 Concentrations of CSF Abeta42 derived from the new immunoassays (modified INNO

130 Here we report fibril propagation of an Abeta42 dodecamer called large fatty acid-derived oligom

131 The hereditary Arctic mutation of Abeta42 (E22G) leads to increased intracellular accumula

132 -INNOTEST (r = 0.97), Abeta42-FL (r = 0.93), Abeta42-EI (r = 0.93), and Abeta42-MSD (r = 0.95) assays

133 The mixing of Abeta42 enantiomers thus accelerates the formation of no

134 the less stable [Formula: see text] state of Abeta42, encoding for the U-bend fibril, should form ear

135 nteracting with the Abeta peptide to inhibit Abeta42 fiber formation.

136 ciently reduce neurotoxicity associated with Abeta42 fibril formation both in vitro and in vivo In th

137 and A42 side chains which are exposed on the Abeta42 fibril surface as continuous hydrophobic patches

138 L3.3, giving rise to stronger inhibition of Abeta42 fibrillation and better rescue of behavioral imp

139 on assays, antioxidant assays, and assays of Abeta42 fibrillation.

140 Quiescent Abeta42 fibrils adopt a long and twisted morphology, whi

141 i) selection of scFvs with high affinity for Abeta42 fibrils after removal of scFvs that bind Abeta42

142 Data for Abeta42 fibrils indicate structural heterogeneity in mos

143 esonance (ssNMR) measurements on Abeta40 and Abeta42 fibrils prepared by seeded growth from extracts

144 Here we studied two types of Abeta42 fibrils prepared under quiescent and agitated co

145 At the same time, agitated Abeta42 fibrils show stronger interactions between spin

146 EPR studies of these two types of Abeta42 fibrils show that the secondary structure is sim

147 n Abeta40 fibrils in alternative structures, Abeta42 fibrils, or amyloid fibrils formed from other se

148 e resulting candidate scFvs that bind to the Abeta42 fibrils; and (iii) kinetic screening and analysi

149 th the modified Abeta42-INNOTEST (r = 0.97), Abeta42-FL (r = 0.93), Abeta42-EI (r = 0.93), and Abeta4

150 ter model of AD expressing the Arctic mutant Abeta42 gene.

151 changes of the cytosolic side of TMD4 affect Abeta42-generating gamma-secretase activity.

152 Co-oligomerized Abeta42-hIAPP mixtures displayed distinct amorphous stru

153 r studies, HSV-1-infected 2D cultures showed Abeta42 immunoreactivity in cells expressing the HSV-1 a

154 Specifically, 2D neuronal cultures showed Abeta42-immunoreactivity mainly in HSV-1-infected cells

155 they implicate mechanisms underlying low CSF Abeta42 in Alzheimer's disease pathogenesis and progress

156 Recently, we showed that abnormal levels of Abeta42 in cerebrospinal fluid (CSF) can be detected bef

157 cline induced by extracellular deposition of Abeta42 in Drosophila.

158 Conversely, accumulation of Abeta42 in ICP4+ cells in infected organoids was rarely

159 ly enhance accumulation of aggregation-prone Abeta42 in intracellular acidic compartments.

160 a42 fibrils after removal of scFvs that bind Abeta42 in its monomeric form; (ii) ranking, by surface

161 on average, 28% lower levels of Abeta40 and Abeta42 in plasma as compared to the controls and the ca

162 s already evident in individuals with normal Abeta42 in the CSF and normal amyloid PET who subsequent

163 prove memory performance in flies expressing Abeta42 in the mushroom body neurons, which are intimate

164 s able to remodel the aggregation process of Abeta42 in vitro and to reduce its associated toxicity i

165 the two primary forms of Abeta (Abeta40 and Abeta42) in a primary human cell culture model.

166 sing substantial effects in both Abeta40 and Abeta42 include His14, Gln15, Ala30, Ile31, Met35, and V

167 , Leu17, and Asn 27, whereas sites unique to Abeta42 include Phe20 and Ala21.

168 of the aggregation process of amyloid beta (Abeta42) induce the disruption of lipid bilayers and an

169 support the application of this paradigm of Abeta42-induced memory loss in Drosophila to investigate

170 Furthermore, Abeta42-induced upregulation of the phagolysosomal marke

171 t, expression of human mutant APP in mice or Abeta42 infusion into control diet-fed mice to mimic obe

172 showed higher correlations with the modified Abeta42-INNOTEST (r = 0.97), Abeta42-FL (r = 0.93), Abet

173 (r = 0.95) assays compared with the classic Abeta42-INNOTEST assay (r = 0.88; P </= .01).

174 However, the classic Abeta42-INNOTEST assay showed better concordance with vi

175 The signal in the classic Abeta42-INNOTEST assay was partly quenched by recombinan

176 tivity impact the degradation of Abeta40 and Abeta42 into a common Abeta34 intermediate.

177 a that combined reduction of CSF Abeta40 and Abeta42 is a specific biomarker for vascular amyloid.

178 tion, the aggregation free energy profile of Abeta42 is more downhill, with a computed solubility tha

179 ithin the A2T-bound monomer, while A2V-bound Abeta42 is often enhanced in overall disorder.

180 Nascent Abeta42 is predominantly disordered but samples alpha-he

181 Abeta42 is the principal component of amyloid deposits w

182 The 42-amino-acid beta-amyloid (Abeta42) is a critical causative agent in the pathology

183 42-residue form of the amyloid-beta peptide (Abeta42) is a pivotal event in Alzheimer's disease (AD).

184 A notable reorganization of the Abeta42 landscape is revealed due to hexapeptide associa

185 eta6 hexapeptide binding on the monomeric WT Abeta42 landscape.

186 n adult-onset model of AD, without affecting Abeta42 level.

187 The concordance of CSF Abeta42 levels and Abeta42:Abeta40 and Abeta42:tau ratio

188 biogenesis and synaptic activity and reduces Abeta42 levels and protects AD neurons against Abeta-ind

189 erebrospinal fluid (CSF) p-tau and lower CSF Abeta42 levels in a cohort of human AD patients.

190 educed CD33 mRNA and TBS-soluble Abeta40 and Abeta42 levels in brain extracts.

191 To determine the concordance between CSF Abeta42 levels measured using 5 different immunoassays a

192 Abeta42 levels were significantly reduced in DDQ-treated

193 gth on AD-associated differences in cortical Abeta42 levels, wheel-running activity, and circadian fr

194 y, 3D brain organoids showed accumulation of Abeta42 mainly in non-infected cells surrounding HSV-1-i

195 n by different soluble aggregated species of Abeta42 may contribute to the onset and progression of A

196 The agreement between CSF Abeta42 measures from different immunoassays and visual

197 d by computations of the infrared spectra of Abeta42 model structures, suggesting that the conformati

198 Concurrently, Abeta6-bound Abeta42 monomer exhibits alternative structural features

199 of the N-terminal hexapeptide binding on the Abeta42 monomer structure, which might help in explainin

200 42-FL (r = 0.93), Abeta42-EI (r = 0.93), and Abeta42-MSD (r = 0.95) assays compared with the classic

201 study the aggregation kinetics of the Arctic Abeta42 mutant peptide and its heterogeneous structural

202 Thus, the holdase activity of secHsp70 masks Abeta42 neurotoxicity by promoting the accumulation of n

203 veal, in molecular detail, the mechanisms of Abeta42 oligomer dynamics during amyloid fibril formatio

204 een developed to efficiently eliminate toxic Abeta42 oligomers as a promising treatment strategy for

205 solvent-exposure of hydrophobic residues in Abeta42 oligomers contributes to the different aggregati

206 Picomolar concentrations of Abeta42 oligomers could be observed to induce Ca(2+) inf

207 t originate as oligomers, we found that most Abeta42 oligomers dissociate into their monomeric precur

208 Moreover, the binding of Abeta42 oligomers to beta1-integrin triggers the cofilin

209 avenous opioid usage (P = 0.04), and low CSF Abeta42 (P < 0.01) were independent predictors of postop

210 nd compared with that of CSF core biomarkers Abeta42, P-tau and T-tau.

211 However, in AD cases, Abeta42 pathology might be associated with WML, especial

212 and spermidine significantly correlated with Abeta42 (pearson r = -0.32; P = 0.018).

213 cies populated during the aggregation of the Abeta42 peptide have been identified as potent cytotoxin

214 dividual synthetic vesicles, we show for the Abeta42 peptide implicated in Alzheimer's disease that t

215 Excess of Abeta42 peptide is considered a hallmark of the disease.

216 d (RC) and the [Formula: see text] states of Abeta42 peptide is smaller than that for Abeta40.

217 Here we express the human Abeta42 peptide to assay the neuroprotective effects of

218 ultures causes intracellular accumulation of Abeta42 peptide, but these 2D models do not recapitulate

219 d 2a significantly reduced production of the Abeta42 peptide, when administered (100 mg/kg, twice dai

220 d stability and affinity for the Alzheimer's Abeta42 peptide.

221 aggregation and secondary nucleation of the Abeta42 peptide.

222 y brain accumulation of the amyloid-beta-42 (Abeta42) peptide generated from the amyloid-beta precurs

223 of soluble assemblies of the amyloid-beta42 (Abeta42) peptide.

224 on enhances the levels and assembly of toxic Abeta42 peptides and impairs the self-renewal and neuron

225 We show that this allows Abeta42 peptides to assemble pore-like structures that m

226 ion not just of an increase in the levels of Abeta42 peptides, but to impairments in the self-renewal

227 ly relationships of 76 different Abeta40 and Abeta42 peptides.

228 xhibited low levels of Abeta38, Abeta40, and Abeta42 peptides.

229 the few direct comparisons, beta-amyloid 42 (Abeta42)/phosphorylated tau (p-tau) ratio, total tau (t-

230 Despite comparably low CSF Abeta40 and Abeta42, PiB retention was substantially less in D-CAA t

231 In AD/MCI, lower CSF Abeta42 predicted Abeta deposition and Abeta burden reci

232 In healthy elderly, lower CSF Abeta42 predicted Abeta deposition and reciprocally, Abe

233 Lower CSF Abeta42 predicted an increase in CSF p-tau, and CSF p-ta

234 t hoc models examining cognitive status, CSF Abeta42 predicted Mini Mental State Examination (MMSE) s

235 rmacological reduction of BACE1 activity and Abeta42 prevented and reversed, respectively, these outc

236 PICALM has been implicated in Abeta42 production and turnover, but whether it plays a

237 between the cytosolic sides of TMD4/TMD7 and Abeta42 production levels, suggesting that allosteric co

238 Interestingly, NUCB1 prevents Abeta42 protofibril toxicity in a cellular assay.

239 ns of Abeta40 (r = -0.55, p = 0.021) but not Abeta42 (r = 0.01, p = 0.991).

240 rylated tau (p-tau) ratio, total tau (t-tau)/Abeta42 ratio, and p-tau appeared more accurate than Abe

241 se), we further demonstrate that the Abeta34/Abeta42 ratio, representing Abeta degradation and cortic

242 ides and an increased Abeta38 to Abeta40 and Abeta42 ratio.

243 peptoid nanosheet containing surface-exposed Abeta42-recognizing loops is constructed, and a label-fr

244 Mechanistically, higher Abeta42 reduced endothelial NO synthase (eNOS), cyclic G

245 This lead compound demonstrated robust Abeta42 reductions and subsequent Abeta37 increases in b

246 dues 16-21 and 29-36 that is dominant in the Abeta42 reference ensemble.

247 ngly stabilize the oligomeric structures for Abeta42 relative to Abeta40, and greatly facilitate the

248 ases, result in an increase in the amount of Abeta42 relative to Abeta40.

249 uantitatively the faster aggregation rate of Abeta42 relative to Abeta40.

250 e that overexpression of secreted Abeta40 or Abeta42 resulted in dramatic induction of drusen-like de

251 Lowering Abeta42 reversed the DIO deficit in the eNOS/cGMP/PKG pa

252 e/putrescine) was enhanced by ratio with CSF Abeta42 (ROC > 0.8), and spermidine significantly correl

253 c to study, and we identify sites within the Abeta42 sequence that could be potential targets for the

254 een spin labels across the full range of the Abeta42 sequence, suggesting a more tightly packed struc

255 Mechanistically, we suggest that Abeta42-Ser26 could be a candidate residue for direct or

256 thesized that the addition of mirror-image d-Abeta42 should reduce the concentration of toxic oligome

257 enzyme 1 (BACE-1), gamma-secretase, soluble Abeta42, soluble amyloid precursor protein (sAPP)beta, s

258 population shift in a subset of the original Abeta42 structural sub-populations, including a sevenfol

259 Abeta40 aggregation landscape disappears for Abeta42, suggesting that the Abeta42 tetramer has a more

260 t of implementing the CSF Abeta42:Abeta40 or Abeta42:tau ratios as a biomarker of amyloid deposition

261 f CSF Abeta42 levels and Abeta42:Abeta40 and Abeta42:tau ratios with visual [18F]flutemetamol PET sta

262 assessment when using the Abeta42:Abeta40 or Abeta42:tau ratios.

263 disappears for Abeta42, suggesting that the Abeta42 tetramer has a more diverse structural range.

264 The Abeta42 tetramer unit that formed in the initial simulat

265 (DIO) in mice increased plasma and vascular Abeta42 that correlated with decreased NO bioavailabilit

266 in blocks the autocatalytic proliferation of Abeta42 (the 42-residue form of Abeta) fibrils, fibrilla

267 In contrast to Abeta42, the short Abeta peptides were not toxic and, wh

268 otal tau (T-tau) (AUCs, 0.94; P </= .05), or Abeta42 to phosphorylated tau (P-tau) (AUCs, 0.94-0.95;

269 ng fluorescent-tagged wildtype (WT) and E22G Abeta42 to study the aggregation kinetics of the Arctic

270 (scFv9) and C-terminal (scFv42.2) regions of Abeta42 to suppress the progressive memory decline induc

271 Baseline age, MoCA and UPSIT scores, and CSF Abeta42 to t-tau ratio were associated with MoCA score a

272 ibrillization leads to reduced adsorption of Abeta42 to the nanoparticles increasing the TR-LRET sign

273 beta42:Abeta40 (AUCs, 0.93-0.95; P </= .01), Abeta42 to total tau (T-tau) (AUCs, 0.94; P </= .05), or

274 uctural ensembles of the IDP amyloid-beta42 (Abeta42) to an alternative sequence in which a nitroxide

275 nventory Test (UPSIT) scores, CSF amyloid - (Abeta42) to t-tau ratio, and APOE status were associated

276 taneous overexpression of BRI-Abeta40 or BRI-Abeta42 together resulted in dose-dependent and cumulati

277 PPbeta), Abeta species (Abeta38, Abeta40 and Abeta42), total tau (T-tau), phosphorylated tau, neurofi

278 protein (GFAP), amyloid-beta (Abeta) 40 and Abeta42, total tau (t-tau) and phosphorylated tau (p-tau

279 hese in vivo experiments, we further analyze Abeta42 toxicity and its suppression by PI3K activation

280 rosophila PICALM orthologue lap could rescue Abeta42 toxicity in an adult-onset model of AD, without

281 whether it plays a direct role in modulating Abeta42 toxicity remains unclear.

282 Finally, we show that the Abeta42 toxicity syndrome includes the transcriptional s

283 toxicity and potential modulatory effects on Abeta42 toxicity.

284 These lipoproteins facilitate Abeta42 transport more efficiently than Abeta40, consist

285 regation in three unrelated amyloid species: Abeta42, transthyretin, and human islet amylin polypepti

286 g followed by a decrease of both Abeta40 and Abeta42 upon CAA onset, supporting the idea that combine

287 The mass spectrometry-derived Abeta42 values showed higher correlations with the modif

288 ed chiral mutant library (FCML) of 16 chiral Abeta42 variants, we identified several point D-substitu

289 nhanced fibril formation propensity, racemic Abeta42 was less prone to form soluble oligomers.

290 ur experiments revealed that the assembly of Abeta42 was more sensitive to chiral substitutions than

291 al fluid Abeta40 was reduced at 6 months and Abeta42 was reduced at 12 months in the nilotinib group

292 Levels of CSF Abeta42 were analyzed using the classic INNOTEST and the

293 The amplitude and linear rise of Abeta42 were both associated with turnover (r = -0.38; P

294 erences in extracellular amylin, Abeta40, or Abeta42 were detected, yet only supernatant from VZV-inf

295 e was performed, and kinetics of Abeta40 and Abeta42 were measured.

296 ound that aggregates formed by Arctic mutant Abeta42 were more resistant to intracellular degradation

297 CD81-normalized EDE levels of Abeta40 and Abeta42 were significantly higher in the pAD/MCI with SC

298 es were not toxic and, when coexpressed with Abeta42, were protective in a dose-dependent fashion.

299 tion and greater ability to uptake and clear Abeta42, which is reversed with the active (S3A) but not

300 lations, elucidating preferential binding of Abeta42 with the A2V and A2T hexapeptides compared to WT