ライフサイエンスコーパス: Abeta

1 lux of desmosterol and amyloid-beta peptide (Abeta).

2 wn to be dephosphorylated in the presence of Abeta.

3 tations increased the rate of aggregation of Abeta.

4 n previously implicated in interactions with Abeta.

5 ecretase complex, cleaves betaCTF to produce Abeta.

6 SA), which binds approximately 90% of plasma Abeta.

7 and deficits of axonal transport induced by Abeta.

8 gher age in the subjects without evidence of Abeta.

9 milial AD that produces high brain levels of Abeta.

10 ue to its ability to seed the aggregation of Abeta.

11 n with the differential neurotoxic effect of Abeta(1-40) and Abeta(1-42) in Alzheimer's disease.

12 ce in the channel forming properties between Abeta(1-40) and Abeta(1-42).

13 istinct structural changes occurring in both Abeta(1-40) oligomers and EGCG during remodeling offer a

14 sidues in the Abeta(1-42) isoform but not in Abeta(1-40).

15 a monomers is lower for Abeta(1-42) than for Abeta(1-40).

16 Our findings demonstrate that only Abeta(1-42) contains unique structural features that fac

17 rential neurotoxic effect of Abeta(1-40) and Abeta(1-42) in Alzheimer's disease.

18 ium extend to the C-terminal residues in the Abeta(1-42) isoform but not in Abeta(1-40).

19 HSA affinity of Abeta monomers is lower for Abeta(1-42) than for Abeta(1-40).

20 l forming properties between Abeta(1-40) and Abeta(1-42).

21 tiaggregation activity against amyloid-beta (Abeta)1-42 peptide aggregation.

22 mpared with stability of the dimer formed by Abeta(14-23) hairpin.

23 el beta hairpin structure, consisting of two Abeta(14-23) monomers connected by a turn forming YNGK p

24 rformed with the all-atom MD simulations for Abeta(14-23) peptide shows that surface interactions ind

25 echin-3-gallate (EGCG) on the aggregation of Abeta(17-36) peptides.

26 t cannot inhibit the formation of a U-shaped Abeta(17-36) protofilament.

27 e segments from both Abeta and hIAPP, termed Abeta(24-34) WT and hIAPP(19-29) S20G, with 64% sequence

28 y, and an increase in the ratio of insoluble Abeta 42/40.

29 have been developed to measure beta-amyloid (Abeta) 42 in cerebrospinal fluid (CSF).

30 The amyloid-beta peptide (Abeta), a key pathogenic factor in Alzheimer disease, in

31 gamma-secretase produces multiple species of Abeta: Abeta40, short Abeta peptides (Abeta37-39), and l

32 es 12-28 of Abeta and this binding modulates Abeta accumulation and disease progression.

33 AD-type pathologies related to the Abeta accumulation including tau hyperphosphorylation, n

34 This early pattern of Abeta accumulation is already evident in individuals wit

35 on at baseline was associated with increased Abeta accumulation.

36 results in decreased, rather than increased, Abeta accumulation.

37 and nicotine (NT) can enhance amyloid-beta (Abeta) accumulation in BMEC through Alpha7 nicotinic ace

38 beta-amyloid (Abeta) accumulation in the brain is 1 of 2 pathologic ha

39 Live imaging studies reveal Abeta activates NgRs on the dendritic shaft of neurons,

40 First, all force fields predict that Abeta adopts unfolded structure dominated by turn and ra

41 ocalizing to synapses and binding of soluble Abeta aggregates to synapses requires the expression of

42 could contribute to the neurotoxic effect of Abeta aggregates.

43 Different amyloid beta (Abeta) aggregates can be discriminated by a combinatoria

44 The antagonist activity of 5 toward Abeta aggregation diminishes with sequence and positiona

45 uated the apoE4 pro-fibrillogenic effects on Abeta aggregation in vitro as well as apoE4 potentiation

46 rved that addition of IAPP seeds accelerates Abeta aggregation in vitro in a seeding-like manner and

47 The model accurately predicted Abeta aggregation kinetics at various CatB and CysC conc

48 Abeta, CatB, or CysC concentration, whether Abeta aggregation or degradation will result.

49 uence of biological interfaces in modulating Abeta aggregation pathways.

50 used to track dynamic changes that occur in Abeta aggregation states, which result from the formatio

51 ely predicts the effects of CysC and CatB on Abeta aggregation.

52 whether alpha-synuclein promotes or inhibits Abeta aggregation.

53 lso plays a role in regulating amyloid-beta (Abeta) aggregation and degradation.

54 etin (TTR) is known to inhibit amyloid-beta (Abeta) aggregation in vitro and suppress the Alzheimer's

55 beta-Amyloid (Abeta) aggregation is thought to initiate a cascade of n

56 These findings indicate that polymorphic Abeta-amyloid deposits within the brain cluster as cloud

57 ) ions are especially prone to interact with Abeta and affect its aggregation.

58 The complex interplay between Abeta and alpha-synuclein has led to seemingly contradic

59 such relationship in the association between Abeta and cognitive impairment.

60 model, we show that Abcg4 was able to export Abeta and desmosterol at the BBB level and these process

61 so can inhibit abnormal interactions between Abeta and Drp1 in AD neurons.

62 Interaction between Abeta and Drp1 is reduced in DDQ-treated AD neurons.

63 ng and immunostaining analyses revealed that Abeta and Drp1 levels were reduced in DDQ-treated AD neu

64 develop a therapeutic target that can reduce Abeta and Drp1 levels, and also can inhibit abnormal int

65 stigate the heterotypic interactions between Abeta and fatty acids (FAs) by two independent tool-sets

66 structures of 11-residue segments from both Abeta and hIAPP, termed Abeta(24-34) WT and hIAPP(19-29)

67 structural similarity between aggregates of Abeta and hIAPP.

68 ecedented view of how albumin interacts with Abeta and illustrate the potential of dark-state exchang

69 ely, 5 induces strong secondary structure in Abeta and inhibits its functions including oligomerizati

70 tein and neuronal nitric-oxide synthase, and Abeta and p-Tau(Ser-202) also increased during that time

71 sulted in more effective reductions of brain Abeta and plaque deposits, gliosis, and behavioral memor

72 and MCI, possess effective phagocytosis for Abeta and protect homeostasis of the brain and, furtherm

73 unction and cognitive deficits by triggering Abeta and Tau accumulation through increases in oxidativ

74 d tau imaging, we demonstrate that increased Abeta and tau are both associated with aberrant fMRI act

75 Using in vivo human Abeta and tau imaging, we demonstrate that increased Abe

76 the relationship of the pathological role of Abeta and tau in synapse dysfunction, several questions

77 function, several questions remain as to how Abeta and tau interdependently cause impairments in syna

78 The link between Abeta and tau, however, remains controversial.

79 /Abeta interaction with Abeta12-28 P reduced Abeta and tau-related pathology, leading to cognitive im

80 t to tethered contacts between the monomeric Abeta and the protofibril surface.

81 d-beta (Abeta) peptides at residues 12-28 of Abeta and this binding modulates Abeta accumulation and

82 ulation of protein aggregates; amyloid-beta (Abeta) and tau in the brain during AD, and islet amyloid

83 Accumulation of amyloid beta (Abeta) and tau represent the two major pathological hall

84 ta deposition per year, were assessed across Abeta+ and Abeta- groups.

85 The examination of Abeta- and non-Abeta-derived peptides in complex with he

86 locking Abeta function, by using anti-murine Abeta antibodies or APP knock-out mice, prevents the cGM

87 red for glial recognition and destruction of Abeta are still unclear.

88 roglia in wt mice in vivo Thus, most soluble Abeta assemblies in AD cortex are large and inactive but

89 etry compatible with experimentally observed Abeta assemblies.

90 Abnormal accumulation of Abeta at nerve terminals leads to synaptic pathology and

91 ic cleavage of APP and produce amyloid beta (Abeta) at the expense of sAPPalpha and other non-amyloid

92 ficance of the triangular trimer assembly of Abeta beta-hairpins and may offer a deeper understanding

93 a functional interplay between amyloid beta (Abeta), beta-adrenergic signaling, and altered Ca(2+) si

94 es and genetic ablation of APP prevents both Abeta binding and Abeta-mediated synaptic dysfunctions.

95 Additionally, unbiased docking also showed Abeta binding at this site.

96 participants oversampled for elevated brain Abeta, both the middle (hazard ratio [HR], 2.43; 95% CI,

97 efore estimated symptom onset, higher global Abeta brain burden, and with lower delayed total recall

98 beta = 0.35; 95% CI, 0.19-.52; P < .001) and Abeta burden (beta = 0.24; 95% CI, 0.08-.40; P = .005),

99 To determine if tau pathology influences Abeta burden and to assess prophylactic benefits, 3xTg a

100 Furthermore, Abeta burden was reduced by 84% overall (61% in males an

101 depressed phagocytosis of amyloid-beta1-42 (Abeta) by monocytes and macrophages.

102 omeric, oligomeric, and fibril amyloid-beta (Abeta) by three homologous antibodies (solanezumab, cren

103 ratio can be used to estimate, at any given Abeta, CatB, or CysC concentration, whether Abeta aggreg

104 gested that decreasing CysC would facilitate Abeta clearance by relieving CatB inhibition.

105 These results suggest that CR3 limits Abeta clearance from the ISF, illustrating a novel role

106 xicity of amyloid beta (Abeta) or to promote Abeta clearance.

107 capability at interacting sites of Drp1 and Abeta complex.

108 In contrast, canonical Abeta comprised the minority of the identified proteofor

109 is underway to develop strategies to reduce Abeta concentration or inhibit aggregation.

110 We measured Abeta concentrations and kinetics in 77 adults aged 60 t

111 regation of Abeta probably by modulating the Abeta conformation into a fiber incompetent structure.

112 g soluble and aggregated brain amyloid-beta (Abeta) continues to dominate clinical research in AD, a

113 Whether circulating Abeta contributes to brain AD-type pathologies remains l

114 Compared with their Abeta+ counterparts, all patients with MCI SNAP subtypes

115 on in vitro as well as apoE4 potentiation of Abeta cytotoxicity.

116 teraction between neprilysins and Drosophila Abeta (dAbeta), a cleavage product of APPL.

117 al, we show that the synaptotoxic effects of Abeta depend on expression of APP and that the Abeta-med

118 It is believed that Abeta deposited in the brain originates from the brain t

119 r that renders the aging brain vulnerable to Abeta deposition and the development of AD.

120 However, factors that underlie Abeta deposition are incompletely understood.

121 t with the well-established role of apoE4 in Abeta deposition in AD.

122 ospiraceae and S24-7) and reduction in brain Abeta deposition in aged APPSWE/PS1DeltaE9 mice.

123 e from baseline to 1 and 2 y, and percentage Abeta deposition per year, were assessed across Abeta+ a

124 ke phenotypes in a transgenic mouse model of Abeta deposition.

125 tic pathway has clearly been associated with Abeta deposits and neuronal apoptosis, the critical upst

126 The examination of Abeta- and non-Abeta-derived peptides in complex with heme revealed tha

127 While Pb(IV) ions affected mainly Abeta dimer and trimer formation, hydrophobic toluene ma

128 We observe that FAs influence Abeta dynamics distinctively in three broadly-defined FA

129 ity of Abeta, while dimers strongly suppress Abeta fibril formation.

130 mining region loops can effectively bind the Abeta fibril lateral surface around the same 13-16 regio

131 ction is first-order in the concentration of Abeta fibrils and a pseudo-first-order reaction in the c

132 is mostly likely that the mPPCs disassemble Abeta fibrils through a direct interaction.

133 It is not known exactly where amyloid-beta (Abeta) fibrils begin to accumulate in individuals with A

134 n animals of both sexes showed that blocking Abeta function, by using anti-murine Abeta antibodies or

135 Finally, within the Abeta+ group, increasing levels of flortaucipir tau bind

136 on per year, were assessed across Abeta+ and Abeta- groups.

137 ator of CR3 reduces soluble Abeta levels and Abeta half-life in brain interstitial fluid (ISF), as me

138 These findings indicate that Abeta has a differential effect on hippocampal prolifera

139 ifying specific signaling pathways involving Abeta has allowed for the development of more precise th

140 isease (AD), and the spatial distribution of Abeta has been studied extensively ex vivo.

141 point of view the peroxidase activity of the Abeta-heme complex seemed quite attractive to pursue thi

142 ve shed important new light on how sleep and Abeta homeostasis may be connected in the setting of AD.

143 ivity, we show that the predominant forms of Abeta in aqueous extracts of AD brain are high molecular

144 CHL1) in mouse cerebrospinal fluid (CSF) and Abeta in the mouse brains.

145 regional associations between gait speed and Abeta in the whole sample and the CN subsample.

146 sphorylation, a process that is perturbed by Abeta, in regulating the membrane sorting decision that

147 er this ubiquitin signaling pathway mediates Abeta-induced loss of surface AMPARs is unknown.

148 d that the protective effects of BAY against Abeta-induced memory deficits might involve the regulati

149 ion of Ephexin5 expression critically drives Abeta-induced memory impairment, and strategies aimed at

150 t cofilin activation plays a pivotal role in Abeta-induced mitochondrial and synaptic dysfunction.

151 both enhances Abeta production and mediates Abeta-induced neurotoxicity.

152 arization in the affected brain region after Abeta injection.

153 Conversely, FoxO1 responded to Abeta insult by binding to the Trib3 gene promoter, enha

154 ounds, CPO_Abeta17-21 P, diminished the apoE/Abeta interaction and attenuated the apoE4 pro-fibrillog

155 some TTR stabilizers for modulating the TTR-Abeta interaction have been previously studied.

156 Our Abeta interaction results suggest a molecular rationale

157 transgenic mice lines that blocking the apoE/Abeta interaction with Abeta12-28 P reduced Abeta and ta

158 These HSA-Abeta interactions are isoform-specific, because the HSA

159 The aggregation of the amyloid beta peptide (Abeta) into amyloid fibrils is a defining characteristic

160 Cerebral vessels play a major role in AD, as Abeta is cleared from the brain by pathways involving th

161 Here, we have reported that Abeta is sufficient to acutely promote the production of

162 A key enzyme involved in the generation of Abeta is the beta-secretase BACE, for which powerful inh

163 The amyloid beta peptide (Abeta) is a key player in the etiology of Alzheimer dise

164 Amyloid-beta (Abeta) is thought to play an essential pathogenic role i

165 PP, resulting in the overproduction of toxic Abeta isoforms.

166 ly kinetics, morphology, and toxicity of all Abeta isoforms.

167 etase cleavage of the mutant C99 to generate Abeta, leading to recessively inherited AD.

168 ll molecule modulator of CR3 reduces soluble Abeta levels and Abeta half-life in brain interstitial f

169 uggesting a potential approach of modulating Abeta levels and attenuating synaptic deficits in AD.SIG

170 anisms, here we studied whether cGMP affects Abeta levels and function during LTP.

171 The correlation between CSF Abeta levels and WM-LL suggests a direct link between am

172 sphorylation of PS1 on Ser367 also decreases Abeta levels by increasing betaCTF degradation through a

173 e phosphorylation of PS1 on Ser367 decreases Abeta levels by increasing betaCTF degradation through a

174 ssays revealed significantly reduced soluble Abeta levels in the SS31-treated APP mice relative to th

175 p-regulation of the ALOX5 pathway, increased Abeta levels, tau phosphorylation, and synaptic patholog

176 in the rodent brain, where it rapidly lowers Abeta levels.

177 eriodontitis is related to the amyloid beta (Abeta) load in blood and the role of any such relationsh

178 inhibition of plasticity are associated with Abeta localizing to synapses and binding of soluble Abet

179 These effects are associated with Abeta localizing to synapses and genetic ablation of APP

180 ere we report that Gleevec also achieves its Abeta-lowering effects through an additional cellular me

181 g appreciation that oligomeric amyloid-beta (Abeta) may contribute to cognitive decline of Alzheimer

182 eta depend on expression of APP and that the Abeta-mediated impairment of synaptic plasticity is acco

183 ation of APP prevents both Abeta binding and Abeta-mediated synaptic dysfunctions.

184 se results uncover a novel role for mDia1 in Abeta-mediated synaptotoxicity and demonstrate that inhi

185 a novel role for CR3 and microglia in brain Abeta metabolism and defining a potential new therapeuti

186 lzheimer's disease the amyloid-beta peptide (Abeta) misfolds into neurotoxic oligomers and assembles

187 soform-specific, because the HSA affinity of Abeta monomers is lower for Abeta(1-42) than for Abeta(1

188 30 FDG+, 33 HV+, and 11 FDG+HV+) and 37 were Abeta+N+ (17.7%; 22 FDG+, 26 HV+, and 11 FDG+HV+).

189 3 FDG+, 82 HV+, and 38 FDG+HV+) and 187 were Abeta+N+ (39.9%; 135 FDG+, 147 HV+, and 95 FDG+HV+ cases

190 omarkers did not differ between Abeta-N+ and Abeta+N+ cases.

191 ism (mean [SD] FDG: Abeta-N+, 1.25 [0.11] vs Abeta+N+, 1.19 [0.11]), less severe atrophy of the later

192 nately low APOE epsilon4 (Abeta-N+, 18.7% vs Abeta+N+, 70.6%) and disproportionately high APOE epsilo

193 tion biomarkers; of these patients, 107 were Abeta-N+ (22.8%; 63 FDG+, 82 HV+, and 38 FDG+HV+) and 18

194 rodegeneration biomarkers; of these, 52 were Abeta-N+ (24.9%; 30 FDG+, 33 HV+, and 11 FDG+HV+) and 37

195 generation biomarkers did not differ between Abeta-N+ and Abeta+N+ cases.

196 mporoparietal FDG metabolism (mean [SD] FDG: Abeta-N+, 1.25 [0.11] vs Abeta+N+, 1.19 [0.11]), less se

197 d with disproportionately low APOE epsilon4 (Abeta-N+, 18.7% vs Abeta+N+, 70.6%) and disproportionate

198 rences (Cohen d; Abeta-positive impaired vs. Abeta-negative normal) were evaluated in another phase 2

199 efine T-type calcium channels as a target of Abeta-NgR signaling, mediating Abeta's inhibitory effect

200 We found that Abeta oligomer binding to CNS synaptosomes isolated from

201 Thus, Abeta oligomer elimination by RD2 treatment may be also

202 nd TEM show that 5 effectively inhibits both Abeta oligomerization and fibrillation.

203 ines was screened to identify antagonists of Abeta oligomerization, amyloid formation, and cytotoxici

204 ecognizes structural features common to both Abeta oligomers and fibril ends and that this interactio

205 of evidence suggests that the highly dynamic Abeta oligomers are the main causal agent associated wit

206 ppression of long term potentiation (LTP) by Abeta oligomers was prevented.

207 nt assay confirmed the presence of bona fide Abeta oligomers, whereas immunoprecipitation-Western blo

208 red (NIR) light on synaptic vulnerability to Abeta oligomers.

209 on microscopy to elucidate how EGCG remodels Abeta oligomers.

210 We assessed cerebral Abeta on Pittsburgh Compound B (PiB) positron emission t

211 ent mutants inhibited the adverse effects of Abeta on the surface expression of AMPARs in neurons.

212 , aggregation, and toxicity of amyloid beta (Abeta) or to promote Abeta clearance.

213 Pronounced tau and Abeta pathologies were primarily detected in the subicul

214 te penetrance of AD dementia with respect to Abeta pathology, we hypothesized that factors present in

215 the response of the innate immune system to Abeta pathology.

216 on and turnover rates suggest that day/night Abeta patterns are modulated by both production and clea

217 sence of aberrant deposits containing by the Abeta peptide (amyloid plaques) and the tau protein (neu

218 value of 1.6 x 10(9) M(-1) at pH 7.1 for the Abeta peptide and to a coordination model for the Cu(II)

219 UV-vis competition was performed on the Abeta peptide as well as on a wide series of modified pe

220 resenilin 2) and are accompanied by elevated Abeta peptide levels.

221 ination model for the Cu(II) site within the Abeta peptide that agrees with the one mostly accepted c

222 utic for AD by directly interacting with the Abeta peptide to inhibit Abeta42 fiber formation.

223 er's disease (AD) is the Abeta42 alloform of Abeta peptide, which is dominant in the amyloid plaques

224 , with the Alzheimer's disease amyloid-beta (Abeta) peptide modulates their self-assembly into amyloi

225 es multiple species of Abeta: Abeta40, short Abeta peptides (Abeta37-39), and longer Abeta peptides (

226 hort Abeta peptides (Abeta37-39), and longer Abeta peptides (Abeta42-43).

227 dings, we propose that glia clear neurotoxic Abeta peptides in the AD model Drosophila brain through

228 ection against AD by engulfing extracellular Abeta peptides, but the repertoire of molecules required

229 his dipeptide forms the central motif of the Abeta peptides, which are associated with Alzheimer's di

230 ) lead to production of longer amyloidogenic Abeta peptides.

231 apoE4 in particular, binds to amyloid-beta (Abeta) peptides at residues 12-28 of Abeta and this bind

232 characterized by deposition of amyloid beta (Abeta) peptides into senile plaques in the brain.

233 Aggregation of amyloid beta (Abeta) peptides is a significant event that underpins Al

234 The ability of transthyretin (TTR) to bind Abeta-peptides and the positive effect exerted by some T

235 rmediate M1-M2 phenotype that is optimal for Abeta phagocytosis and the stabilization of cognitive de

236 a-3 mediator, resolvin D1, in vitro increase Abeta phagocytosis by Mvarphis of patients with MCI.

237 kinase RNA-like ER kinase (PERK) expression, Abeta phagocytosis, intermediate M1-M2 Mvarphi type, and

238 s by fish-derived omega-3 emulsion increased Abeta phagocytosis, PERK expression, and UPR RNA signatu

239 al research in AD, a deeper understanding of Abeta physiology has led to the recognition of distinct

240 ved eicosanoids are thought to contribute to Abeta plaque deposition, these 1,5-diarylimidazoles prov

241 brain-derived pathological tau (AD-tau) into Abeta plaque-bearing mouse models that do not overexpres

242 ggregates in dystrophic neurites surrounding Abeta plaques (NP tau), AD-like neurofibrillary tangles

243 characterized by extracellular amyloid-beta (Abeta) plaques and intracellular tau inclusions.

244 ANCE STATEMENT Tau tangles and beta-amyloid (Abeta) plaques are key lesions in Alzheimer's disease (A

245 by the presence of parenchymal amyloid-beta (Abeta) plaques, cerebral amyloid angiopathy (CAA) and ne

246 zheimer's disease (AD) include amyloid-beta (Abeta) plaques, neurofibrillary tangles, and reactive gl

247 Oligomeric Amyloid beta1-42 (Abeta) plays a crucial synaptotoxic role in Alzheimer's

248 Amyloid-beta (Abeta) plays a key role in the pathogenesis of Alzheimer

249 effect sizes for group differences (Cohen d; Abeta-positive impaired vs. Abeta-negative normal) were

250 for cerebral small vessel disease (CSVD) and Abeta-positivity.

251 Processing of amyloid-beta (Abeta) precursor protein (APP) by gamma-secretase produc

252 Abeta preparations were characterized with transmission

253 d that desmosterol antagonized the export of Abeta, presumably as both bind at the sterol-binding sit

254 inhibiting the seed-catalyzed aggregation of Abeta probably by modulating the Abeta conformation into

255 ins of AD and AD mouse models, both enhances Abeta production and mediates Abeta-induced neurotoxicit

256 otein processing and support a model wherein Abeta production is amplified by plaque-induced axonal l

257 These mice exhibit age-related increases in Abeta production, plaque deposition, as well as contextu

258 indings indicate that SS31 treatment reduces Abeta production, reduces mitochondrial dysfunction, mai

259 site to generate C89, resulting in truncated Abeta production.

260 small molecule modulators that would reduce Abeta production.

261 can increase microglia activation and induce Abeta production.

262 te to generate C99 for amyloid beta protein (Abeta) production, and predominantly at major Glu(11) si

263 ts beta secretase activity and amyloid-beta (Abeta) production.

264 e, we used the most disease-relevant form of Abeta, protein isolated from AD brain.

265 To understand the etiology of Abeta proteostasis in AMD, we delivered recombinant aden

266 In both Abeta protofibrils and monomers, HSA targets key Abeta s

267 2D potentiates AD pathology by cross-seeding Abeta, providing a molecular explanation for the link be

268 te the Nogo receptor family (NgR1-3) acts as Abeta receptors mediating an inhibition of synapse assem

269 etylase inhibitor M344 reduces beta-amyloid (Abeta), reduces tau Ser(396) phosphorylation, and decrea

270 CPO_Abeta17-21 P reduced Abeta-related pathology coupled with cognitive improveme

271 Abeta release from and transport across HBMEC were signi

272 s a target of Abeta-NgR signaling, mediating Abeta's inhibitory effects on calcium, synapse assembly,

273 gment, Abeta1-6A2V, which supports a role of Abeta's N-terminal domain in amyloid fibril formation.

274 ith baseline, the composite SUVR increase in Abeta+ scans was significantly larger than in Abeta- sca

275 beta+ scans was significantly larger than in Abeta- scans at 1 y (P = 0.04 [CGM]; P = 0.03 [WCER]) an

276 A key endogenous inhibitor of Abeta self-association is human serum albumin (HSA), whi

277 a protofibrils and monomers, HSA targets key Abeta self-recognition sites spanning the beta strands f

278 c fragment of APP, the amyloid beta-protein (Abeta), self-associates to form soluble aggregates that

279 (A673V), or position 2 of the amyloid-beta (Abeta) sequence.

280 rlies memory decline in old age even without Abeta.SIGNIFICANCE STATEMENT Tau tangles and beta-amyloi

281 inally truncated pyroglutamate (pE)-modified Abeta species (AbetapE3) exhibit enhanced aggregation po

282 Passive immunization using Abeta-specific antibodies has been demonstrated to reduc

283 d florbetapir imaging (to determine amyloid [Abeta] status) at screening and flortaucipir F 18 imagin

284 mune activation in the brain with concurrent Abeta suppression could enhance plaque clearance and cou

285 egenerative disorders, such as amyloid-beta (Abeta), tau, or alpha-synuclein (alphaSyn) might be the

286 s could significantly increase the levels of Abeta, Tau and Ubiquitin C-Terminal Hydrolase L1 (UCHL1)

287 Among the anti-Abeta therapeutic approaches, the most extensively devel

288 distinct neuronal signaling pathways linking Abeta to synaptotoxicity and neurodegeneration and to ne

289 ase, and hyperphosphorylated tau facilitates Abeta toxicity.

290 ioactive components are important drivers of Abeta toxicity.

291 ty lipoprotein, HDL) synergize to facilitate Abeta transport across bioengineered human cerebral vess

292 E4 is less effective than apoE2 in promoting Abeta transport, also consistent with the well-establish

293 in vivo evidence showing that p62 regulates Abeta turnover.

294 g fMRI and subsequent longitudinal change in Abeta using PIB-PET imaging in cognitively normal older

295 Abeta was then exposed to the extracellular face of exci

296 Concentrations of CSF Abeta were assessed using an antibody-independent mass s

297 brogates the deleterious vascular effects of Abeta, whereas wild-type PVM reconstitute the vascular d

298 eneration of distinct conformeric strains of Abeta, which may have profound phenotypic outcomes.

299 otently prevent neuronal network toxicity of Abeta, while dimers strongly suppress Abeta fibril forma

300 In Abeta(+), WM-LL correlated with WM microstructural damag