ライフサイエンスコーパス: amyloid beta-peptide

1 activity is inhibited in the presence of the amyloid beta peptide.

2 P does not require the generation of AICD or amyloid beta peptide.

3 ioactive peptides, including insulin and the amyloid beta peptide.

4 rs resistance to the proteotoxicity of human amyloid beta peptide.

5 ads to a number of metabolites including the amyloid beta peptide.

6 the proteolytic generation of the neurotoxic amyloid beta-peptide.

7 the precursor by the secretases to generate amyloid beta-peptide.

8 plaques, which are predominantly composed of amyloid-beta peptide.

9 f cross-seeding other TDP-43 peptides and an amyloid-beta peptide.

10 r constituent of these plaques is aggregated amyloid-beta peptide.

11 beta1-42, the most amyloidogenic form of the amyloid-beta peptide.

12 r constituent of these plaques is aggregated amyloid-beta peptide.

13 -catalyzed cleavage of APP to the pathogenic amyloid-beta peptide.

14 ysosomes/lysosomes and reduced intraneuronal amyloid-beta peptide.

15 of neuronal autophagic substrates including amyloid-beta peptide.

16 igned antibody DesAb-Abeta against the human Amyloid-beta peptide.

17 disease characterized by aggregation of the amyloid-beta peptide.

18 ualitatively different IDP ensembles for the amyloid-beta peptide.

19 odegenerative diseases caused by variants in amyloid-beta peptide.

20 Trehalose also reduced the secretion of the amyloid-beta peptide.

21 or, leading to a decreased generation of the amyloid-beta peptide.

22 the position of isoaspartic acid residues in amyloid beta peptides.

23 peptides, including insulin, amylin, and the amyloid beta peptides.

24 ncoding for Neprilysin, the enzyme degrading amyloid beta-peptides.

25 , we measured total tau, phosphorylated tau, amyloid beta peptide 1-42 (Abeta(1-42)), Flt3 ligand, an

26 ilized proteins including oxidized LDL, IgG, amyloid beta peptide 1-42, C4b-binding protein, and fact

27 ele carrier status; plasma concentrations of amyloid beta peptides 1-42 and 1-40 and their ratio (Abe

28 it has been possible to detect underivatized Amyloid-beta peptide 1-40, one of the potential Alzheime

29 The accumulation of amyloid beta peptide(1-42) (Abeta(1-42)) in extracellula

30 acellular amyloid deposition and total brain amyloid-beta peptide 40 and 42 levels, and prevented the

31 romoted the cellular uptake of extracellular amyloid beta peptide 42 (Abeta42) by human neuroblastoma

32 synaptotagmin, and synaptophysin, but not of amyloid beta-peptide 42 or P-T181-tau, were correlated s

33 ntramembrane-cleaving protease that produces amyloid-beta peptide 42 (Abeta42), which is the toxic an

34 s study, we aimed to identify the effects of amyloid-beta peptide 42 (amyloid-beta42) and phosphoryla

35 nimpaired participants (22 with elevated CSF amyloid-beta peptide 42 levels, 15 with elevated CSF pho

36 s, synaptic dysfunction, and accumulation of amyloid beta-peptides (A beta) are major hallmarks of Al

37 In addition, amyloid-beta peptide (A beta) also enhances the dynamin-

38 and without shaking) on the fibrilization of amyloid-beta peptide, a major player in AD pathogenesis.

39 ed long-term depression induced by exogenous amyloid beta peptide Abeta((1-42)).

40 We report the structures of amyloid beta peptide (Abeta(1-40) and Abeta(1-42)) as we

41 In Alzheimer disease (AD), amyloid beta peptide (Abeta) accumulates in plaques in t

42 oglia activated by extracellularly deposited amyloid beta peptide (Abeta) act as a two-edged sword in

43 Intermediate amyloidogenic states along the amyloid beta peptide (Abeta) aggregation pathway have be

44 R by the scrapie prion protein (PrP(Sc)) and amyloid beta peptide (Abeta) and investigated whether an

45 curs early and promotes the disease-defining amyloid beta peptide (Abeta) and Tau pathologies.

46 Massive deposition of amyloid beta peptide (Abeta) as senile plaques in the br

47 not accompanied by altered APP processing or amyloid beta peptide (Abeta) deposition.

48 Accumulating amyloid beta peptide (Abeta) in brain is linked to neuro

49 protein (APP) and accumulation of neurotoxic amyloid beta peptide (Abeta) in the brain is central to

50 (AD) is the accumulation of the APP-derived amyloid beta peptide (Abeta) in the brain.

51 Emerging evidence indicates that amyloid beta peptide (Abeta) initially induces subtle al

52 The aggregation of the amyloid beta peptide (Abeta) into amyloid fibrils is a d

53 The amyloid beta peptide (Abeta) is a key player in the etio

54 The interaction between lipid bilayers and Amyloid beta peptide (Abeta) plays a critical role in pr

55 oid precursor protein (APP) and formation of amyloid beta peptide (Abeta) species.

56 egation of misfolded proteins, including the amyloid beta peptide (Abeta) that is implicated in preec

57 links prefibrillar oligomeric species of the amyloid beta peptide (Abeta) to cellular toxicity in Alz

58 athy (CAA) is characterized by deposition of amyloid beta peptide (Abeta) within walls of cerebral ar

59 plaques are primarily composed of aggregated amyloid beta peptide (Abeta), a proteolytic fragment of

60 tracellular plaques, primarily consisting of amyloid beta peptide (Abeta), in the brain is the confir

61 mall molecules that inhibit the secretion of amyloid beta peptide (Abeta), the major component of Alz

62 beta precursor protein (APP) to release the amyloid beta peptide (Abeta).

63 versus HC subjects and studied the effect of amyloid beta peptide (Abeta, a hallmark of AD pathology)

64 Full-length amyloid beta peptides (Abeta(1-40/42)) form neuritic amy

65 characterized by accumulation of neurotoxic amyloid beta peptides (Abeta) in brain and retina.

66 Our results show that accumulation of amyloid beta peptides (Abeta) leads to Golgi fragmentati

67 AD is characterized by excessive amount of amyloid beta peptides (Abeta), which results in a signif

68 that HSV-1 catalyzes the aggregation of the amyloid beta-peptide (Abeta(42)), a major constituent of

69 In AMD, amyloid beta-peptide (Abeta) accumulates in subretinal d

70 tance, we perform pulling simulations of the amyloid beta-peptide (Abeta) and alpha-synuclein (alphaS

71 restriction worsens memory impairments, and amyloid beta-peptide (Abeta) and pTau accumulations in t

72 Accumulation of amyloid beta-peptide (Abeta) and tau aggregates, possibl

73 thesis that soluble, diffusible forms of the amyloid beta-peptide (Abeta) are pathogenically importan

74 Oligomers formed by the amyloid beta-peptide (Abeta) are pathogens in Alzheimer'

75 Since the identification of the amyloid beta-peptide (Abeta) as the principal toxic enti

76 Pathogenic generation of amyloid beta-peptide (Abeta) by sequential cleavage of b

77 Wild-type, full-length (40- and 42-residue) amyloid beta-peptide (Abeta) fibrils have been shown by

78 Amyloid beta-peptide (Abeta) has a central role in the p

79 ade and peptide-membrane interactions of the amyloid beta-peptide (Abeta) have been implicated as tox

80 Active amyloid beta-peptide (Abeta) immunization of patients wi

81 ptor-related protein-1 (sLRP1) binds ~70% of amyloid beta-peptide (Abeta) in human plasma.

82 ked to the aggregation and deposition of the amyloid beta-peptide (Abeta) in neural tissue.

83 Amyloid beta-peptide (Abeta) pathology is an invariant f

84 lation and BBB breakdown, and to accelerated amyloid beta-peptide (Abeta) pathology, reduced Abeta cl

85 the deposition of beta-sheet-rich, insoluble amyloid beta-peptide (Abeta) plaques; however, plaque bu

86 that GLUT1 deficiency in mice overexpressing amyloid beta-peptide (Abeta) precursor protein leads to

87 ies in advanced phases of development target amyloid beta-peptide (Abeta) production, aggregation, or

88 irst proteolytic cleavage of APP, leading to amyloid beta-peptide (Abeta) production.

89 heimer's disease (AD) are elevated levels of amyloid beta-peptide (Abeta) species generated via amylo

90 In Alzheimer disease, oligomeric amyloid beta-peptide (Abeta) species lead to synapse los

91 athological polymerization of the endogenous amyloid beta-peptide (Abeta) that ultimately forms amylo

92 een recently shown to mediate key actions of amyloid beta-peptide (Abeta) through a dysregulation of

93 taining gamma-secretase complex produces the amyloid beta-peptide (Abeta) through intramembrane prote

94 Amyloid beta-peptide (Abeta), a cleavage product of the

95 amyloid precursor protein (APP) to yield the amyloid beta-peptide (Abeta), a key pathogenic agent in

96 the generation of the Alzheimer disease (AD) amyloid beta-peptide (Abeta), are tightly regulated by t

97 Amyloid beta-peptide (Abeta), found outside neuronal cel

98 imer's disease, characterized by deposits of amyloid beta-peptide (Abeta), is the most common neurode

99 ovascular dysfunction, abnormal elevation of amyloid beta-peptide (Abeta), tau pathology and neuronal

100 ation of an aggregation-prone isoform of the amyloid beta-peptide (Abeta).

101 Constituents of the amyloid beta-peptide (Abeta)42-generating system now are

102 ri2 and pro-SP-C prevent fibril formation of amyloid beta-peptides (Abeta(40) and Abeta(42)) far belo

103 pivotal role in the production of neurotoxic amyloid beta-peptides (Abeta) in Alzheimer disease (AD)

104 pairments may involve aberrant deposition of amyloid beta-peptides (Abeta).

105 of the 42-residue variant of the Alzheimer's amyloid-beta peptide (Abeta(1-42)).

106 gation process of the 42-residue form of the amyloid-beta peptide (Abeta(42)) are key pathogenic agen

107 Amyloid-beta peptide (Abeta) accumulation in the brain i

108 et when the therapeutic strategy is to alter amyloid-beta peptide (Abeta) aggregation in Alzheimer di

109 An early role of amyloid-beta peptide (Abeta) aggregation in Alzheimer's

110 The coaggregation of the amyloid-beta peptide (Abeta) and alpha-synuclein is comm

111 samples for systemic and brain inflammation; amyloid-beta peptide (Abeta) and Ser-202-phosphorylated

112 for SorCS1 in metabolism of the Alzheimer's amyloid-beta peptide (Abeta) and the Abeta precursor pro

113 n hippocampal slices treated with oligomeric amyloid-beta peptide (Abeta) and was shown to restore sy

114 Passive immunization with anti-amyloid-beta peptide (Abeta) antibodies is effective in

115 Proteases that degrade the amyloid-beta peptide (Abeta) are important in protecting

116 ta precursor protein (APP) and generation of amyloid-beta peptide (Abeta) are key events in Alzheimer

117 er's Disease (AD) focuses on accumulation of amyloid-beta peptide (Abeta) as the main culprit for the

118 Increased deposition of amyloid-beta peptide (Abeta) at the cerebral endothelial

119 We report that transgenic mice overproducing amyloid-beta peptide (Abeta) but deficient in CD45 (PSAP

120 The amyloid-beta peptide (Abeta) deposited in plaques in Alz

121 based glutamate sensor imaging, we show that amyloid-beta peptide (Abeta) engages alpha7 nicotinic ac

122 omers, oligomers, and amyloid fibrils of the amyloid-beta peptide (Abeta) has been implicated in the

123 Given that synthetic amyloid-beta peptide (Abeta) has been shown to adopt dis

124 molecular-weight aggregates of the Alzheimer amyloid-beta peptide (Abeta) have attracted increasing i

125 High levels of amyloid-beta peptide (Abeta) have been related to Alzhei

126 The aggregation of amyloid-beta peptide (Abeta) in brain is an early event

127 dy was to investigate the role of endogenous amyloid-beta peptide (Abeta) in healthy brain.

128 aracterized by extracellular accumulation of amyloid-beta peptide (Abeta) in the brain interstitium.

129 Accumulation of amyloid-beta peptide (Abeta) in the brain is regarded as

130 Aggregation of the amyloid-beta peptide (Abeta) in the brain leads to the f

131 ciated with the pathological accumulation of amyloid-beta peptide (Abeta) in the brain.

132 entate gyrus, and the clearance of fibrillar amyloid-beta peptide (Abeta) in the hippocampus.

133 tion cortex and limbic system, deposition of amyloid-beta peptide (Abeta) in the neuropil and around

134 sis, according to which the self-assembly of amyloid-beta peptide (Abeta) is a causative process in A

135 The accumulation of amyloid-beta peptide (Abeta) is associated with AD.

136 Amyloid-beta peptide (Abeta) is believed to play a centr

137 d cascade hypothesis, cerebral deposition of amyloid-beta peptide (Abeta) is critical for Alzheimer's

138 Dyshomeostasis of amyloid-beta peptide (Abeta) is responsible for synaptic

139 Amyloid-beta peptide (Abeta) is the amyloid component of

140 The amyloid hypothesis postulates that amyloid-beta peptide (Abeta) is the causative agent in A

141 Amyloid-beta peptide (Abeta) isoforms of different lengt

142 d pharmacokinetic profiles to reduce central amyloid-beta peptide (Abeta) levels in wild-type rats fo

143 In Alzheimer's disease the amyloid-beta peptide (Abeta) misfolds into neurotoxic ol

144 merous aromatic small molecule modulators of amyloid-beta peptide (Abeta) monomer aggregation and neu

145 ression of IL-4, reduced astro/microgliosis, amyloid-beta peptide (Abeta) oligomerization and deposit

146 The formation of amyloid-beta peptide (Abeta) oligomers at the cellular m

147 Soluble amyloid-beta peptide (Abeta) oligomers have been hypothe

148 We found that amyloid-beta peptide (Abeta) oligomers, synaptotoxins th

149 in old apoE4 TR mice in the absence of human amyloid-beta peptide (Abeta) overexpression, suggesting

150 Amyloid-beta peptide (Abeta) plaque in the brain is the

151 er disease (AD) and synergistic effects with amyloid-beta peptide (Abeta) suggest interactions among

152 t increases APP processing and production of amyloid-beta peptide (Abeta) that is deposited in the br

153 Failure of anti-amyloid-beta peptide (Abeta) therapies against Alzheimer

154 The ability of amyloid-beta peptide (Abeta) to disrupt membrane integri

155 crotubule-associated protein tau may mediate amyloid-beta peptide (Abeta) toxicity by modulating the

156 research have correlated increased levels of amyloid-beta peptide (Abeta) with neuropathological prog

157 The amyloid-beta peptide (Abeta), a key pathogenic factor in

158 on of amyloid plaques, which are composed of amyloid-beta peptide (Abeta), in HIV-infected brains, th

159 eta precursor protein (APP) alpha and -beta, amyloid-beta peptide (Abeta), tau (tau) and inflammatory

160 rstand the structures of oligomers formed by amyloid-beta peptide (Abeta), we have incorporated a key

161 As a model system, we chose amyloid-beta peptide (Abeta), which is implicated in Alz

162 r results show intraneuronal accumulation of amyloid-beta peptide (Abeta)-like, alpha-synuclein-like,

163 leading to the production and deposition of amyloid-beta peptide (Abeta).

164 ration of cholinergic neurons induced by the amyloid-beta peptide (Abeta).

165 he interaction of model lipid membranes with amyloid-beta peptide (Abeta).

166 a common cross-beta-subunit of the Alzheimer Amyloid-beta peptide (Abeta).

167 and regulates APP traffic and processing to amyloid-beta peptide (Abeta).

168 te in the cellular efflux of desmosterol and amyloid-beta peptide (Abeta).

169 small peptides, in particular the mammalian amyloid-beta peptide (Abeta).

170 rized by the pathological aggregation of the amyloid-beta peptide (Abeta).

171 brain and responsible for the production of amyloid-beta peptide (Abeta).

172 species; and suppressing the fibrillation of amyloid-beta peptide (Abeta).

173 Neurotoxic amyloid-beta peptides (Abeta) are major drivers of Alzhe

174 Amyloid-beta peptides (Abeta) assemble into both rigid a

175 ificantly increased the levels of AD-related amyloid-beta peptides (Abeta) both in vitro and in vivo.

176 senilin-1 (PS1(M146V)) display extracellular amyloid-beta peptides (Abeta) deposits and Tau tangles.

177 Accumulation of amyloid-beta peptides (Abeta) in the brain is a common p

178 The deposition of amyloid-beta peptides (Abeta) in the cerebral vasculatur

179 Amylin, a pancreatic peptide, and amyloid-beta peptides (Abeta), a major component of Alzh

180 tigated because its processing generates the amyloid-beta-peptide (Abeta), which is a likely cause of

181 Here we show that the amyloid-beta peptide Abeta1-42 markedly prolongs the ext

182 pe hippocampal slices treated with exogenous amyloid beta peptide (Abeta1-42) and in slices from APP/

183 inogen, oxidized LDL, and native or oxidized amyloid beta-peptide (Abeta1-42).

184 a synergistic toxic interaction between the amyloid-beta peptide (Abeta1-42) and the pro-domains of

185 ngth on the microscopic aggregation rates of amyloid beta peptide (Abeta40) self-association, implica

186 nteractions of the two full-length Alzheimer amyloid beta peptides (Abeta40 and Abeta42) with the ful

187 ibrils formed in vitro by 40- and 42-residue amyloid-beta peptides (Abeta40 and Abeta42) are polymorp

188 Oligomers of the 40 and 42 residue amyloid-beta peptides (Abeta40 and Abeta42) have been im

189 E. coli cells overexpressing the 40-residue amyloid-beta peptide, Abeta40, wild-type and 24 charge m

190 Although soluble species of the amyloid-beta peptide Abeta42 correlate with disease symp

191 To explore the initial stages of amyloid beta peptide (Abeta42) deposition on membranes,

192 esidues 31-42) of the 42-residue form of the amyloid beta peptide (Abeta42), a protein fragment whose

193 he aggregation of the 42-residue form of the amyloid-beta peptide (Abeta42) is a pivotal event in Alz

194 re we study the role of adsorbed Alzheimer's amyloid-beta peptide (Abeta42) on surface-mediated fibri

195 The aggregation of the amyloid beta peptide, Abeta42, implicated in Alzheimer's

196 an even more aggregation-prone peptide (the amyloid-beta peptide, Abeta42, implicated in Alzheimer d

197 cess glutamate, or the dimer/trimer forms of amyloid-beta peptide (Abetad/t), the most synaptotoxic A

198 t to be instigated by toxic oligomers of the amyloid beta peptide (AbetaOs).

199 Soluble oligomers of the amyloid-beta peptide (AbetaOs) are thought to be proxima

200 neuronal impact of soluble oligomers of the amyloid-beta peptide (AbetaOs).

201 The amyloid beta peptide aggregates into amyloid plaques at

202 Amyloid beta peptides also induce a depressive state in

203 ified and characterized marked intraneuronal amyloid-beta peptide/amyloid and lysosomal system pathol

204 Comparison of the binding of an amyloid beta peptide analog to wild-type IDE and to the

205 model, SKN-1A/Nrf1 slows accumulation of the amyloid beta peptide and delays adult-onset cellular dys

206 Extraneuronal plaque comprising mostly the amyloid beta peptide and intraneuronal tangles of hyperp

207 es and differing oligoreactivity directed to amyloid beta peptide and microbial superantigen proteins

208 n proteostasis, influencing clearance of the amyloid beta peptide and phosphorylation of tau, which a

209 n as a receptor for soluble oligomers of the amyloid beta peptide and possibly other toxic protein ag

210 to inhibit accumulation and toxicity of the amyloid-beta peptide and alpha-synuclein.

211 of brain pathologies such as accumulation of amyloid-beta peptide and mitochondrial damage.

212 eurotoxic agent is an oligomeric form of the amyloid-beta peptide and one of the treatment options cu

213 's disease (AD) is accumulation of misfolded amyloid-beta peptides and hyperphosphorylated tau protei

214 irect toxic effects imparted by pathological amyloid-beta peptides and/or through signals derived fro

215 ta40 (the 42- and 40-residue isoforms of the amyloid-beta peptide), and knockdown of PLD3 leads to a

216 phenotype in transgenic models of tauopathy, amyloid beta-peptide, and polyglutamine expansion.

217 100/calgranulins, high-mobility group box-1, amyloid-beta peptide, and beta-sheet fibrils.

218 acts with lipoprotein particles and with the amyloid-beta peptide, and it is associated with increase

219 biological effects of soluble and aggregated Amyloid-beta peptides are difficult to separate in vivo.

220 An improved understanding of the ways that amyloid-beta peptides are formed could help efforts to f

221 Amyloid-beta peptides are proteolytic fragments of the t

222 s containing amyloidogenic peptides from the amyloid-beta peptide associated with Alzheimer's disease

223 Decamers of amyloid beta peptide capable of dimer formation were sel

224 ment of this clearance step, for example, by amyloid beta peptides, causes feedback inhibition of MPP

225 t characterize the kinetic pathways by which amyloid-beta peptides convert from monomers to oligomers

226 Neprilysins in particular are the major amyloid-beta peptide-degrading enzymes.

227 The amyloid beta-peptide deposit found in the brain tissue o

228 lytic complex that may facilitate removal of amyloid beta peptide deposits from the normal brain and

229 The spatial localization of amyloid-beta peptide deposits, the major component of se

230 The age-dependent deposition of amyloid-beta peptides, derived from amyloid precursor pr

231 Soluble oligomeric and aggregated forms of amyloid beta peptides, especially amyloid beta 42, impai

232 egradation of fibrillar forms of Alzheimer's amyloid beta peptide (fAbeta).

233 beta-secretase inhibitors with a fragment of amyloid-beta peptide facilitates entrance into the centr

234 growth of alpha-synuclein from Parkinson and amyloid beta peptide from Alzheimer disease in the prese

235 excising the hydrophobic, aggregation-prone amyloid beta-peptide from the beta-amyloid precursor pro

236 zheimer's disease pathogenesis by regulating amyloid-beta peptide generation.

237 raluminal vesicles of endosomes and enhances amyloid-beta peptide generation.

238 Copper(II) binding to the amyloid-beta peptide has been proposed to be a key event

239 Soluble oligomers of the amyloid-beta peptide have been implicated as proximal ne

240 including the mitochondrial poison rotenone, amyloid beta-peptide, hydrogen peroxide, and high levels

241 yzes the final step in the production of the amyloid beta-peptides implicated in the pathogenesis of

242 rminants of the aggregation mechanism of the amyloid-beta peptide implicated in Alzheimer's disease.

243 The toxic role of amyloid beta peptides in Alzheimer's disease is well doc

244 avage contributes to the generation of toxic amyloid beta peptides in Alzheimer's disease, whereas cl

245 Deposits of amyloid beta peptides in the brains of demented individu

246 etylation contributes to the accumulation of amyloid beta-peptide in Alzheimer's disease and to impai

247 (AD) is to decrease deposition of neurotoxic amyloid beta-peptide in the brain and to boost repair of

248 used to measure the early rise of different amyloid-beta peptides in a mouse model of increasing amy

249 including pathologically elevated levels of amyloid-beta peptides in brain, aberrant neural network

250 ort how relative levels of different soluble amyloid-beta peptides in hippocampus, preceding plaque d

251 loss induced by Alzheimer-related aggregated amyloid-beta peptides in primary neurons.

252 we revealed that nanomolar concentrations of amyloid beta-peptide increased inositol-1,4,5-triphospha

253 e is linked to excessive production of toxic amyloid-beta peptide, initiated by beta-secretase cleava

254 The aberrant aggregation of the amyloid-beta peptide into beta-sheet rich, fibrillar str

255 Aggregation of amyloid-beta peptides into fibrils or other self-assembl

256 The aggregation of amyloid-beta peptides into protein fibres is one of the

257 yloidogenic peptides, such as the well-known amyloid-beta peptide involved in Alzheimer's disease.

258 grading enzyme (IDE) can degrade insulin and amyloid-beta, peptides involved in diabetes and Alzheime

259 dies have suggested that when the 40-residue amyloid beta peptide is encapsulated in a reverse micell

260 The amyloid beta peptide is the major protein constituent of

261 ction between the two internally immobilized amyloid beta peptides is measured by pulling of the teth

262 The amyloid-beta peptide is correlated with Alzheimer's dise

263 Accumulation of amyloid-beta peptides is a dominant feature in the patho

264 and rate-limiting step in the production of amyloid-beta peptides, is an attractive target for the t

265 eating a molecular beacon reporter to detect amyloid-beta peptides, known to be involved in the patho

266 se posits that the excessive accumulation of amyloid-beta peptide leads to neurofibrillary tangles co

267 cleavage of the precursor of the neurotoxic amyloid-beta peptide leads to the secretion of the neuro

268 Non-fibrillar soluble oligomeric forms of amyloid-beta peptide (oAbeta) and tau proteins are likel

269 The binding of amyloid-beta peptides of different concentrations to the

270 hobic residues designed from the Alzheimer's amyloid-beta peptide onto a large beta-sheet protein for

271 The formation of oligomers of the amyloid-beta peptide plays a key role in the onset of Al

272 microglial-mediated uptake of extracellular amyloid-beta peptide pools.

273 ecapitulate human disease phenotypes such as amyloid beta peptide production, hyperphosphorylation of

274 b (a monoclonal antibody targeting misfolded amyloid-beta peptides), revitalizing the "amyloid cascad

275 of gamma-secretase activity to reduce toxic amyloid-beta peptide species is one plausible therapeuti

276 contained more than 10-fold higher levels of amyloid-beta peptide than the most concentrated soluble

277 yloid precursor protein (APP) to produce the amyloid beta peptides that accumulate in Alzheimer's dis

278 nd to a GXXXG repeat motif commonly found in amyloid beta peptides that is necessary for aggregation

279 tracellular domain but not the production of amyloid beta peptides that occurs in endosomal and recyc

280 e disorder that is linked to the presence of amyloid beta-peptides that can form insoluble fibrils or

281 eveloped a fluorescently tagged, optogenetic Amyloid-beta peptide that oligomerizes rapidly in the pr

282 se best known for its role in generating the amyloid-beta peptides that are present in plaques of Alz

283 III PI3 kinase and autophagy in response to amyloid beta peptide, the main pathogenic mediator of Al

284 l factors influencing the aggregation of the amyloid-beta peptide, the islet amyloid polypeptide, alp

285 APP is cleaved by proteases, generating amyloid-beta peptide, the main component of the amyloid

286 ing by secretases to generate the pathogenic amyloid-beta peptide, the major component in Alzheimer p

287 egation, effectively reduces the toxicity of amyloid-beta peptide to cells.

288 esis assays on islet amyloid polypeptide and amyloid-beta peptide to demonstrate why, at experimental

289 be relevant to biological processes such as amyloid-beta peptide toxicity and lipid oxidation.

290 ain O-GlcNAcylation protects against tau and amyloid-beta peptide toxicity.

291 misfolded endogenous proteins and the human amyloid beta peptide trigger activation of proteasome su

292 pathology, reduced abnormal accumulations of amyloid-beta peptide, ubiquitinated proteins and other a

293 gatively charged and hydrophobic Alzheimer's amyloid beta peptide using weak and stringent selections

294 le system (Abeta(16-22), a sequence from the amyloid-beta peptide) was used to examine cross-linking

295 In the third postnatal week, several amyloid-beta peptides were above the limit of detection,

296 tabolism of apolipoprotein E/lipoprotein and amyloid-beta peptide, whether LRP1 also plays a direct r

297 tumour necrosis factor alpha (TNF-alpha) and amyloid beta-peptide, which increase production of ADP-r

298 lzheimer's disease is the aggregation of the amyloid-beta peptide, which was shown to follow differen

299 the enzyme responsible for the formation of amyloid-beta peptides, which have a major role in Alzhei

300 he production and accumulation of neurotoxic amyloid-beta peptides, which is widely considered an ess