ライフサイエンスコーパス: amyloid beta-peptide

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

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

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

4 , intracellular accumulation and toxicity of amyloid beta peptide.

5 activity is inhibited in the presence of 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 (APP) during the neuronal production of the amyloid beta-peptide.

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

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

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

12 igned antibody DesAb-Abeta against the human 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 poptotic ligands pro-nerve growth factor and amyloid-beta peptide.

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

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

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

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

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

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

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

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

25 ils of the Alzheimer's disease Abeta(16-22) (amyloid beta) peptide.

26 detergents or fatty acids in preparations of amyloid beta-peptides.

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

28 brane adhesion protein and the progenitor of amyloid-beta peptides.

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

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

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

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

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

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

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

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

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

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

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

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

41 The amyloid-beta peptide Abeta(42) has been implicated in th

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

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

44 Neurotoxic amyloid beta peptide (Abeta) accumulates in the brains o

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

62 Accumulation of extracellular amyloid beta peptide (Abeta), generated from amyloid pre

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

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

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

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

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

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

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

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

71 to be caused by the neurotoxic effect of the Amyloid beta peptides (Abeta).

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

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

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

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

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

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

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

79 Toxic forms of amyloid beta-peptide (Abeta) can induce Ca(2+) influx in

80 Apoe(-/-) mice: there was significantly less amyloid beta-peptide (Abeta) deposition, a redistributio

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

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

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

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

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

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

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

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

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

90 Genetic alterations of amyloid beta-peptide (Abeta) production caused by mutati

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

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

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

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

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

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

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

98 Production of the amyloid beta-peptide (Abeta) via sequential proteolytic

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

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

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

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

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

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

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

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

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

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

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

110 Amyloid-beta peptide (Abeta(42)) has been implicated in

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

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

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

114 zheimer's disease patients directly bound to amyloid-beta peptide (Abeta) and are linked to the neuro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 f Alzheimer's disease is the accumulation of amyloid-beta peptide (Abeta) in the brain both in the fo

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

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

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

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

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

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

138 athologically characterized by deposition of amyloid-beta peptide (Abeta) into beta-amyloid plaques,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

153 The effects of amyloid-beta peptide (Abeta) on astrocyte responses to a

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

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

156 The amyloid-beta peptide (Abeta) plays a central pathophysio

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

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

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

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

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

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

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

164 Recent evidence suggests that amyloid-beta peptide (Abeta), the same peptide found in

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

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

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

168 Microglia are critical for amyloid-beta peptide (Abeta)-mediated neuronal perturbat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

184 proposed to cause AD by elevating levels of amyloid-beta peptides (Abeta), which are thought to be n

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

204 The amyloid beta peptide aggregates into amyloid plaques at

205 Amyloid beta peptides also induce a depressive state in

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

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

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

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

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

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

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

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

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

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

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

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

218 100/calgranulins, high-mobility group box-1, amyloid-beta peptide, and beta-sheet fibrils.

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

220 Amyloid beta peptides are the major components of the va

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

222 Amyloid-beta peptides are proteolytic fragments of the t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

237 steady-state levels of BACE1 and the rate of amyloid beta-peptide generation.

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

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

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

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

242 f presenilin activity and/or accumulation of amyloid-beta peptides have been proposed to mediate the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

263 The amyloid beta peptide is the major protein constituent of

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

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

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

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

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

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

270 umulation of insoluble plaque containing the amyloid-beta peptide of 40-42 amino acid residues.

271 In vitro, copper binds to the amyloid-beta peptide of AD, and in vivo, copper is assoc

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

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

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

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

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

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

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

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

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

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

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

283 r protein (APP) leading to the generation of amyloid-beta peptides that is central to the pathogenesi

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

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 sforming growth factor beta2 rapidly targets amyloid beta peptide to the lysosomal compartment in cor

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

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

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

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

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 ve peptide substrates, including insulin and amyloid-beta, peptides vital to the development of diabe

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

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

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

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

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

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