ライフサイエンスコーパス: beta-amyloid peptide

1 growth factor-beta1 (TGF-beta1), and carries beta-amyloid peptide.

2 such as huntingtin, alpha-synuclein, and the beta-amyloid peptide.

3 inhibit the AChE-induced aggregation of the beta-amyloid peptide.

4 arily of deposits of fibrillar aggregates of beta-amyloid peptide.

5 lockade by noncompetitive inhibitors such as beta-amyloid peptide.

6 suring the affinities of small molecules for beta-amyloid peptide.

7 ge of beta-amyloid precursor protein to form beta-amyloid peptide.

8 inding domain (RBD), which also binds to the beta-amyloid peptide.

9 ing of RBD to domains of the receptor and to beta-amyloid peptide.

10 following hypoxic conditions or exposure of beta-amyloid peptide.

11 f beta-amyloid, resulted in formation of the beta-amyloid peptide.

12 ta-secretase site to initiate the release of beta-amyloid peptide.

13 ta APP) and decreasing that of amyloidogenic beta-amyloid peptide.

14 tau and extracellular plaques formed by the beta-amyloid peptide.

15 senile plaques, whose major component is the beta-amyloid peptide.

16 d cultures of cortical cells challenged with beta-amyloid peptide.

17 tein (APP), which releases Alzheimer disease beta-amyloid peptide.

18 s amyloid precursor protein (APP) to release beta-amyloid peptide.

19 ociated in 4 cases with vascular deposits of beta-amyloid peptide.

20 ed tau protein and extracellular deposits of beta-amyloid peptide.

21 nitiates interactions with lipids, HSPG, and beta amyloid peptides.

22 possessed the capacity to produce or degrade beta-amyloid peptides.

23 t-Leu-Phe, lipoxin A(4), serum amyloid A and beta-amyloid peptides.

24 n that membranes promote self-association of beta-amyloid peptides.

25 tase (BACE1), a key enzyme for generation of beta-amyloid peptides.

26 ure of fibrils formed by various segments of beta-amyloid peptides.

27 e via the production and deposition of toxic beta-amyloid peptides.

28 -normalized NDE levels of usually pathologic beta-amyloid peptide 1-42 (1.6-fold, P < 0.0001), P-T181

29 beta-Amyloid peptide 1-42 (A beta(1-42)) is generated fr

30 The beta-amyloid peptide 1-42 (Abeta), a major constituent o

31 The beta-amyloid peptide 1-42 (Abeta1-42), a major component

32 onstrated by following the fibrillization of beta-amyloid peptide 1-42 (Abeta42) as a function of tim

33 p recordings, characterizing the response to beta-amyloid peptide 1-42 applied at concentrations rang

34 beta-amyloid peptide 1-42 at low concentrations was able

35 In alpha7-expressing oocytes, beta-amyloid peptide 1-42 elicits inward currents at low

36 Expression of the human beta amyloid peptide (A beta) in transgenic Caenorhabdit

37 ase (AD) by increasing the production of the beta amyloid peptide (A beta).

38 beta-amyloid peptide (A beta) and complement-derived mem

39 Deposition of beta-amyloid peptide (A beta) in senile plaques is a hal

40 The deposition of extracellular beta-amyloid peptide (A beta) in the brain is a patholog

41 Alzheimer's beta-amyloid peptide (A beta) is normally present at nan

42 beta-Amyloid peptide (A beta) is the primary constituent

43 beta-Amyloid peptide (A beta) is the primary protein com

44 Elevations in beta-amyloid peptide (A beta) levels after traumatic bra

45 beta-Amyloid peptide (A beta), one of the primary protei

46 ught to determine whether exposure of PBM to beta-amyloid peptide (A beta), the major protein of the

47 beta-Amyloid peptide (A beta), the primary protein compo

48 plaques are predominantly composed of human beta-amyloid peptide (A beta).

49 ily of a 40-43 amino acid peptide, the human beta-amyloid peptide (A beta).

50 g on the cerebrospinal fluid (CSF) levels of beta-amyloid peptide (A, beta-amyloid deposition), phosp

51 tive cascades, including diffuse deposits of beta-amyloid peptides (A beta) in the injured brain.

52 The deposition of beta-amyloid peptides (A beta42 and A beta40) in neuriti

53 tactic peptides, including the 42 aa form of beta amyloid peptide, a causative factor of Alzheimer's

54 east in part, from the neurotoxic effects of beta-amyloid peptides, a set of 39-43 amino acid fragmen

55 lution structures of oligomers formed by the beta-amyloid peptide Abeta are needed to understand the

56 Oligomers of the beta-amyloid peptide Abeta have emerged as important con

57 The assembly of the beta-amyloid peptide Abeta into toxic oligomers plays a

58 re determined by fluorescence titration with beta-amyloid peptide Abeta(1-40) and a fluorescence assa

59 been reported for four peptides derived from beta-amyloid peptide Abeta(1-42): Abeta(1-40), Abeta(10-

60 The 42-aa form of the beta amyloid peptide (Abeta(42)) is implied as a major c

61 d sleep deprivation has been associated with beta amyloid peptide (Abeta) aggregation, which is a maj

62 brain estrogen and early-onset and increased beta amyloid peptide (Abeta) deposition.

63 ein misfolding or amyloid proteopathy of the beta amyloid peptide (Abeta) in Alzheimer's disease (AD)

64 e principal component of amyloid deposits is beta amyloid peptide (Abeta), a peptide derived by prote

65 icity resulting from expression of the human beta amyloid peptide (Abeta).

66 Beta amyloid peptides (Abeta) are known risk factors inv

67 Amyloid fibrils formed by the 40-residue beta-amyloid peptide (Abeta(1-40)) are highly polymorphi

68 esidues 1-9 from the full-length Alzheimer's beta-amyloid peptide (Abeta(1-40)) did not prevent the p

69 ibrils formed by the full-length, 40-residue beta-amyloid peptide (Abeta(1-40)).

70 se events are unclear, but the 42-amino acid beta-amyloid peptide (Abeta(1-42)) is involved.

71 tracellular neuritic plaques composed of the beta-amyloid peptide (Abeta(1-42)).

72 ls from apoptosis induced by incubation with beta-amyloid peptide (Abeta(1-42)).

73 mprised of residues 10-40 of the Alzheimer's beta-amyloid peptide (Abeta(10-40)), prepared under vari

74 pometabolism, mitochondrial dysfunction, and beta-amyloid peptide (Abeta) accumulation are well-chara

75 In AD the beta-amyloid peptide (Abeta) aggregates to form characte

76 t of AChE toward the aggregation of both the beta-amyloid peptide (Abeta) and a prion peptide with a

77 fashion, the mice develop plaques containing beta-amyloid peptide (Abeta) and exhibit neuronal dystro

78 result of the extracellular accumulation of beta-amyloid peptide (Abeta) and intracellular accumulat

79 nts of these two histopathological features, beta-amyloid peptide (Abeta) and tau, respectively, have

80 To determine the stability of beta-amyloid peptide (Abeta) and the glial and neuronal

81 ggregation in two different amyloid systems, beta-amyloid peptide (Abeta) and transthyretin, by these

82 Elevated levels of the beta-amyloid peptide (Abeta) are thought to contribute t

83 The kinetics of amyloid fibril formation by beta-amyloid peptide (Abeta) are typical of a nucleation

84 It has been widely reported that beta-amyloid peptide (Abeta) blocks long-term potentiati

85 the cytotoxicity of the Alzheimer's disease beta-amyloid peptide (Abeta) by remodeling seeding-compe

86 ls of AD, CCEs are found before the onset of beta-amyloid peptide (Abeta) deposition to form senile p

87 s to the onset and/or progression of AD-like beta-amyloid peptide (Abeta) deposits, we studied the lo

88 synapses, has previously been shown to limit beta-amyloid peptide (Abeta) formation in Alzheimer's di

89 Alzheimer's disease, and a putative site of beta-amyloid peptide (Abeta) formation.

90 Spontaneous conversion of beta-amyloid peptide (Abeta) from soluble monomer to ins

91 retase inhibitors which block the release of beta-amyloid peptide (Abeta) has long been an attractive

92 Expression of the human beta-amyloid peptide (Abeta) in a transgenic Caenorhabdi

93 The accumulation of the beta-amyloid peptide (Abeta) in Alzheimer's disease (AD)

94 acterized by the extracellular deposition of beta-amyloid peptide (Abeta) in cerebral plaques and evi

95 ectly observe the aggregation of Alzheimer's beta-amyloid peptide (Abeta) in contact with two model s

96 associate with pathologic deposition of the beta-amyloid peptide (Abeta) in neuritic plaques or in t

97 Accumulation of beta-amyloid peptide (Abeta) in the brain is believed to

98 olocalization of microbial pathogens and the beta-amyloid peptide (Abeta) in the brain of Alzheimer's

99 d by the presence of increased levels of the beta-amyloid peptide (Abeta) in the brain parenchyma and

100 The assembly of the beta-amyloid peptide (Abeta) into amyloid fibrils is ess

101 's disease is characterized by deposition of beta-amyloid peptide (Abeta) into plaques in the brain,

102 Alzheimer's beta-amyloid peptide (Abeta) is a 39- to 43-amino-acid p

103 Since the beta-amyloid peptide (Abeta) is a critical factor in thi

104 Deposition of fibrillar aggregates of the beta-amyloid peptide (Abeta) is a key pathologic feature

105 Immunotherapy against beta-amyloid peptide (Abeta) is a leading therapeutic di

106 The beta-amyloid peptide (Abeta) is a normal product of the

107 The beta-amyloid peptide (Abeta) is directly related to neur

108 beta-amyloid peptide (Abeta) is the primary constituent

109 the rate-limiting step in the production of beta-amyloid peptide (Abeta) is the proteolytric cleavag

110 deficits correlated well with an increase of beta-amyloid peptide (Abeta) level in the mutant hippoca

111 Tissue accumulation of the cytotoxic beta-amyloid peptide (Abeta) occurs in Alzheimer's disea

112 Numerous studies have shown that the beta-amyloid peptide (Abeta) or beta-amyloid deposits im

113 n their soluble form, others, like Alzheimer beta-amyloid peptide (Abeta) or serum amyloid A, must un

114 beta-Amyloid peptide (Abeta) plaques are a cardinal neur

115 zheimer's disease (AD) research is what role beta-amyloid peptide (Abeta) plays in synaptic dysfuncti

116 The applicability of beta-amyloid peptide (Abeta) positron emission tomograph

117 PP) in hippocampal neurons leads to elevated beta-amyloid peptide (Abeta) production and consequent d

118 thium as well as valproic acid (VPA) inhibit beta-amyloid peptide (Abeta) production in HEK293 cells

119 microdomains in Alzheimer disease-associated beta-amyloid peptide (Abeta) production.

120 In Alzheimer's disease, aggregation of the beta-amyloid peptide (Abeta) results in the formation of

121 The assembly of the beta-amyloid peptide (Abeta) to form oligomers and fibri

122 offee extracts can similarly protect against beta-amyloid peptide (Abeta) toxicity in a transgenic Ca

123 tly linked carboxyl-terminal segments of the beta-amyloid peptide (Abeta) were tested for their quali

124 is characterized by the accumulation of the beta-amyloid peptide (Abeta) within the brain along with

125 To determine whether the deposition of the beta-amyloid peptide (Abeta), a key pathological feature

126 ns that specifically interact with the 42-aa beta-amyloid peptide (Abeta), a major constituent of sen

127 The 4-kDa beta-amyloid peptide (Abeta), a principal component of p

128 omposed of a fibrillar insoluble form of the beta-amyloid peptide (Abeta), are found in the hippocamp

129 egeneration and cerebral accumulation of the beta-amyloid peptide (Abeta), but it is unknown what mak

130 /PS1delta, which produce large quantities of beta-amyloid peptide (Abeta), DCP-LA and DHA-CP6 reduced

131 rimarily is composed of the 39-43 amino acid beta-amyloid peptide (Abeta), which forms fibrils of bet

132 at blood clots formed in the presence of the beta-amyloid peptide (Abeta), which has been implicated

133 (AD) is characterized by accumulation of the beta-amyloid peptide (Abeta), which is generated through

134 elevate the Alzheimer's disease (AD) related beta-amyloid peptide (Abeta), which is known to generate

135 (AD) is characterized by accumulation of the beta-amyloid peptide (Abeta), which likely contributes t

136 Beta-amyloid peptide (Abeta), which plays a central role

137 zheimer's disease is thought to be caused by beta-amyloid peptide (Abeta)-dependent synaptic dysfunct

138 of the PI3K pathway leads to rescuing of the beta-amyloid peptide (Abeta)-induced memory loss in the

139 s, or similarly advanced in individuals with beta-amyloid peptide (Abeta)-negative (Abeta-) suspected

140 e of these plaques are fibrillar deposits of beta-amyloid peptide (Abeta).

141 tained in rat PFC slices pretreated with the beta-amyloid peptide (Abeta).

142 itate the cellular uptake and degradation of beta-amyloid peptide (Abeta).

143 om the central and C-terminal regions of the beta-amyloid peptide (Abeta).

144 ave complex effects on the production of the beta-amyloid peptide (Abeta).

145 ers of a family of peptides derived from the beta-amyloid peptide (Abeta).

146 plaques composed of aggregated forms of the beta-amyloid peptide (Abeta).

147 tive against a variety of insults, including beta-amyloid peptide (Abeta); however, the underlying me

148 ques are extracellular deposits of fibrillar beta-amyloid peptide (Abeta); neurofibrillary tangles re

149 Senile plaques formed by beta-amyloid peptides (Abeta) and neurofibrillary tangle

150 deficits, plaque pathology, accumulation of beta-amyloid peptides (Abeta) and oligomers in the brain

151 tracellular plaques consisting of aggregated beta-amyloid peptides (Abeta) and tau protein derived in

152 ly believed to be due to the accumulation of beta-amyloid peptides (Abeta) and their interaction with

153 Alzheimer's disease-associated beta-amyloid peptides (Abeta) are generated by the seque

154 inding kinetics of many of the mAbs with the beta-amyloid peptides (Abeta) are poorly understood.

155 ion and progressive cerebral accumulation of beta-amyloid peptides (Abeta) derived by endoproteolytic

156 Clinical trials targeting beta-amyloid peptides (Abeta) for Alzheimer disease (AD)

157 tia, is characterized by the accumulation of beta-amyloid peptides (Abeta) in senile plaques in the b

158 protein (APP) and to reduce the secretion of beta-amyloid peptides (Abeta) that are associated with A

159 beta-Amyloid peptides (Abeta), derived from proteolytic

160 tein by beta- and gamma-secretases generates beta-amyloid peptides (Abeta), which accumulate in the b

161 is characterized by cerebral accumulation of beta-amyloid peptides (Abeta), which are proteolytically

162 recursor protein (APP) and the generation of beta-amyloid peptides (Abeta).

163 a critical role for PS in the production of beta-amyloid peptides (Abeta).

164 se for initiating the production of neuronal beta-amyloid peptides (Abeta).

165 tudy, we show that the 42 amino acid form of beta amyloid peptide, Abeta(42), is a chemotactic agonis

166 Soluble oligomers of the beta-amyloid peptide, Abeta, are thought to be the synap

167 Oligomers of the beta-amyloid peptide, Abeta, play a central role in the

168 beta-sheet containing residues 16-22 of the beta-amyloid peptide, Abeta.

169 flutemetamol, to the 40-residue Alzheimer's beta-amyloid peptide (Abeta40).

170 APP processing by gamma-secretase produces beta-amyloid peptides (Abeta40 and Abeta42) that accumul

171 generation and accumulation of 40- and 42-aa beta-amyloid peptides (Abeta40/Abeta42) in selectively v

172 tructure and inhibits the aggregation of the beta-Amyloid Peptide Abeta42 and transthyretin.

173 The major components of plaque, beta-amyloid peptides (Abetas), are produced from amyloi

174 beta-Amyloid peptide accumulation in senile plaques in t

175 , but no changes in APP metabolism or Abeta (beta-amyloid peptide) accumulation.

176 We have observed that fibrillar beta-amyloid peptides activate a tyrosine kinase-based s

177 of hippocampal neuronal/glial co-cultures to beta-amyloid peptides activates the glial nicotinamide a

178 Thus, when beta-amyloid peptide activation of alpha7 receptors occu

179 evant to brain oxidative stress accompanying beta-amyloid peptide aggregation, conformationally const

180 Aggregatin as a critical seeding factor for beta-amyloid peptide aggregation.

181 (tg) mice with neuronal expression of human beta-amyloid peptides, alpha-synuclein, or both.

182 Active immunization against the beta-amyloid peptide (Alphabeta) with vaccines or passiv

183 ibodies, we also established the presence of beta-amyloid peptide and abnormally phosphorylated tau p

184 rotein (APP) at a key step in generating the beta-amyloid peptide and presumably causes Alzheimer's d

185 s suggest that BBP is a target of neurotoxic beta-amyloid peptide and provide new insight into the mo

186 ition of extracellular filaments composed of beta-amyloid peptides and intracellular filaments compos

187 xarotene stimulates the clearance of soluble beta-amyloid peptides and results in the reversal of beh

188 strogliosis-inducing stimuli (dibutryl cAMP, beta-amyloid peptide), and (ii) cultures of adult rat hi

189 d-symmetric fibrils formed by the 40-residue beta-amyloid peptide, and for fibrils formed by the yeas

190 ligands exhibiting greater affinity for the beta-amyloid peptide are effective at altering its aggre

191 in which intramyofiber accumulations of the beta-amyloid peptide are pathognomonic.

192 d subsequently gamma-secretase generates the beta-amyloid peptide as well as a cytoplasmic intracellu

193 urements on fibrils formed by the 40-residue beta-amyloid peptide associated with Alzheimer's disease

194 loid fibrils formed by residues 14-23 of the beta-amyloid peptide associated with Alzheimer's disease

195 loid fibrils formed by residues 11-25 of the beta-amyloid peptide associated with Alzheimer's disease

196 of amyloid fibrils formed by the 40-residue beta-amyloid peptide associated with Alzheimer's disease

197 for amyloid fibrils formed by the 40-residue beta-amyloid peptide associated with Alzheimer's disease

198 presenting residues 16-22 of the full-length beta-amyloid peptide associated with Alzheimer's disease

199 for amyloid fibrils formed by the 40-residue beta-amyloid peptide associated with Alzheimer's disease

200 Our approach employs immobilized beta-amyloid peptide at low density to minimize the prob

201 We find that the aggregated beta-amyloid peptide beta AP25-35 opens irreversibly a C

202 by their ability to complex with the tagged beta-amyloid peptide beta AP25-35.

203 ux caused by aggregated, probably fibrillar, beta-amyloid peptides beta AP25-35 and beta AP1-42.

204 The major component of senile plaques is the beta-amyloid peptide (beta A4), which has been shown to

205 ociated with the formation and deposition of beta-amyloid peptide (beta AP) in the brain.

206 f the disease with a gradual increase in the beta-amyloid peptide (beta-AP) concentrations may alter

207 se (AD) is a multifactorial disease in which beta-amyloid peptide (betaAP) plays a critical role.

208 nervous system in AD, dramatically augments beta-amyloid peptide (betaAP)-induced microglial product

209 This report describes a novel beta-amyloid peptide-binding protein (denoted BBP) conta

210 oid precursor protein also resulted in lower beta-amyloid peptide brain levels than controls.

211 unds that block the cellular toxicity of the beta-amyloid peptide, but the relationship between their

212 eurons in Alzheimer's disease is mediated by beta-amyloid peptide by diverse mechanisms, which includ

213 To test whether beta-amyloid peptide can activate alpha7 nicotinic acety

214 Previous work suggests that beta-amyloid peptide can interact with alpha7 nicotinic

215 ing that NO acts at a junction point between beta-amyloid peptides, caspase activation, and tau aggre

216 e demonstrate that neurotoxic agents such as beta-amyloid peptide cause aberrant activation of mitoge

217 In Alzheimer's disease, neurotoxic beta-amyloid peptides cause a deleterious influx of calc

218 ypic defects with a concomitant reduction in beta-amyloid peptide clearly indicate that BACE is an ex

219 that block the production or accumulation of beta-amyloid peptides could benefit a broader spectrum o

220 fragments of the Alzheimer's disease-related beta-amyloid peptide (CuAbeta) show significant oxidativ

221 The beta-amyloid peptide derived from APP is without effect.

222 e inhibitor is composed of residues 15-25 of beta-amyloid peptide, designed to function as the recogn

223 Transgenic flies expressing toxic beta-amyloid peptides develop neurodegeneration.

224 hypothesis that the oligomers formed by the beta-amyloid peptide early in its aggregation process ar

225 ischemic or hypoxic episode, with levels of beta-amyloid peptides elevated in brains from patients.

226 rotein (APP), thus modulating the APP-Abeta (beta-amyloid peptide) environment.

227 he neurotoxic species is challenging because beta-amyloid peptides form oligomers at very low physiol

228 hippocampal neuronal cultures with 10(-5) M beta-amyloid peptide fragment 25-35 (A beta P) for 24 h

229 eus (LC) one week following the injection of beta-amyloid peptide fragment 25-35 (beta (25-35)) into

230 in the cholinergic system, and deposition of beta-amyloid peptides generated by proteolytic processin

231 e with the generation of toxic aggregates of beta-amyloid peptides have been shown to rescue the flie

232 loid precursor protein to produce neurotoxic beta-amyloid peptides (i.e. Abeta42) that have been impl

233 We sought to determine whether abnormal beta-amyloid peptides impair REMS and injure mesopontine

234 The deposition of the beta amyloid peptide in neuritic plaques and cerebral bl

235 e (AD) is characterized by overproduction of beta amyloid peptides in the brain with progressive loss

236 artic protease involved in the production of beta-amyloid peptide in Alzheimer's disease and is a maj

237 disease, up-regulation and association with beta-amyloid peptide in Alzheimer's disease).

238 olinergic signaling, and the accumulation of beta-amyloid peptide in neuritic plaques.

239 The BBP subtype bound human beta-amyloid peptide in vitro with high affinity and spe

240 It is crucial to determine the structures of beta-amyloid peptides in a membrane to provide a molecul

241 eimer's disease (AD) is the overabundance of beta-amyloid peptides in brain fluids, leading to the fo

242 es and demonstrated significant reduction of beta-amyloid peptides in mouse brain following oral dosi

243 contributes to the accumulation of insoluble beta-amyloid peptides in plaques.

244 t exposure may contribute to accumulation of beta-amyloid peptides in the brain fluids, leading to AD

245 Excessive accumulation of beta-amyloid peptides in the brain is a major cause for

246 There were exceptionally high levels of beta-amyloid peptides in the plasma (approximately 17 ti

247 despite extremely high levels of circulating beta-amyloid peptides in the transgenic mice, the result

248 The compound is less effective against the beta-amyloid peptide, indicating specificity in its abil

249 al circuitry in determining the magnitude of beta-amyloid peptide induced cell death in the highly vu

250 onatine, and the agonist 4-OH-GTS-21 blocked beta-amyloid peptide-induced receptor activation.

251 oid precursor protein (APP) and its product, beta-amyloid peptide, initiate pathological changes befo

252 re ascribed to extracellular accumulation of beta-amyloid peptides into plaques.

253 ces neuron viability in an in vitro model of beta-amyloid peptide intoxication, and presents positive

254 tase enzyme that initiates production of the beta-amyloid peptide involved in Alzheimer disease.

255 The pathological beta-amyloid peptide, involved in Alzheimer's disease, d

256 The beta-amyloid peptide is a cleavage product of the amyloi

257 The extracellular accumulation of beta-amyloid peptide is a key trigger in the pathogenesi

258 Alzheimer disease-associated beta-amyloid peptide is generated from its precursor pro

259 beta-Amyloid peptide is the major protein component of A

260 Similarly, when beta-amyloid peptide is used to stimulate cultured prima

261 bral cortex of cKO mice, while generation of beta-amyloid peptides is reduced.

262 Abeta (beta-amyloid peptide) is an important contributor to Alz

263 beta-amyloid precursor protein, and secreted beta-amyloid peptide levels were reduced without affecti

264 ein Swedish mutant mouse increased insoluble beta-amyloid peptide levels, neuronal degeneration, casp

265 Without decreasing beta-amyloid peptide load in the brain, alpha-MSH improv

266 ApoE also interacts with beta amyloid peptide, manifests critical isoform-specifi

267 beta-Amyloid peptides may contribute to the development

268 ssed sensitivity of human Ntera-2 neurons to beta-amyloid peptide mediated toxicity.

269 urements on fibrils formed by the 40-residue beta-amyloid peptide of Alzheimer's disease (Abeta(1-40)

270 ells were challenged with toxic oligomers of beta-amyloid peptide or hydrogen peroxide.

271 A naturally occurring derivative of the beta-amyloid peptide, p3, possesses all of the structura

272 TgCRND8 mice with established beta-amyloid peptide pathology and nontransgenic litterm

273 r the aggregation-disintegration behavior of beta-amyloid peptide plaques in the presence of static a

274 myloid precursor protein (APP) generates the beta-amyloid peptide, postulated to participate in the n

275 llular deposition in the brain of aggregated beta-amyloid peptide, presumed to play a pathogenic role

276 beta-Amyloid peptide produces apoptosis in neurons at mi

277 s, leading to Alzheimer's disease-associated beta-amyloid peptide production by cleavage near the mid

278 beta-Amyloid peptides promoted aggregation of alpha-synu

279 itotoxicity (N-methyl d-aspartate), with the beta amyloid peptide (putative cytotoxin in Alzheimer's

280 nother protein yielded a approximately 4-kDa beta-amyloid peptide, reflecting a loose residue specifi

281 Synaptic activity has been shown to induce beta-amyloid peptide release into the extracellular spac

282 umulation of the cytotoxic 40- to 42-residue beta-amyloid peptide represents the primary pathological

283 onformation and aggregation of the synthetic beta-amyloid peptide, residues 1-40 (betaA4), as a funct

284 d to stably express p75NTR, we find that the beta-amyloid peptide specifically binds the p75NTR.

285 e show here that nanomolar concentrations of beta-amyloid peptides specifically and reversibly block

286 a major constituent of plaques is the 4 kDa beta-amyloid peptide, synthetic Abeta1-40 was incubated

287 similar morphology formed by the 40-residue beta-amyloid peptide that is associated with Alzheimer's

288 ) was originally identified as the source of beta-amyloid peptides that accumulate in Alzheimer's dis

289 induction of Tau phosphorylation by APP and beta-amyloid peptide, the functional connection between

290 .11) has been implicated in the clearance of beta amyloid peptides through hydrolytic cleavage.

291 e induced caspase-dependent vulnerability to beta-amyloid peptide toxicity.

292 o combat the neurotoxic effect of aggregated beta-amyloid peptides, we have devised a series of very

293 IgG rather than IgM, in addition to binding beta-amyloid peptide, whereas the MBP-ghC showed a prefe

294 be cleaved by a beta-secretase to generate a beta-amyloid peptide, which has been implicated in the p

295 A major plaque component is the beta-amyloid peptide, which is a cleavage product of the

296 ological levels of apoE protected cells from beta-amyloid peptides, while higher doses of apoE led to

297 Interactions of beta-amyloid peptides with an elevated level of their no

298 osits of fibrils formed by 39- to 43-residue beta-amyloid peptides with possible neurotoxic effects.