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

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

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

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

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

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

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

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

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

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

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

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

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

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

21 e via the production and deposition of toxic 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 beta-Amyloid peptide 1-42 (A beta(1-42)) is generated fr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 beta-Amyloid peptide accumulation in senile plaques in t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

251 beta-Amyloid peptides may contribute to the development

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

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

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

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

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

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

258 beta-Amyloid peptide produces apoptosis in neurons at mi

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

260 beta-Amyloid peptides promoted aggregation of alpha-synu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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