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1 s effect is exacerbated with the addition of amyloid beta protein.
2 ole in Alzheimer's disease by generating the amyloid beta protein.
3 d by diffusible oligomeric assemblies of the amyloid beta protein.
4 (LVFFAEDVGSNK), a tryptic fragment from the amyloid beta-protein.
5 ipoprotein E4, amyloid precursor protein and amyloid beta-protein.
6 mbrane protein involved in the production of amyloid beta-protein.
7 aved products, Notch intracellular domain or amyloid-beta protein.
8 ys by which hypoperfusion influenced tau and amyloid-beta proteins.
9 rval: 0.64-0.83) and for cerebrospinal fluid amyloid beta protein 1-42 was 0.685 (95% confidence inte
11 nergy landscapes and relative stabilities of amyloid-beta protein (1-40) in the monomer and all of it
12 abilities of amyloid-beta protein (1-42) and amyloid-beta protein (1-40) in their monomeric and oligo
13 nergy landscapes and relative stabilities of amyloid-beta protein (1-42) and amyloid-beta protein (1-
16 ogical folding and oligomer formation of the amyloid beta-protein (A beta) are widely perceived as ce
20 the beta- and gamma-secretases generate the amyloid beta-protein (A beta), which plays a central rol
22 ing soluble aggregation intermediates of the amyloid-beta protein (A beta), as well as the ongoing gr
23 e 1 transmembrane protein, gives rise to the amyloid beta-protein, a neurotoxic peptide postulated to
25 ng the deposition of amyloidogenic proteins, amyloid beta protein (Abeta) and amylin (islet amyloid p
26 ers involved in Alzheimer's disease (AD) are amyloid beta protein (Abeta) and apolipoprotein E (apoE)
31 (APP695SWE) develop Alzheimer's disease-like amyloid beta protein (Abeta) deposits by 8 to 10 months
32 e progress in defining a pathogenic role for amyloid beta protein (Abeta) in Alzheimer's disease, ora
33 e data support a central pathogenic role for amyloid beta protein (Abeta) in Alzheimer's disease, the
34 acterized by the progressive accumulation of amyloid beta protein (Abeta) in areas of the brain servi
35 the progressive deposition of the 42-residue amyloid beta protein (Abeta) in brain regions serving me
36 uction and clearance of the self-aggregating amyloid beta protein (Abeta) in brain regions serving me
39 (AD) maintains that the accumulation of the amyloid beta protein (Abeta) is a critical event in dise
41 odents suggest that soluble oligomers of the amyloid beta protein (Abeta) may discretely interfere wi
43 ic hallmarks of Alzheimer's disease (AD) are amyloid beta protein (Abeta) plaques and neurofibrillary
44 indings suggest that oligomeric forms of the amyloid beta protein (Abeta) play a critical role in Alz
45 APP at minor Asp(1) site to generate C99 for amyloid beta protein (Abeta) production, and predominant
47 en developed to study the pathophysiology of amyloid beta protein (Abeta) toxicity, which is thought
49 heimer's disease (AD) is the accumulation of amyloid beta protein (Abeta), a small peptide derived fr
51 is associated with elevated brain levels of amyloid beta protein (Abeta), particularly neurotoxic Ab
53 rated that the TNFR1 cascade is required for amyloid beta protein (Abeta)-induced neuronal death.
55 ive stress and the accumulation of fibrillar amyloid beta proteins (Abeta) in senile plaques througho
56 Amyloid fibrils, large ordered aggregates of amyloid beta proteins (Abeta), are clinical hallmarks of
57 c differences in structural dynamics between amyloid beta-protein (Abeta) 40 and Abeta42 appear to un
59 ubstrates of insulin-degrading enzyme (IDE), amyloid beta-protein (Abeta) and insulin, are critically
64 e to suggest that ABri and the AD-associated amyloid beta-protein (Abeta) are molecular equivalents t
66 easing evidence supports the hypothesis that amyloid beta-protein (Abeta) assembly is a key pathogeni
70 ved by Lowe et al. to simultaneously enhance amyloid beta-protein (Abeta) fibrillogenesis and decreas
74 cts of isoflurane on apoptosis are linked to amyloid beta-protein (Abeta) generation and aggregation.
75 loid precursor protein (APP) processing, and amyloid beta-protein (Abeta) generation in H4 human neur
76 the structural and assembly dynamics of the amyloid beta-protein (Abeta) has direct relevance to the
78 esenilin 1 (PS1) decreases the production of amyloid beta-protein (Abeta) identified the presenilins
79 e suggests that the accumulation of cerebral amyloid beta-protein (Abeta) in Alzheimer's disease (AD)
81 ntia that involves progressive deposition of amyloid beta-protein (Abeta) in brain regions important
89 We have recently reported that fibrillar amyloid beta-protein (Abeta) inhibits the proteolytic ac
92 ests that the folding and aggregation of the amyloid beta-protein (Abeta) into oligomers is a key pat
98 cture of the 21-30 fragment of the Alzheimer amyloid beta-protein (Abeta) is investigated by replica-
99 (gamma-secretase) that cleave APP to release amyloid beta-protein (Abeta) is likely to be presenilin.
100 c oligomeric and fibrillar structures by the amyloid beta-protein (Abeta) is linked to Alzheimer's di
103 ented LTP inhibition by soluble oligomers of amyloid beta-protein (Abeta) isolated from AD cortex.
104 port on the plasticity-disrupting effects of amyloid beta-protein (Abeta) isolated from Alzheimer's d
105 (AD) is age-dependent, brain accumulation of amyloid beta-protein (Abeta) leading to Abeta self-assoc
108 The final proteolytic step to generate the amyloid beta-protein (Abeta) of Alzheimer's disease (AD)
110 Strong evidence exists for a central role of amyloid beta-protein (Abeta) oligomers in the pathogenes
112 assay using antibodies that are specific for amyloid beta-protein (Abeta) oligomers with sub-femtomol
115 evidence suggests that soluble assemblies of amyloid beta-protein (Abeta) play an important role in t
117 treating Alzheimer's disease (AD), in which amyloid beta-protein (Abeta) plays a key pathogenic role
118 many type I membrane proteins, including the amyloid beta-protein (Abeta) precursor (APP) and the Not
119 many type I membrane proteins, including the amyloid beta-protein (Abeta) precursor (APP) and the Not
126 euronal cell surface receptor that regulates amyloid beta-protein (Abeta) trafficking into the cell.
130 that oligomers of the 42-residue form of the amyloid beta-protein (Abeta), Abeta42, play a critical r
132 TP) can be inhibited by soluble oligomers of amyloid beta-protein (Abeta), but the synaptic elements
133 in Alzheimer's disease, soluble oligomers of amyloid beta-protein (Abeta), have been complicated by t
134 IDE) in mice causes accumulation of cerebral amyloid beta-protein (Abeta), hyperinsulinemia, and gluc
135 hat a small amphipathic fragment of APP, the amyloid beta-protein (Abeta), self-associates to form so
138 Numerous studies have now shown that the amyloid beta-protein (Abeta), the principal component of
139 the amyloid precursor protein (APP) produces amyloid beta-protein (Abeta), the probable causative age
140 ave been examined primarily as inhibitors of amyloid beta-protein (Abeta), whereas testing of inhibit
151 id fibrils formed from long fragments of the amyloid beta-protein (Abeta-protein), the monomers are a
153 neurodegeneration associated with deposited amyloid-beta protein (Abeta) aggregates in the brains of
155 cides with the accumulation of extracellular amyloid-beta protein (Abeta) and intraneuronal tau aggre
156 ctive in inducing an immune response against amyloid-beta protein (Abeta) and reducing brain Abeta lo
158 dies have determined that fibrillar forms of amyloid-beta protein (Abeta) comprise the characteristic
159 loid hypothesis suggests that the process of amyloid-beta protein (Abeta) fibrillogenesis is responsi
161 ggests water-soluble, non-fibrillar forms of amyloid-beta protein (Abeta) have important roles in Alz
162 able evidence supports a causal role for the amyloid-beta protein (Abeta) in AD, a direct link betwee
169 protein (APP) and its pathogenic by-product amyloid-beta protein (Abeta) play central roles in Alzhe
170 that interaction of CypD with mitochondrial amyloid-beta protein (Abeta) potentiates mitochondrial,
172 de hypothesis," linking self-assembly of the amyloid-beta protein (Abeta) to the pathogenesis of Alzh
174 The final step in the generation of the amyloid-beta protein (Abeta), implicated in the etiology
175 croglia are activated by aggregated forms of amyloid-beta protein (Abeta), usually demonstrated in vi
176 generate various polypeptides, including the amyloid-beta protein (Abeta), which forms amyloid plaque
177 amma-secretases results in generation of the amyloid-beta protein (Abeta), which is characteristicall
181 (ELISA) to measure plasma concentrations of amyloid beta proteins Abeta40 and Abeta42 among 55 adult
182 brils formed by the Arctic variant (E22G) of amyloid-beta protein (Abeta40(ARC)) as well as the effec
184 lower the level of the 42-amino-acid form of amyloid beta protein (Abeta42) in a human H4 cell line.
189 h with CLR01 resulted in a decrease in brain amyloid beta protein aggregates, hyperphosphorylated tau
190 lyphenolic extract can significantly inhibit amyloid beta-protein aggregation into high-molecular-wei
192 embly of the two predominant disease-related amyloid beta-protein alloforms, Abeta40 and Abeta42.
195 f multiple amyloidogenic proteins, including amyloid beta protein and tau, by disrupting key interact
196 caused by toxic oligomers and aggregates of amyloid beta protein and the microtubule-associated prot
198 ecursor protein (APP) processing and affects amyloid beta-protein and APP secretion and APP-c-termina
199 longitudinal MRI; (iii) post-mortem regional amyloid-beta protein and tau associated neurofibrillary
200 opment of in vivo imaging probes targeted to amyloid beta protein, and one agent is already available
201 id membranes promote beta-sheet formation by amyloid beta-proteins, and they suggest a possible role
204 eurons are defective in apoptosis induced by amyloid-beta protein but not by staurosporine or trophic
205 how that BSB binds not only to extracellular amyloid beta protein, but also many intracellular lesion
207 glish and the Tottori, the mutations produce amyloid beta-proteins containing amino acid substitution
208 or protein may be another mechanism by which amyloid beta protein contributes to synapse loss and neu
209 ent transgenic mouse models suggest that the amyloid beta-protein contributes to memory loss in Alzhe
211 n of angiotensin-converting enzyme (ACE), an amyloid-beta protein degrading enzyme, to brain resident
212 ectron microscopy in a preparation of seeded amyloid beta protein fibrils that formed at relatively l
213 ion of peptide self-assembly pathways in the amyloid-beta protein fragment Abeta(25-35) by two amyloi
214 s, such as angiotensin I (Agt I) and [Gln11]-amyloid-beta-protein fragment 1-16 (A beta(1-16)), the o
215 ce gamma-secretase can specifically generate amyloid beta-protein from an APP substrate and similarly
217 in the islet and brain (amyloid derived from amyloid beta protein in the brain in Alzheimer disease a
219 as potential contributory factors, including amyloid beta-protein in Alzheimer's disease, tau in fron
221 ntia, increase cell death, and deposition of amyloid-beta proteins in Alzheimer's disease brains.
222 ate early accumulation and spread of tau and amyloid-beta proteins in the pathological cascade of Alz
223 oxicity induced by the 42-residue isoform of amyloid beta protein, including approximately 80% inhibi
225 ence that a defined molecular species of the amyloid-beta protein interferes with cognitive function.
229 dogenic effects of oxidative lipid damage on amyloid beta proteins is demonstrated and the mechanism
231 gests that the aggregation and deposition of amyloid-beta protein is an initiating event in Alzheimer
232 We applied these methods to a number of the amyloid-beta protein isoforms of Abeta40 and Abeta42 and
233 etase cleavage of the mutant C99 to generate amyloid beta protein, leading to recessively inherited A
236 aptic preservation and reduction in cerebral amyloid-beta protein levels and astrogliosis (P < 0.001
237 airment and a 2-3-fold increase in insoluble amyloid-beta protein levels and deposition in the brain.
238 acellular amyloid deposits and intracellular amyloid beta protein may activate caspases, leading to c
239 nges, taken together with toxic insults from amyloid-beta protein, may underlie the observed neuronal
244 amma-secretase, critical to the formation of amyloid-beta protein, on membrane thickness and lipid co
245 rticularly vulnerable to early deposition of amyloid beta-protein, one of the hallmark pathologies of
247 ionship of APP-CTFgamma to the production of amyloid beta protein peptides is not known, we conclude
250 he familial Alzheimer's disease gene product amyloid beta protein precursor (A beta PP) is sequential
253 eta1-40 or Abeta1-42 in the absence of human amyloid beta protein precursor (APP) overexpression.
254 were then tested in acute dosing studies in amyloid beta protein precursor (APP) transgenic mice, an
255 en shown to influence limited proteolysis of amyloid beta protein precursor (APP), Notch and ErbB4, a
256 ease-causing mutations in the genes encoding amyloid beta protein precursor and presenilins, raising
258 ed increase in the levels of cell-associated amyloid beta-protein precursor (AbetaPP) and cell death.
261 vidence suggests that dysregulated levels of amyloid beta-protein precursor (APP) and its catabolites
262 rous type I membrane proteins, including the amyloid beta-protein precursor (APP) and the Notch recep
263 se A beta is produced from the processing of amyloid beta-protein precursor (APP) by beta- and gamma-
265 idation of the proteolytic processing of the amyloid beta-protein precursor (APP) has revealed that o
266 ated with Alzheimer disease, is derived from amyloid beta-protein precursor (APP) through sequential
269 nal presenilins and cleaves substrates (e.g. amyloid beta-protein precursor and Notch) with very loos
270 I integral membrane proteins, including the amyloid beta-protein precursor and the Notch receptor, a
271 I integral membrane proteins, including the amyloid beta-protein precursor and the Notch receptor.
272 ns of a variety of substrates, including the amyloid beta-protein precursor and the Notch receptor.
274 nd able to produce amyloid beta-peptides and amyloid beta-protein precursor intracellular domain.
275 is of a variety of substrates, including the amyloid beta-protein precursor of Alzheimer's disease an
277 peptide inhibitors and designed to mimic the amyloid beta-protein precursor substrate bind specifical
278 ate the possibility that caspase cleavage of amyloid beta-protein precursor with the generation of C3
279 mice, an AD mouse model overexpressing human amyloid beta-protein precursor with the Swedish double m
280 agulant protein, an aprotinin mutant (6L15), amyloid beta-protein precursor, or tissue factor pathway
283 own to attenuate amyloidogenic processing of amyloid-beta protein precursor (APP) in cell culture stu
284 P) binds to and regulates the translation of amyloid-beta protein precursor (App) mRNA, but the detai
288 99 amino acids, and measured the effects on amyloid-beta protein production and Notch signaling, res
290 loid precursor protein to generate the toxic amyloid beta protein, the major component of plaques in
292 ocytic receptor conferred protection against amyloid beta-protein toxicity in the presence of activat
293 y protects neurons from oxidative stress and amyloid beta-protein toxicity, and conditional deletion
297 se, lactate, pyruvate, glutamate and tau and amyloid-beta proteins, were measured every 1-2 h in the
298 2-nonenal modifies the three His residues in amyloid beta proteins, which increases their membrane af
299 ta-amyloid precursor protein (APP) generates amyloid beta-protein, which can assemble into oligomers
300 ease is a dense plaque composed of fibrillar amyloid beta-proteins with a characteristic and well-ord