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1 model of AD; Tg19959 mice express the human amyloid precursor gene (APP) with 2 familial AD mutation
2 pidly detecting small molecules that bind to amyloid precursors, identifying the interacting protein
6 human Kunitz protease inhibitor domains from amyloid precursor-like protein 2 (APLP2), bikunin, hepat
9 kidney cells bearing the Swedish mutation of amyloid precursor protein (APP(sw) HEK cells) as a cellu
10 set Alzheimer's disease-causing mutations in amyloid precursor protein (APP(Swe)) and presenilin 1 (P
11 owed significant amounts of beta-amyloid and amyloid precursor protein (APP) aggregates in the cortex
15 eavage product of the ubiquitously expressed amyloid precursor protein (APP) and is able to self-asso
20 ha-, beta-, and gamma-secretases, cleave the amyloid precursor protein (APP) and modulate beta-amyloi
21 uitin aggregates and increased expression of amyloid precursor protein (APP) and phosphorylated tau (
23 ysosomal cysteine protease that cleaves both amyloid precursor protein (APP) and tau, mediating the a
25 beta due to a change in the approximation of amyloid precursor protein (APP) and the beta-site APP cl
26 l invasion and colonization by destabilizing amyloid precursor protein (APP) and ZNF395 transcripts,
27 Overexpression and/or abnormal cleavage of amyloid precursor protein (APP) are linked to Alzheimer'
28 es whether C-terminal fragments (CTF) of the amyloid precursor protein (APP) are present in cerebrosp
29 ally neurotoxic Abeta fragments derived from amyloid precursor protein (APP) at synapses may be a key
31 generated during sequential cleavage of the amyloid precursor protein (APP) by beta- and gamma-secre
32 ta (Abeta) peptide, derived from cleavage of amyloid precursor protein (APP) by beta- and gamma-secre
33 and are formed by sequential cleavage of the amyloid precursor protein (APP) by beta-secretase (BACE)
34 eta is generated by a sequential cleavage of amyloid precursor protein (APP) by beta-secretase 1 (BAC
35 ides derived from sequential cleavage of the amyloid precursor protein (APP) by beta-site APP cleavin
36 tion of Abeta peptide from the processing of amyloid precursor protein (APP) by clipping enzymes (bet
37 ovel regulation of proteolytic processing of amyloid precursor protein (APP) by DISC1, a major risk f
42 dels of Alzheimer's disease suggest that the amyloid precursor protein (APP) can cause changes in syn
44 APP/PS1 Tg mice, the critical molecules for amyloid precursor protein (APP) cleavage and signaling p
45 icits in AD.SIGNIFICANCE STATEMENT beta-Site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1
50 d beta-peptide (Abeta) species generated via amyloid precursor protein (APP) endoproteolysis and clea
51 reviously that the Alzheimer-associated beta-amyloid precursor protein (APP) facilitates neuronal iro
54 EG recordings in tet-off mice overexpressing amyloid precursor protein (APP) from birth display frequ
61 ng evidence suggests that the copper-binding amyloid precursor protein (APP) has an essential synapti
62 Activation of nonamyloidogenic processing of amyloid precursor protein (APP) has been hypothesized to
63 p family proteins.SIGNIFICANCE STATEMENT The amyloid precursor protein (App) has been intensively stu
67 ion of amyloid-beta (Abeta) derived from the amyloid precursor protein (APP) in the brain is thought
68 yloid beta (Abeta) peptides originating from amyloid precursor protein (APP) in the endosomal-lysosom
69 ecretase (BACE1) initiates processing of the amyloid precursor protein (APP) into Abeta peptides, whi
70 retase is responsible for the proteolysis of amyloid precursor protein (APP) into short, aggregation-
71 a growing body of evidence suggests that the amyloid precursor protein (APP) intracellular C-terminal
73 retase component, the enzyme responsible for amyloid precursor protein (APP) intramembraneous cleavag
78 associated with Alzheimer disease (AD), the amyloid precursor protein (APP) is cleaved by beta-secre
79 Here, we reveal that the membrane-associated amyloid precursor protein (APP) is highly expressed in m
82 nce of earlier complications occurring while amyloid precursor protein (APP) is trafficking through t
83 nked mutations in Presenilins (PSEN) and the amyloid precursor protein (APP) lead to production of lo
85 ACH) and presenilin (PSH) hypotheses and the amyloid precursor protein (APP) matrix approach (AMA), o
89 beta-secretase 1 (BACE-1) and BACE-1-cleaved amyloid precursor protein (APP) metabolites (secreted AP
92 death: 50.0 +/- 8.6 years) with mutations in amyloid precursor protein (APP) or presenilin 1 (PSEN1),
95 ly involvement of endosomes and lysosomes in amyloid precursor protein (APP) processing and clearance
96 D) as it results directly in the decrease of amyloid precursor protein (APP) processing through the b
97 of APOE varepsilon3/4 allele exhibit altered amyloid precursor protein (APP) processing, abnormally i
100 and Abeta42 secretion, and the amount of the amyloid precursor protein (APP) secreted at the cell sur
102 mplicated a pathway involving binding of the Amyloid Precursor Protein (APP) to Death Receptor 6 (DR6
103 enic mouse model expressing a mutant form of amyloid precursor protein (APP) to distinguish the impac
104 ns of alpha-syn-containing preparations into amyloid precursor protein (APP) transgenic mice (express
105 hat Abeta pathology and neuroinflammation in amyloid precursor protein (APP) transgenic mice are wors
109 ng studies revealed that the dynamics of the amyloid precursor protein (APP) were significantly impai
110 in, and scyllo-inositol, in cells expressing amyloid precursor protein (APP) with the Osaka (E693Delt
113 in 4 (CNTN4) or one of its binding partners, amyloid precursor protein (APP), a subset of direction-s
114 transport of the Alzheimer's disease-related amyloid precursor protein (APP), although neuronal morph
115 nerated by the proteolytic processing of the amyloid precursor protein (APP), and alterations to this
116 laques resulting from abnormal processing of amyloid precursor protein (APP), and presence of neurofi
117 eferring to an interaction between DISC1 and amyloid precursor protein (APP), and to an association o
119 a-peptide (Abeta), a cleavage product of the amyloid precursor protein (APP), exerts detrimental effe
120 erated through sequential proteolysis of the amyloid precursor protein (APP), first by the action of
121 oid-beta generation from its precursor, beta-amyloid precursor protein (APP), in a competitive manner
122 tide, a metabolite of sequential cleavage of amyloid precursor protein (APP), is a critical step in t
123 ition of amyloid-beta peptides, derived from amyloid precursor protein (APP), is a neuropathological
124 proteins linked to familial AD (FAD), mutant amyloid precursor protein (APP), or APP and presenilin (
125 eta), derived from proteolytic processing of amyloid precursor protein (APP), play a central role in
126 and fully penetrant pathogenic mutations in amyloid precursor protein (APP), presenilin 1 and 2 (PSE
129 ) peptide because of increased processing of amyloid precursor protein (APP), resulting in loss of sy
130 Missense mutations in alanine 673 of the amyloid precursor protein (APP), which corresponds to th
131 ilar to that of transgenic mice that express amyloid precursor protein (APP), which is duplicated in
132 tween these conditions may be constituted by amyloid precursor protein (APP), which plays a pivotal r
133 idue protein produced by the cleavage of the amyloid precursor protein (APP), which subsequently aggr
138 udies implicate death receptor 6 (DR6) in an amyloid precursor protein (APP)-dependent pathway regula
150 Here, we examined the impact of CXCR3 in the amyloid precursor protein (APP)/presenilin 1 (PS1) trans
151 ne beta-hydroxylase (DBH) knockout mice with amyloid precursor protein (APP)/presenilin-1 (PS1) mice
153 well as an Alzheimer's disease mouse model, amyloid precursor protein (APP)/PSEN1dE9(+/-) (PS1) that
155 TgF344-AD) expressing disease-causing mutant amyloid precursor protein (APPsw) and presenilin-1 (PS1D
156 criptomic changes in control and mutant beta-amyloid precursor protein (APPSw,Ind) transgenic mice du
157 SY5Y neuroblastoma cells expressing the beta-amyloid precursor protein (betaAPP) harboring the famili
158 The 99 amino acid C-terminal fragment of amyloid precursor protein (C99), consisting of a single
159 ocampal neurons and in mice expressing human amyloid precursor protein (hAPP mice), a model for famil
160 compared transgenic mice that express human amyloid precursor protein (hAPP) and patients with mild
161 humans with AD, aging mice expressing human amyloid precursor protein (hAPP) showed increased levels
162 cking in the axon of AD-related mutant human amyloid precursor protein (hAPP) transgenic (Tg) mouse n
163 e mortality and network dysfunction in human amyloid precursor protein (hAPP) transgenic mice, which
166 he AD mouse model carrying human mutation of amyloid precursor protein (mhAPP) expressing human Abeta
167 Here, we have uncovered a role for soluble amyloid precursor protein (sAPP) as a vascular niche sig
168 soluble metabolites alpha and beta (soluble amyloid precursor protein (sAPP)alpha, sAPPbeta) and two
169 ), gamma-secretase, soluble Abeta42, soluble amyloid precursor protein (sAPP)beta, sAPPalpha, glial-d
171 (+/-)) in a mouse model of familial AD (FAD; amyloid precursor protein [APP]/presenilin 1 [PS1]) amel
172 odel of AD (transgenic mice expressing human amyloid precursor protein [hAPP]) and patients in the ea
173 hese observations, anterogradely transported amyloid precursor protein accumulated in ligated sciatic
174 ion on transmembrane proteins other than the amyloid precursor protein affects the nervous system is
178 C-terminal domain (residues 672-770) of the amyloid precursor protein and is the immediate precursor
179 Alzheimer's disease we used a double mutant amyloid precursor protein and presenilin 1 (APPswe/PSEN1
180 Here we report that FAD mutations in beta-amyloid precursor protein and presenilin 1 are able to i
181 expression of human familial AD mutations in amyloid precursor protein and presenilin 1 leads to sens
182 nd transgenic APPPS1 mice (overexpression of amyloid precursor protein and presenilin 1 with Swedish
183 r's disease (AD), mice overexpressing mutant amyloid precursor protein and presenilin-1 (APP/PS1) wer
184 numerous proteins besides ApoER2, including amyloid precursor protein and the synaptic adaptor prote
185 at initiates amyloidogenic processing of the amyloid precursor protein and which is a substrate for t
186 Abeta43, a product of the proteolysis of the amyloid precursor protein APP, is related to Abeta42 by
187 known that mutations in the gene coding for amyloid precursor protein are responsible for autosomal
188 transmembrane aspartyl protease that cleaves amyloid precursor protein at the beta-secretase site to
189 hemistry; white matter showed Abeta and beta-amyloid precursor protein by immunocytochemistry, but no
190 accompanied by a decrease in BACE1-mediated amyloid precursor protein cleavage and amyloid-beta leve
191 hway represses the transcription of the beta-amyloid precursor protein cleaving enzyme (BACE1) via bi
192 sufficient to unleash a global and beta-site amyloid precursor protein cleaving enzyme 1 (bace-1) DNA
193 ide derivative, is a high-affinity beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) inhi
195 nooxazoline xanthene inhibitors of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) is d
196 sion causes an increase in APP and beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) prot
197 bustly reduces Abeta by inhibiting beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), a k
198 he beta secretase, widely known as beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), ini
199 S6K1 levels reduced translation of beta-site amyloid precursor protein cleaving enzyme 1 and tau, two
201 reduced translation of tau and the beta-site amyloid precursor protein cleaving enzyme 1, a key enzym
202 of Group II mGluR in Dutch APP (Alzheimer's amyloid precursor protein E693Q) transgenic mice that ac
205 pressing a shorter FE65 isoform able to bind amyloid precursor protein family members (APP, APLP1, AP
206 s of the Alzheimer's disease (AD)-implicated amyloid precursor protein gene (APP) and comprehensively
208 t over-express the Swedish mutant human beta-amyloid precursor protein gene with G protein-coupled re
209 TgCRND8 (Tg) transgenic mice express human amyloid precursor protein harboring the Swedish and Indi
210 examined [3H]PiB binding and Abeta and beta-amyloid precursor protein immunocytochemistry in autopsy
211 ochemistry for beta-amyloid (Abeta) and beta-amyloid precursor protein in brain tissue were obtained
213 iple similarities, strengthening the role of amyloid precursor protein in normal brain function and d
214 human induced neurons overexpressing mutant amyloid precursor protein in the background of APOE vare
215 l PDAPP mice, which overexpress mutant human amyloid precursor protein in the brain, exhibit two cryp
216 screpancy is likely due to overexpression of amyloid precursor protein in the transformed cellular mo
218 e of the Alzheimer's disease-associated beta-amyloid precursor protein in vitro and in human embryoni
219 affected brain regions caused by cleavage of amyloid precursor protein into the pathogenic peptide am
223 ogy of Alzheimer's disease, it is clear that amyloid precursor protein is expressed in numerous cell
224 umulation of the C-terminal fragments of the amyloid precursor protein is inversely correlated with P
226 vine pancreatic trypsin inhibitor (BPTI) and amyloid precursor protein Kunitz protease inhibitor (APP
228 hand, gamma-secretase-mediated processing of amyloid precursor protein leads to the production of amy
230 ) identify novel genetic factors involved in amyloid precursor protein metabolism and (ii) highlight
236 endosomes was coupled with reduced levels of amyloid precursor protein processing and Abeta productio
237 In the latter case, proteins related to amyloid precursor protein processing and secretion are S
238 sosome transport in regulating amyloidogenic amyloid precursor protein processing and support a model
240 immunoreactivity without detectably altering amyloid precursor protein processing or extracellular Ab
242 ht chain (NFL), alpha-synuclein (alpha-syn), amyloid precursor protein soluble metabolites alpha and
243 smic reticulum retrograde transport, affects amyloid precursor protein subcellular localization, cell
244 ral transmembrane proteins, most notably the amyloid precursor protein that results in Abeta, a trans
245 efflux by lowering tau protein that traffics amyloid precursor protein to facilitate iron efflux.
246 m for Golgi fragmentation and its effects on amyloid precursor protein trafficking and processing in
247 gomeric Abeta or in slices from mutant human amyloid precursor protein transgenic mice (mhAPP J20).
249 dated miRNA data using AD postmortem brains, amyloid precursor protein transgenic mice and AD cell li
251 creases brain beta-amyloid (Abeta) levels in amyloid precursor protein transgenic mice, but no data a
255 of intracellular C-terminal fragments of the amyloid precursor protein via the MVB/lysosomal pathway.
258 the absence of any changes in the amounts of amyloid precursor protein, amyloid-beta or synaptic prot
261 at bind a variety of proteins, including the amyloid precursor protein, and that mediate the assembly
262 e result of alterations in expression of the amyloid precursor protein, as confirmed by both immunost
264 havioural signs, astrogliosis, deposition of amyloid precursor protein, synaptic loss and neuronal de
265 e proteolytic fragments of the transmembrane amyloid precursor protein, whereas tau is a brain-specif
266 teins including several, such as tau and the amyloid precursor protein, which are involved in the pat
267 he diversion of the membrane-bound beta-site amyloid precursor protein-(APP) cleaving enzyme (BACE1)
268 ant factors amyloid beta (Abeta) and soluble amyloid precursor protein-alpha (sAPPalpha) and present
269 to measure amyloid beta (Abeta) and soluble amyloid precursor protein-alpha (sAPPalpha), analytes ce
272 inistration of an inhibitor of the beta-site amyloid precursor protein-cleaving enzyme 1 (BACE1) on A
273 gical substrate of beta-secretase (beta-site amyloid precursor protein-cleaving enzyme 1 (BACE1)).
288 d with doxycycline (dox) to suppress further amyloid precursor protein/Abeta production, and at the s
289 ells via intracerebroventricular infusion in amyloid precursor protein/presenilin 1 (APP/PS1) double-
290 e effect of CLU on Abeta pathology using the amyloid precursor protein/presenilin 1 (APP/PS1) mouse m
291 content of mitochondrial 5-methylcytosine in amyloid precursor protein/presenilin 1 mice along with A
292 t spines and boutons distant from plaques in amyloid precursor protein/presenilin 1-GFP (APPPS1-GFP)
293 al glutathione (mGSH) depletion in older age amyloid precursor protein/presenilin-1 (APP/PS1) mice.
295 Down syndrome critical region 1 (DSCR1) and amyloid-precursor protein (APP), proteins upregulated in
296 /Down syndrome critical region 1 (DSCR1) and amyloid-precursor protein (APP), proteins upregulated in
297 One major target has been the beta-site amyloid-precursor-protein-cleaving enzyme 1 (BACE-1), wi
299 protease complex involved in the cleavage of amyloid precursor proteins that lead to the formation of
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