コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
2 pidly detecting small molecules that bind to amyloid precursors, identifying the interacting protein
8 kidney cells bearing the Swedish mutation of amyloid precursor protein (APP(sw) HEK cells) as a cellu
9 set Alzheimer's disease-causing mutations in amyloid precursor protein (APP(Swe)) and presenilin 1 (P
10 zheimer's disease, as they are produced from amyloid precursor protein (APP) along the endocytic path
11 HIV, brain region-specific up-regulation of amyloid precursor protein (APP) and Abeta (40 and 42) in
14 s the interaction between astrocyte-released amyloid precursor protein (APP) and death receptor-6 (DR
15 and increased Abeta production by modulating amyloid precursor protein (APP) and gamma-secretase leve
16 eavage product of the ubiquitously expressed amyloid precursor protein (APP) and is able to self-asso
17 ly onset AD, requires the extra gene copy of amyloid precursor protein (APP) and is specifically medi
22 cretase and gamma-secretase cleavages of the amyloid precursor protein (APP) and mediates a synergist
23 ha-, beta-, and gamma-secretases, cleave the amyloid precursor protein (APP) and modulate beta-amyloi
24 disease (fAD) results from mutations in the amyloid precursor protein (APP) and presenilin (PSEN1 an
26 ysosomal cysteine protease that cleaves both amyloid precursor protein (APP) and tau, mediating the a
27 beta due to a change in the approximation of amyloid precursor protein (APP) and the beta-site APP cl
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
30 in cell and animal models to edit endogenous amyloid precursor protein (APP) at the extreme C-terminu
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
36 ides derived from sequential cleavage of the amyloid precursor protein (APP) by beta-site APP cleavin
37 tion of Abeta peptide from the processing of amyloid precursor protein (APP) by clipping enzymes (bet
39 and are formed by successive cleavage of the amyloid precursor protein (APP) by the beta and gamma se
42 dels of Alzheimer's disease suggest that the amyloid precursor protein (APP) can cause changes in syn
45 APP/PS1 Tg mice, the critical molecules for amyloid precursor protein (APP) cleavage and signaling p
46 al Alzheimer's disease (fAD) mutations alter amyloid precursor protein (APP) cleavage by gamma-secret
47 icits in AD.SIGNIFICANCE STATEMENT beta-Site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1
50 inesterase, butyrylcholinesterase, beta-site amyloid precursor protein (APP) cleaving enzyme-1 (BACE-
52 reviously that the Alzheimer-associated beta-amyloid precursor protein (APP) facilitates neuronal iro
56 of DS models that one extra copy of a normal amyloid precursor protein (APP) gene impairs lysosomal a
57 in AD, as compared to rodent Abeta, the rat Amyloid Precursor Protein (App) gene was mutated to prod
60 p family proteins.SIGNIFICANCE STATEMENT The amyloid precursor protein (App) has been intensively stu
64 yloid beta (Abeta) peptides originating from amyloid precursor protein (APP) in the endosomal-lysosom
65 mediate amyloid beta (Abeta) formation from amyloid precursor protein (APP) in vitro To determine wh
66 ecretase (BACE1) initiates processing of the amyloid precursor protein (APP) into Abeta peptides, whi
67 retase is responsible for the proteolysis of amyloid precursor protein (APP) into short, aggregation-
68 a growing body of evidence suggests that the amyloid precursor protein (APP) intracellular C-terminal
69 retase component, the enzyme responsible for amyloid precursor protein (APP) intramembraneous cleavag
73 associated with Alzheimer disease (AD), the amyloid precursor protein (APP) is cleaved by beta-secre
74 Here, we reveal that the membrane-associated amyloid precursor protein (APP) is highly expressed in m
78 nce of earlier complications occurring while amyloid precursor protein (APP) is trafficking through t
79 and cortical slices from male wild-type and amyloid precursor protein (APP) knock-out (KO) mice to a
80 nked mutations in Presenilins (PSEN) and the amyloid precursor protein (APP) lead to production of lo
82 ACH) and presenilin (PSH) hypotheses and the amyloid precursor protein (APP) matrix approach (AMA), o
83 lipid metabolism, tau binding proteins, and amyloid precursor protein (APP) metabolism, showing that
86 beta-secretase 1 (BACE-1) and BACE-1-cleaved amyloid precursor protein (APP) metabolites (secreted AP
88 xpressing human genes such as those encoding amyloid precursor protein (APP) or presenilins (PSEN1 or
90 ly involvement of endosomes and lysosomes in amyloid precursor protein (APP) processing and clearance
91 of APOE varepsilon3/4 allele exhibit altered amyloid precursor protein (APP) processing, abnormally i
95 and Abeta42 secretion, and the amount of the amyloid precursor protein (APP) secreted at the cell sur
97 oduce Abeta by the proteolytic processing of amyloid precursor protein (APP) through the endocytic pa
100 (AD) is associated with the cleavage of the amyloid precursor protein (APP) to produce the toxic amy
101 ns of alpha-syn-containing preparations into amyloid precursor protein (APP) transgenic mice (express
102 hat Abeta pathology and neuroinflammation in amyloid precursor protein (APP) transgenic mice are wors
103 rodissected neurons extracted from preplaque amyloid precursor protein (APP) transgenic rats were fou
105 ng studies revealed that the dynamics of the amyloid precursor protein (APP) were significantly impai
106 in, and scyllo-inositol, in cells expressing amyloid precursor protein (APP) with the Osaka (E693Delt
107 laque pathology and astrogliosis in the male amyloid precursor protein (APP)(SWE) /presenilin 1 (PS1)
110 in 4 (CNTN4) or one of its binding partners, amyloid precursor protein (APP), a subset of direction-s
111 transport of the Alzheimer's disease-related amyloid precursor protein (APP), although neuronal morph
113 cholesterol homeostasis and cleavage of the amyloid precursor protein (APP), and how this relationsh
114 laques resulting from abnormal processing of amyloid precursor protein (APP), and presence of neurofi
115 eferring to an interaction between DISC1 and amyloid precursor protein (APP), and to an association o
116 mory deficits as well as the upregulation of amyloid precursor protein (APP), BACE-1, a trending incr
117 erated through sequential proteolysis of the amyloid precursor protein (APP), first by the action of
118 els of total-Tau, phosphorylated-Tau (pTau), amyloid precursor protein (APP), GFAP, Iba1, alphaII-spe
119 oid-beta generation from its precursor, beta-amyloid precursor protein (APP), in a competitive manner
120 tide, a metabolite of sequential cleavage of amyloid precursor protein (APP), is a critical step in t
121 ition of amyloid-beta peptides, derived from amyloid precursor protein (APP), is a neuropathological
122 proteins linked to familial AD (FAD), mutant amyloid precursor protein (APP), or APP and presenilin (
123 eta), derived from proteolytic processing of amyloid precursor protein (APP), play a central role in
125 use models overexpress mutant forms of human amyloid precursor protein (APP), producing high levels o
127 ) peptide because of increased processing of amyloid precursor protein (APP), resulting in loss of sy
128 illar aggregates of peptide fragments of the amyloid precursor protein (APP), typically 40 or 42 resi
129 ilar to that of transgenic mice that express amyloid precursor protein (APP), which is duplicated in
130 tween these conditions may be constituted by amyloid precursor protein (APP), which plays a pivotal r
131 idue protein produced by the cleavage of the amyloid precursor protein (APP), which subsequently aggr
132 wn primarily for its initial cleavage of the amyloid precursor protein (APP), which ultimately leads
136 It was recently suggested that beta-site amyloid precursor protein (APP)-cleaving enzyme 2 (BACE2
147 Here, we examined the impact of CXCR3 in the amyloid precursor protein (APP)/presenilin 1 (PS1) trans
149 well as an Alzheimer's disease mouse model, amyloid precursor protein (APP)/PSEN1dE9(+/-) (PS1) that
150 on within the Kunitz inhibitor domain of the amyloid precursor protein (APPI) that incorporated a new
152 TgF344-AD) expressing disease-causing mutant amyloid precursor protein (APPsw) and presenilin-1 (PS1D
153 SY5Y neuroblastoma cells expressing the beta-amyloid precursor protein (betaAPP) harboring the famili
154 ocampal neurons and in mice expressing human amyloid precursor protein (hAPP mice), a model for famil
155 compared transgenic mice that express human amyloid precursor protein (hAPP) and patients with mild
156 humans with AD, aging mice expressing human amyloid precursor protein (hAPP) showed increased levels
157 cking in the axon of AD-related mutant human amyloid precursor protein (hAPP) transgenic (Tg) mouse n
158 e mortality and network dysfunction in human amyloid precursor protein (hAPP) transgenic mice, which
160 he AD mouse model carrying human mutation of amyloid precursor protein (mhAPP) expressing human Abeta
161 Here, we have uncovered a role for soluble amyloid precursor protein (sAPP) as a vascular niche sig
162 ), gamma-secretase, soluble Abeta42, soluble amyloid precursor protein (sAPP)beta, sAPPalpha, glial-d
164 young transgenic mice overexpressing mutated amyloid precursor protein (Tg2576), Abeta causes dysfunc
166 ntracellular amyloidogenic proteins (amylin, amyloid precursor protein [APP], and amyloid-beta [Abeta
167 odel of AD (transgenic mice expressing human amyloid precursor protein [hAPP]) and patients in the ea
168 hese observations, anterogradely transported amyloid precursor protein accumulated in ligated sciatic
170 This occurred prior to the appearance of amyloid precursor protein accumulation, an indicator of
171 e transmembrane alpha-helical portion of the amyloid precursor protein after the latter values were a
174 Furthermore, we observed increased levels of amyloid precursor protein and amyloid beta in PITRM1-kno
176 led increased phosphorylation of full-length amyloid precursor protein and its associated neurotoxic
177 a-secretase association with substrates like amyloid precursor protein and N-cadherin, but not with i
179 ransgenic mouse model carrying mutated human amyloid precursor protein and presenilin 1 (APP/PS1-Tg).
180 Methods: Nine wild-type (WT) mice and 9 amyloid precursor protein and presenilin 1 double-transg
181 expression of human familial AD mutations in amyloid precursor protein and presenilin 1 leads to sens
182 at initiates amyloidogenic processing of the amyloid precursor protein and which is a substrate for t
183 Abeta43, a product of the proteolysis of the amyloid precursor protein APP, is related to Abeta42 by
184 known that mutations in the gene coding for amyloid precursor protein are responsible for autosomal
185 Here, we used a mouse model expressing human amyloid precursor protein bearing two familial mutations
187 accompanied by a decrease in BACE1-mediated amyloid precursor protein cleavage and amyloid-beta leve
188 nduce an "endosomal traffic jam" that drives amyloid precursor protein cleavage to amyloid-beta in en
189 ncoding RNA (miR-188-3p) targeting beta-site amyloid precursor protein cleaving enzyme (BACE)-1, a ke
190 sufficient to unleash a global and beta-site amyloid precursor protein cleaving enzyme 1 (bace-1) DNA
191 ide derivative, is a high-affinity beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) inhi
195 sion causes an increase in APP and beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) prot
196 S6K1 levels reduced translation of beta-site amyloid precursor protein cleaving enzyme 1 and tau, two
198 reporter gene driven by the BACE1 (beta-site amyloid precursor protein cleaving enzyme 1) promoter, w
199 reduced translation of tau and the beta-site amyloid precursor protein cleaving enzyme 1, a key enzym
200 ro-amyloidogenic processing enzyme beta-site amyloid precursor protein cleaving enzyme 1, and both to
203 pressing a shorter FE65 isoform able to bind amyloid precursor protein family members (APP, APLP1, AP
204 these rats, such as increased deposition of amyloid precursor protein fragments associated with the
206 s of the Alzheimer's disease (AD)-implicated amyloid precursor protein gene (APP) and comprehensively
207 t over-express the Swedish mutant human beta-amyloid precursor protein gene with G protein-coupled re
208 TgCRND8 (Tg) transgenic mice express human amyloid precursor protein harboring the Swedish and Indi
210 s involved in anterograde trafficking of the amyloid precursor protein in neurons and in the secretio
211 iple similarities, strengthening the role of amyloid precursor protein in normal brain function and d
212 human induced neurons overexpressing mutant amyloid precursor protein in the background of APOE vare
213 l PDAPP mice, which overexpress mutant human amyloid precursor protein in the brain, exhibit two cryp
215 e of the Alzheimer's disease-associated beta-amyloid precursor protein in vitro and in human embryoni
216 affected brain regions caused by cleavage of amyloid precursor protein into the pathogenic peptide am
218 Acting as synapse-to-nucleus messengers, amyloid precursor protein intracellular domain associate
219 ogical feature of AD, and endocytosis of the amyloid precursor protein is an important step in its su
221 ogy of Alzheimer's disease, it is clear that amyloid precursor protein is expressed in numerous cell
223 n called "remapping." We tested remapping in amyloid precursor protein knockin (APP-KI) mice with imp
224 vine pancreatic trypsin inhibitor (BPTI) and amyloid precursor protein Kunitz protease inhibitor (APP
225 t to be primarily due to triplication of the amyloid precursor protein located on chromosome 21, the
230 endosomes was coupled with reduced levels of amyloid precursor protein processing and Abeta productio
231 In the latter case, proteins related to amyloid precursor protein processing and secretion are S
232 sosome transport in regulating amyloidogenic amyloid precursor protein processing and support a model
234 immunoreactivity without detectably altering amyloid precursor protein processing or extracellular Ab
235 itory fragment of Nogo-A is generated by the amyloid precursor protein protease BACE1 and presented o
237 smic reticulum retrograde transport, affects amyloid precursor protein subcellular localization, cell
238 PPSwDI transgenic mice expressing human beta-amyloid precursor protein Swedish (Tg-SwDI), a model of
239 , we identified the protein interacting with amyloid precursor protein tail 1 (PAT1) as a potential p
240 ral transmembrane proteins, most notably the amyloid precursor protein that results in Abeta, a trans
241 efflux by lowering tau protein that traffics amyloid precursor protein to facilitate iron efflux.
244 dated miRNA data using AD postmortem brains, amyloid precursor protein transgenic mice and AD cell li
247 of intracellular C-terminal fragments of the amyloid precursor protein via the MVB/lysosomal pathway.
248 ring AD-related mutations in presenilin-1 or amyloid precursor protein vs. isogenic gene corrected co
249 and low sAPPbeta (a soluble beta fragment of amyloid precursor protein) in cerebrospinal fluid (CSF)
253 the absence of any changes in the amounts of amyloid precursor protein, amyloid-beta or synaptic prot
255 of AD, GR signaling pathways, processing of amyloid precursor protein, and enzymes involved in Tau p
257 at bind a variety of proteins, including the amyloid precursor protein, and that mediate the assembly
258 e result of alterations in expression of the amyloid precursor protein, as confirmed by both immunost
260 's disease (AD) are tied to mutations in the amyloid precursor protein, but the cellular mechanisms t
261 ial forms of AD are tied to mutations in the amyloid precursor protein, but the cellular mechanisms t
262 egion from >100 substrates, including Notch, amyloid precursor protein, cadherins, growth factors, an
263 iation is partially due to overexpression of amyloid precursor protein, encoded by APP, as a result o
264 cases, hippocampal levels of phosphorylated amyloid precursor protein, its pro-amyloidogenic process
265 teins, including those derived from the same amyloid precursor protein, such as Aeta or sAPPalpha, an
266 havioural signs, astrogliosis, deposition of amyloid precursor protein, synaptic loss and neuronal de
267 are caused by mutations in the gene encoding amyloid precursor protein, whose processing can result i
268 he diversion of the membrane-bound beta-site amyloid precursor protein-(APP) cleaving enzyme (BACE1)
269 ant factors amyloid beta (Abeta) and soluble amyloid precursor protein-alpha (sAPPalpha) and present
271 cilitate LTP.SIGNIFICANCE STATEMENT Secreted amyloid precursor protein-alpha (sAPPalpha) is a neurotr
272 to measure amyloid beta (Abeta) and soluble amyloid precursor protein-alpha (sAPPalpha), analytes ce
275 becestat is an orally administered beta-site amyloid precursor protein-cleaving enzyme 1 (BACE-1) inh
278 inistration of an inhibitor of the beta-site amyloid precursor protein-cleaving enzyme 1 (BACE1) on A
279 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 rt, liver, and brain tissues in a late-stage amyloid precursor protein/presenilin-1 (APP/PS-1) human
294 Down syndrome critical region 1 (DSCR1) and amyloid-precursor protein (APP), proteins upregulated in
295 /Down syndrome critical region 1 (DSCR1) and amyloid-precursor protein (APP), proteins upregulated in
296 One major target has been the beta-site amyloid-precursor-protein-cleaving enzyme 1 (BACE-1), wi
297 protease complex involved in the cleavage of amyloid precursor proteins that lead to the formation of