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1 t light and the soluble fraction beta of the amyloid precursor protein).
2 ations in presenilin 1, presenilin 2, or the amyloid precursor protein.
3 protein, phosphorylated tau 181, and soluble amyloid precursor protein.
4 s alpha-secretase of the Alzheimer's disease amyloid precursor protein.
5 imer disease-associated mutations within the amyloid precursor protein.
6 expressing familial AD-linked forms of human amyloid precursor protein.
7 d to increased proteolytic processing of the amyloid precursor protein.
8 n lipid-related processes and degradation of amyloid precursor proteins.
10 d with doxycycline (dox) to suppress further amyloid precursor protein/Abeta production, and at the s
11 hese observations, anterogradely transported amyloid precursor protein accumulated in ligated sciatic
14 ion on transmembrane proteins other than the amyloid precursor protein affects the nervous system is
15 e transmembrane alpha-helical portion of the amyloid precursor protein after the latter values were a
18 ant factors amyloid beta (Abeta) and soluble amyloid precursor protein-alpha (sAPPalpha) and present
20 cilitate LTP.SIGNIFICANCE STATEMENT Secreted amyloid precursor protein-alpha (sAPPalpha) is a neurotr
21 to measure amyloid beta (Abeta) and soluble amyloid precursor protein-alpha (sAPPalpha), analytes ce
22 the absence of any changes in the amounts of amyloid precursor protein, amyloid-beta or synaptic prot
23 Furthermore, we observed increased levels of amyloid precursor protein and amyloid beta in PITRM1-kno
25 led increased phosphorylation of full-length amyloid precursor protein and its associated neurotoxic
26 a-secretase association with substrates like amyloid precursor protein and N-cadherin, but not with i
28 ransgenic mouse model carrying mutated human amyloid precursor protein and presenilin 1 (APP/PS1-Tg).
29 Alzheimer's disease we used a double mutant amyloid precursor protein and presenilin 1 (APPswe/PSEN1
31 expression of human familial AD mutations in amyloid precursor protein and presenilin 1 leads to sens
32 at initiates amyloidogenic processing of the amyloid precursor protein and which is a substrate for t
34 of AD, GR signaling pathways, processing of amyloid precursor protein, and enzymes involved in Tau p
36 at bind a variety of proteins, including the amyloid precursor protein, and that mediate the assembly
37 Abeta43, a product of the proteolysis of the amyloid precursor protein APP, is related to Abeta42 by
39 kidney cells bearing the Swedish mutation of amyloid precursor protein (APP(sw) HEK cells) as a cellu
40 set Alzheimer's disease-causing mutations in amyloid precursor protein (APP(Swe)) and presenilin 1 (P
41 zheimer's disease, as they are produced from amyloid precursor protein (APP) along the endocytic path
42 HIV, brain region-specific up-regulation of amyloid precursor protein (APP) and Abeta (40 and 42) in
45 s the interaction between astrocyte-released amyloid precursor protein (APP) and death receptor-6 (DR
46 and increased Abeta production by modulating amyloid precursor protein (APP) and gamma-secretase leve
47 eavage product of the ubiquitously expressed amyloid precursor protein (APP) and is able to self-asso
48 ly onset AD, requires the extra gene copy of amyloid precursor protein (APP) and is specifically medi
53 cretase and gamma-secretase cleavages of the amyloid precursor protein (APP) and mediates a synergist
54 ha-, beta-, and gamma-secretases, cleave the amyloid precursor protein (APP) and modulate beta-amyloi
55 disease (fAD) results from mutations in the amyloid precursor protein (APP) and presenilin (PSEN1 an
57 ysosomal cysteine protease that cleaves both amyloid precursor protein (APP) and tau, mediating the a
58 beta due to a change in the approximation of amyloid precursor protein (APP) and the beta-site APP cl
59 es whether C-terminal fragments (CTF) of the amyloid precursor protein (APP) are present in cerebrosp
60 ally neurotoxic Abeta fragments derived from amyloid precursor protein (APP) at synapses may be a key
61 in cell and animal models to edit endogenous amyloid precursor protein (APP) at the extreme C-terminu
63 ta (Abeta) peptide, derived from cleavage of amyloid precursor protein (APP) by beta- and gamma-secre
64 and are formed by sequential cleavage of the amyloid precursor protein (APP) by beta-secretase (BACE)
65 eta is generated by a sequential cleavage of amyloid precursor protein (APP) by beta-secretase 1 (BAC
67 ides derived from sequential cleavage of the amyloid precursor protein (APP) by beta-site APP cleavin
68 tion of Abeta peptide from the processing of amyloid precursor protein (APP) by clipping enzymes (bet
70 and are formed by successive cleavage of the amyloid precursor protein (APP) by the beta and gamma se
73 dels of Alzheimer's disease suggest that the amyloid precursor protein (APP) can cause changes in syn
76 APP/PS1 Tg mice, the critical molecules for amyloid precursor protein (APP) cleavage and signaling p
77 al Alzheimer's disease (fAD) mutations alter amyloid precursor protein (APP) cleavage by gamma-secret
78 icits in AD.SIGNIFICANCE STATEMENT beta-Site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1
81 inesterase, butyrylcholinesterase, beta-site amyloid precursor protein (APP) cleaving enzyme-1 (BACE-
83 reviously that the Alzheimer-associated beta-amyloid precursor protein (APP) facilitates neuronal iro
88 of DS models that one extra copy of a normal amyloid precursor protein (APP) gene impairs lysosomal a
89 in AD, as compared to rodent Abeta, the rat Amyloid Precursor Protein (App) gene was mutated to prod
92 p family proteins.SIGNIFICANCE STATEMENT The amyloid precursor protein (App) has been intensively stu
96 yloid beta (Abeta) peptides originating from amyloid precursor protein (APP) in the endosomal-lysosom
97 mediate amyloid beta (Abeta) formation from amyloid precursor protein (APP) in vitro To determine wh
98 ecretase (BACE1) initiates processing of the amyloid precursor protein (APP) into Abeta peptides, whi
99 retase is responsible for the proteolysis of amyloid precursor protein (APP) into short, aggregation-
100 a growing body of evidence suggests that the amyloid precursor protein (APP) intracellular C-terminal
101 retase component, the enzyme responsible for amyloid precursor protein (APP) intramembraneous cleavag
105 associated with Alzheimer disease (AD), the amyloid precursor protein (APP) is cleaved by beta-secre
106 Here, we reveal that the membrane-associated amyloid precursor protein (APP) is highly expressed in m
111 nce of earlier complications occurring while amyloid precursor protein (APP) is trafficking through t
112 and cortical slices from male wild-type and amyloid precursor protein (APP) knock-out (KO) mice to a
113 nked mutations in Presenilins (PSEN) and the amyloid precursor protein (APP) lead to production of lo
115 ACH) and presenilin (PSH) hypotheses and the amyloid precursor protein (APP) matrix approach (AMA), o
116 lipid metabolism, tau binding proteins, and amyloid precursor protein (APP) metabolism, showing that
119 beta-secretase 1 (BACE-1) and BACE-1-cleaved amyloid precursor protein (APP) metabolites (secreted AP
121 xpressing human genes such as those encoding amyloid precursor protein (APP) or presenilins (PSEN1 or
123 ly involvement of endosomes and lysosomes in amyloid precursor protein (APP) processing and clearance
124 of APOE varepsilon3/4 allele exhibit altered amyloid precursor protein (APP) processing, abnormally i
128 and Abeta42 secretion, and the amount of the amyloid precursor protein (APP) secreted at the cell sur
130 oduce Abeta by the proteolytic processing of amyloid precursor protein (APP) through the endocytic pa
133 (AD) is associated with the cleavage of the amyloid precursor protein (APP) to produce the toxic amy
134 ns of alpha-syn-containing preparations into amyloid precursor protein (APP) transgenic mice (express
135 hat Abeta pathology and neuroinflammation in amyloid precursor protein (APP) transgenic mice are wors
136 rodissected neurons extracted from preplaque amyloid precursor protein (APP) transgenic rats were fou
138 ng studies revealed that the dynamics of the amyloid precursor protein (APP) were significantly impai
139 in, and scyllo-inositol, in cells expressing amyloid precursor protein (APP) with the Osaka (E693Delt
140 laque pathology and astrogliosis in the male amyloid precursor protein (APP)(SWE) /presenilin 1 (PS1)
143 in 4 (CNTN4) or one of its binding partners, amyloid precursor protein (APP), a subset of direction-s
144 transport of the Alzheimer's disease-related amyloid precursor protein (APP), although neuronal morph
146 cholesterol homeostasis and cleavage of the amyloid precursor protein (APP), and how this relationsh
147 laques resulting from abnormal processing of amyloid precursor protein (APP), and presence of neurofi
148 eferring to an interaction between DISC1 and amyloid precursor protein (APP), and to an association o
149 mory deficits as well as the upregulation of amyloid precursor protein (APP), BACE-1, a trending incr
150 erated through sequential proteolysis of the amyloid precursor protein (APP), first by the action of
151 els of total-Tau, phosphorylated-Tau (pTau), amyloid precursor protein (APP), GFAP, Iba1, alphaII-spe
152 oid-beta generation from its precursor, beta-amyloid precursor protein (APP), in a competitive manner
153 tide, a metabolite of sequential cleavage of amyloid precursor protein (APP), is a critical step in t
154 ition of amyloid-beta peptides, derived from amyloid precursor protein (APP), is a neuropathological
155 proteins linked to familial AD (FAD), mutant amyloid precursor protein (APP), or APP and presenilin (
156 eta), derived from proteolytic processing of amyloid precursor protein (APP), play a central role in
158 use models overexpress mutant forms of human amyloid precursor protein (APP), producing high levels o
161 ) peptide because of increased processing of amyloid precursor protein (APP), resulting in loss of sy
162 illar aggregates of peptide fragments of the amyloid precursor protein (APP), typically 40 or 42 resi
163 ilar to that of transgenic mice that express amyloid precursor protein (APP), which is duplicated in
164 tween these conditions may be constituted by amyloid precursor protein (APP), which plays a pivotal r
165 idue protein produced by the cleavage of the amyloid precursor protein (APP), which subsequently aggr
166 wn primarily for its initial cleavage of the amyloid precursor protein (APP), which ultimately leads
170 It was recently suggested that beta-site amyloid precursor protein (APP)-cleaving enzyme 2 (BACE2
181 Here, we examined the impact of CXCR3 in the amyloid precursor protein (APP)/presenilin 1 (PS1) trans
183 well as an Alzheimer's disease mouse model, amyloid precursor protein (APP)/PSEN1dE9(+/-) (PS1) that
184 Down syndrome critical region 1 (DSCR1) and amyloid-precursor protein (APP), proteins upregulated in
185 /Down syndrome critical region 1 (DSCR1) and amyloid-precursor protein (APP), proteins upregulated in
186 ntracellular amyloidogenic proteins (amylin, amyloid precursor protein [APP], and amyloid-beta [Abeta
187 he diversion of the membrane-bound beta-site amyloid precursor protein-(APP) cleaving enzyme (BACE1)
188 on within the Kunitz inhibitor domain of the amyloid precursor protein (APPI) that incorporated a new
190 TgF344-AD) expressing disease-causing mutant amyloid precursor protein (APPsw) and presenilin-1 (PS1D
191 known that mutations in the gene coding for amyloid precursor protein are responsible for autosomal
192 e result of alterations in expression of the amyloid precursor protein, as confirmed by both immunost
194 Here, we used a mouse model expressing human amyloid precursor protein bearing two familial mutations
195 SY5Y neuroblastoma cells expressing the beta-amyloid precursor protein (betaAPP) harboring the famili
196 's disease (AD) are tied to mutations in the amyloid precursor protein, but the cellular mechanisms t
197 ial forms of AD are tied to mutations in the amyloid precursor protein, but the cellular mechanisms t
199 egion from >100 substrates, including Notch, amyloid precursor protein, cadherins, growth factors, an
200 accompanied by a decrease in BACE1-mediated amyloid precursor protein cleavage and amyloid-beta leve
201 nduce an "endosomal traffic jam" that drives amyloid precursor protein cleavage to amyloid-beta in en
202 ncoding RNA (miR-188-3p) targeting beta-site amyloid precursor protein cleaving enzyme (BACE)-1, a ke
203 sufficient to unleash a global and beta-site amyloid precursor protein cleaving enzyme 1 (bace-1) DNA
204 ide derivative, is a high-affinity beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) inhi
208 sion causes an increase in APP and beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) prot
209 S6K1 levels reduced translation of beta-site amyloid precursor protein cleaving enzyme 1 and tau, two
211 reporter gene driven by the BACE1 (beta-site amyloid precursor protein cleaving enzyme 1) promoter, w
212 reduced translation of tau and the beta-site amyloid precursor protein cleaving enzyme 1, a key enzym
213 ro-amyloidogenic processing enzyme beta-site amyloid precursor protein cleaving enzyme 1, and both to
216 becestat is an orally administered beta-site amyloid precursor protein-cleaving enzyme 1 (BACE-1) inh
219 inistration of an inhibitor of the beta-site amyloid precursor protein-cleaving enzyme 1 (BACE1) on A
220 gical substrate of beta-secretase (beta-site amyloid precursor protein-cleaving enzyme 1 (BACE1)).
221 One major target has been the beta-site amyloid-precursor-protein-cleaving enzyme 1 (BACE-1), wi
222 iation is partially due to overexpression of amyloid precursor protein, encoded by APP, as a result o
225 pressing a shorter FE65 isoform able to bind amyloid precursor protein family members (APP, APLP1, AP
226 these rats, such as increased deposition of amyloid precursor protein fragments associated with the
228 s of the Alzheimer's disease (AD)-implicated amyloid precursor protein gene (APP) and comprehensively
230 t over-express the Swedish mutant human beta-amyloid precursor protein gene with G protein-coupled re
231 ocampal neurons and in mice expressing human amyloid precursor protein (hAPP mice), a model for famil
232 compared transgenic mice that express human amyloid precursor protein (hAPP) and patients with mild
233 humans with AD, aging mice expressing human amyloid precursor protein (hAPP) showed increased levels
234 cking in the axon of AD-related mutant human amyloid precursor protein (hAPP) transgenic (Tg) mouse n
235 e mortality and network dysfunction in human amyloid precursor protein (hAPP) transgenic mice, which
237 odel of AD (transgenic mice expressing human amyloid precursor protein [hAPP]) and patients in the ea
238 TgCRND8 (Tg) transgenic mice express human amyloid precursor protein harboring the Swedish and Indi
240 s involved in anterograde trafficking of the amyloid precursor protein in neurons and in the secretio
241 iple similarities, strengthening the role of amyloid precursor protein in normal brain function and d
242 human induced neurons overexpressing mutant amyloid precursor protein in the background of APOE vare
243 l PDAPP mice, which overexpress mutant human amyloid precursor protein in the brain, exhibit two cryp
245 e of the Alzheimer's disease-associated beta-amyloid precursor protein in vitro and in human embryoni
246 and low sAPPbeta (a soluble beta fragment of amyloid precursor protein) in cerebrospinal fluid (CSF)
247 affected brain regions caused by cleavage of amyloid precursor protein into the pathogenic peptide am
249 Acting as synapse-to-nucleus messengers, amyloid precursor protein intracellular domain associate
250 ogical feature of AD, and endocytosis of the amyloid precursor protein is an important step in its su
252 ogy of Alzheimer's disease, it is clear that amyloid precursor protein is expressed in numerous cell
254 cases, hippocampal levels of phosphorylated amyloid precursor protein, its pro-amyloidogenic process
255 n called "remapping." We tested remapping in amyloid precursor protein knockin (APP-KI) mice with imp
256 vine pancreatic trypsin inhibitor (BPTI) and amyloid precursor protein Kunitz protease inhibitor (APP
257 t to be primarily due to triplication of the amyloid precursor protein located on chromosome 21, the
258 he AD mouse model carrying human mutation of amyloid precursor protein (mhAPP) expressing human Abeta
263 ells via intracerebroventricular infusion in amyloid precursor protein/presenilin 1 (APP/PS1) double-
264 e effect of CLU on Abeta pathology using the amyloid precursor protein/presenilin 1 (APP/PS1) mouse m
265 content of mitochondrial 5-methylcytosine in amyloid precursor protein/presenilin 1 mice along with A
266 rt, liver, and brain tissues in a late-stage amyloid precursor protein/presenilin-1 (APP/PS-1) human
267 endosomes was coupled with reduced levels of amyloid precursor protein processing and Abeta productio
268 In the latter case, proteins related to amyloid precursor protein processing and secretion are S
269 sosome transport in regulating amyloidogenic amyloid precursor protein processing and support a model
271 immunoreactivity without detectably altering amyloid precursor protein processing or extracellular Ab
273 itory fragment of Nogo-A is generated by the amyloid precursor protein protease BACE1 and presented o
275 Here, we have uncovered a role for soluble amyloid precursor protein (sAPP) as a vascular niche sig
276 soluble metabolites alpha and beta (soluble amyloid precursor protein (sAPP)alpha, sAPPbeta) and two
277 ), gamma-secretase, soluble Abeta42, soluble amyloid precursor protein (sAPP)beta, sAPPalpha, glial-d
278 ht chain (NFL), alpha-synuclein (alpha-syn), amyloid precursor protein soluble metabolites alpha and
279 smic reticulum retrograde transport, affects amyloid precursor protein subcellular localization, cell
280 teins, including those derived from the same amyloid precursor protein, such as Aeta or sAPPalpha, an
281 PPSwDI transgenic mice expressing human beta-amyloid precursor protein Swedish (Tg-SwDI), a model of
282 havioural signs, astrogliosis, deposition of amyloid precursor protein, synaptic loss and neuronal de
283 , we identified the protein interacting with amyloid precursor protein tail 1 (PAT1) as a potential p
286 young transgenic mice overexpressing mutated amyloid precursor protein (Tg2576), Abeta causes dysfunc
288 ral transmembrane proteins, most notably the amyloid precursor protein that results in Abeta, a trans
289 protease complex involved in the cleavage of amyloid precursor proteins that lead to the formation of
290 efflux by lowering tau protein that traffics amyloid precursor protein to facilitate iron efflux.
293 dated miRNA data using AD postmortem brains, amyloid precursor protein transgenic mice and AD cell li
298 of intracellular C-terminal fragments of the amyloid precursor protein via the MVB/lysosomal pathway.
299 ring AD-related mutations in presenilin-1 or amyloid precursor protein vs. isogenic gene corrected co
300 are caused by mutations in the gene encoding amyloid precursor protein, whose processing can result i