ライフサイエンスコーパス: APP

1 APP metabolite levels were determined by enzyme-linked i

2 APP promotes neuronal iron efflux by stabilizing the cel

3 APP's non-pathogenic functions include regulating intrac

4 APP-103 reduces tissue injury and IRI-associated inflamm

5 93, P = 0.001; PS2APP: R = 0.485, P = 0.019; APP-SL70: R = 0.410, P = 0.037; App (NL-G-F) : R = 0.385

6 amyloid precursor protein and presenilin 1 (APP/PS1-Tg).

7 tage amyloid precursor protein/presenilin-1 (APP/PS-1) human transgenic double-knock-in mouse model o

8 (1) APP V717I mutations alter gamma-secretase cleavage site

9 ed cognitive deficits in old Gen-1 and Gen-2 APP/PS1 mice.

10 We demonstrated that Abetaos/APP interaction increases the amyloidogenic processing o

11 es of BACE1 and predicts to inhibit abnormal APP processing and reduce Abeta levels in AD neurons.

12 sphorylate APP Y687 residue that accumulates APP in the TGN (Trans-Golgi Network) and diminishes its

13 Aged APP/PS1 mice reveal an increased sensitivity also to LPS

14 Moreover, the impaired LTP in aged APP/PS1 mice is rescued by incubation with a TNFalpha an

15 now show that in an independent, aggressive APP(SWE)/PS1(L166P) (APPPS1-21) mouse model of Abeta amy

16 translational modifications of APP can alter APP processing and increase Abeta generation.

17 ocytotic trafficking associated with altered APP processing could contribute to the neuronal iron ele

18 Although APP metabolism is being intensively investigated, a larg

19 ted qHA-sps, contained intracellular amylin, APP, and/or Abeta, and amyloid.

20 quently, non-amyloidogenic and amyloidogenic APP metabolites are increased and decreased, respectivel

21 oid burden and potentiated non-amyloidogenic APP processing), and oxidative stress (reduced cortical

22 model of AD-type cerebral Abeta amyloidosis (APP(KM670/671NL)/PSEN1(Deltaexon9)) recapitulates the ex

23 nnectivity, and long-term potentiation in an APP-dependent manner.

24 density of neighboring healthy neurons in an APP-dependent manner.

25 -40) and prevents cognitive impairment in an APP/PS1 mouse model through microglial phagocytosis of e

26 ed with subspecialty consultation without an APP (OR 0.91 [0.87, 0.95].

27 growth of DNs in AD mouse brains (5xFAD and APP/PS1DeltaE9 mice) by multiple approaches, including t

28 rong negative correlation between ADAM17 and APP gene expression in human brain and present in vitro

29 ions following cognitive decline in aged and APP/PS1 (AD) mice.

30 infertility; and overexpression of ANXA2 and APP proteins in secondary infertility.

31 Although newly synthesized BACE1 and APP are transported along the secretory pathway, it is n

32 findings reveal that Golgi exit of BACE1 and APP in primary neurons is tightly regulated, resulting i

33 y pathway, it is not known whether BACE1 and APP share the same post-Golgi trafficking pathways or ar

34 e hippocampus, cerebellum, and brainstem and APP protein level was greater in cerebellum of blast vs

35 ugh competition between APP dimerization and APP cholesterol binding.

36 atin-induced changes in APP dimerization and APP-BACE1 are dependent on cholesterol binding to APP.

37 irect interaction between NCT ectodomain and APP(C99) influences the stability of GSEC-Abetan assembl

38 omparing two AD mouse models, APP NL-G-F and APP PS1, we identified distinct heterogeneous plaque pop

39 and beta-APP carboxyl-terminal fragments and APP intracellular domain accumulate in EVs over time and

40 The dissociation between increased pTau and APP in different regions in the absence of neurobehavior

41 ssociated with disease progression rates and APP levels.

42 icity shift in memory-impaired aged rats and APP/PS1 mice modeling AD, which was rescued upon A(2A)R

43 ith iNPH had lower concentrations of tau and APP-derived proteins in combination with elevated MCP-1

44 Notably, both TrkB and APP are robustly cleaved by delta-secretase in AD brains

45 Vs isolated from the brains of wild-type and APP overexpressing Tg2576 mice.

46 In in vivo studies on wild-type and APP/presenilin 1 (PS1) mice, two selected compounds were

47 Methods: Groups of wild-type and APP/PS1-21 mice aged 50 or 170 d underwent (11)C-metoclo

48 ons exposed to oligomeric Abeta in vitro and APP mutant mouse models, modulation of p75(NTR) signalin

49 Six-month-old WT and APP/PS1 mice were fed with standard mouse chow or OLT117

50 etween gastroenterologists/hepatologists and APPs were associated with the best performance and lower

51 ta-cleaved carboxy-terminal fragment of APP (APP-betaCTF).

52 ta cleaved carboxy terminal fragment of APP (APP-betaCTF, C99).

53 se the amyloid-beta precursor protein (APP), APP metabolites, and key APP cleaving enzymes were ident

54 inked APPswe mutant variant upregulates APP, APP carboxyl terminal fragments, and Abeta levels.

55 genes mutated in Familial dementia, such as APP, PSEN1/PSEN2, are implicated in glutamatergic synapt

56 in-cleaving (APP-cleaving) enzyme 1 (BACE1), APP, and beta-amyloid (Abeta) are linked with vascular d

57 ession of beta-site cleaving enzyme (BACE1), APP, and Abeta in human primary astrocytes (HPAs) expose

58 t in excitatory neurons did not alter BACE1, APP, C-terminal fragments derived from BACE1 cleavage of

59 ogenesis of Alzheimer's disease (AD) because APP mutations that influence this processing either indu

60 resulting metabolites, both alpha- and beta-APP carboxyl-terminal fragments and APP intracellular do

61 may be regulated through competition between APP dimerization and APP cholesterol binding.

62 as an important endogenous regulator of both APP processing to Abeta, and oligodendrocyte survival, i

63 quality and outcomes for patients managed by APPs using a retrospective analysis of a nationally repr

64 gy consultation showed that patients seen by APPs were more likely to receive consistent HCC and vari

65 contrast, none of the full-length, cellular APP proteins exhibited Fpn co-localization or FRET.

66 eta-site amyloid precursor protein-cleaving (APP-cleaving) enzyme 1 (BACE1), APP, and beta-amyloid (A

67 These collective APPs accurately reflect disease burden, progression rate

68 Conclusion: APPs, particularly when working with gastroenterologists

69 n particular, signaling pathways controlling APP transport to the synapse in axons and dendrites rema

70 Concentrations of 9 different APPs were measured in eluates from neonatal dried blood

71 for modifiers whose own reduction diminished APP in human cell lines and transgenic Drosophila.

72 fd, impaired social interactions with either APP/PS1 genotype or a Hfd, and synergistic impairment of

73 protects from sporadic dementia, emphasizing APP's role in dementia pathogenesis.

74 o resulted in the accumulation of endogenous APP in the TGN and enhanced alpha-secretase processing.

75 ase flAPP interaction with BACE1 and enhance APP dimerization.

76 e, truncated Abeta2-40/42 peptides, enhanced APP processing by this enzyme could contribute to AD pat

77 3E) cofilin reduces sAPP levels by enhancing APP endocytosis.

78 ncrease in signaling, possibly via enhancing APP expression.SIGNIFICANCE STATEMENT Humans express thr

79 rtical neuronal network-on-a-chip to examine APP transport and localization to the pre- and post-syna

80 sted links between obesity and AD by feeding APP/PS1 mice a high fat diet (Hfd) and evaluating behavi

81 Last, aged male and female APP/PS1 transgenic mice, genetically null for the beta2

82 thermore, we provide evidence that following APP processing, extracellular release of Abetaos mediate

83 ociates with nuclear export of the mRNAs for APP protein processing enzymes, including beta-site amyl

84 ay distinct from the trafficking pathway for APP.

85 Further, RNA-Seq data from APP/PS1 hippocampal tissue revealed that ChS significant

86 cleavage of APP inactivates this functional APP domain promoting excitatory neurotransmitter release

87 We interrogated innate pathways governing APP stability using a siRNA screen for modifiers whose o

88 EATLGGFGSLGL, which is capable of en-hancing APP expression.

89 of interest to clarify in future studies how APP-Ser-675 phosphorylation promotes meprin beta-mediate

90 enic mouse line to model the impact of human APP (hAPP)/Abeta accumulation on tauopathy in the entorh

91 riant on gamma-secretase processing of human APP, the murine Notch derivative mNDeltaE and human neur

92 the MHC-I antigen processing pathway (MHC-I APP), promoting evasion of T cell-mediated immunity.

93 lzheimer's disease (AD), while the Icelandic APP mutation near the BACE1-cleavage site protects from

94 -type' tau aggregate secondarily to Abeta in APP(swe)/PS1(DeltaE9) mice, this study suggests that amy

95 on combinatorial and opposite alterations in APP metabolism rather than simply on Abeta levels.

96 ional plaque morphology in the cerebellum in APP/PS1 transgenic mouse, as a model of AD.

97 Additionally, statin-induced changes in APP dimerization and APP-BACE1 are dependent on choleste

98 llaries or a worsening of the CBF deficit in APP/PS1 mice fed a Hfd as compared to controls, suggesti

99 stic impairment of sensory-motor function in APP/PS1 mice fed a Hfd.

100 proved CBF and short-term memory function in APP/PS1 mice, even when fed a Hfd.

101 fiber synapses are unaltered at 6 months in APP/PS1 mice.

102 These alterations were not observed in APP KO neurons, suggesting that APP expression is requir

103 d trends toward poorer memory performance in APP/PS1 mice fed a Hfd, impaired social interactions wit

104 ases in amyloid-beta monomers and plaques in APP/PS1 mice, as well as increased brain inflammation.

105 on4 allele, as well as rare substitutions in APP (p.S198P), NOTCH3 (p.H1235L) and SORL1 (p.W1563C).

106 n increase performance on cognitive tasks in APP/PS1 mice; however, the potential effects of environm

107 with saracatinib, hippocampal SUVR((WB)) in APP/PS1 mice was significantly increased (P = 0.037, pai

108 Finally, intracranial infection of ZIKV in APP-null neonatal mice resulted in higher mortality and

109 onal maturation was accompanied by increased APP processing, resulting in increased secretion of Abet

110 acts with APP, and viral infection increases APP expression via enhancing protein stability.

111 dimensional culture AD model, virus-infected APP/PS1 mice and the brains of patients with AD.

112 w altering cholesterol metabolism influences APP processing.

113 icial microRNA targeting CD33 (miRCD33) into APP/PS1 mice reduced CD33 mRNA and TBS-soluble Abeta40 a

114 Our data introduce APP-103 as a novel, nontoxic, and site-activating therap

115 rsor protein (APP), APP metabolites, and key APP cleaving enzymes were identified in association with

116 apping in amyloid precursor protein knockin (APP-KI) mice with impaired spatial memory.

117 Furthermore, hippocampal neurons lacking APP family exhibit hyperexcitability, as evidenced by in

118 e APP, and Western analysis, for full length APP, betaCTF and alphaCTF.

119 sAPPbeta and increased levels of full-length APP (flAPP), indicative of reduced processing of APP by

120 We found that full-length APP is cleaved in EVs incubated in the absence of cells.

121 ong different transport routes, which limits APP processing.

122 age in three APP-overexpression mouse lines (APP/PS1, Tg2576, and hAPP-J20) using in vivo labeling wi

123 Lowering APP expression with siRNA or BACE1 inhibition reversed c

124 s of miR-346 and IRP/Fe interact to maintain APP homeostasis.

125 P in the CNS and participates in maintaining APP regulation of Fe, which is disrupted in late stages

126 hosphorylation promotes meprin beta-mediated APP cleavage.

127 sing an EAI smart case connected to a mobile APP) with functions that overcome most of the EAI limita

128 t the BBB in a beta-amyloidosis mouse model (APP/PS1-21 mice) and in wild-type mice.

129 PET scans of 5 different Abeta mouse models (APP/PS1, PS2APP, APP-SL70, App (NL-G-F) , and APPswe) to

130 PO PET in 4 investigated Abeta mouse models (APP/PS1: R = 0.593, P = 0.001; PS2APP: R = 0.485, P = 0.

131 Comparing two AD mouse models, APP NL-G-F and APP PS1, we identified distinct heterogen

132 euroblastoma (N2a) cells that express mutant APP.

133 In contrast, expression of human mutant APP in mice or Abeta42 infusion into control diet-fed mi

134 chondrial fission in ligand 1-treated mutant APP cells.

135 Neonatal APPs varied with perinatal environmental factors and mat

136 risk for ASD were observed between neonatal APPs and maternal infection during late pregnancy, mater

137 abundance of ABCA1 and elevated abundance of APP in brain tissue.

138 er-675 phosphorylation alters the balance of APP processing, increasing meprin beta-mediated and decr

139 bserved at the protein level in the brain of APP/PS1 mice treated with miRCD33 vector.

140 expression therapeutically in the brains of APP/PS1 male mice.

141 results in an increase in BACE1 cleavage of APP and increased production of both Abeta40 and Abeta42

142 Cleavage of APP by BACE1/beta-secretase initiates the amyloidogenic

143 state the sequential proteolytic cleavage of APP by beta secretase 1 enzyme (BACE1) and gamma-secreta

144 These findings suggest that cleavage of APP by either beta- or alpha-secretase may inactivate th

145 tegies targeting the proteolytic cleavage of APP disrupt the relationship between extracellular and i

146 As meprin beta cleavage of APP has been shown to result in formation of highly aggr

147 ur data suggest that beta-/alpha cleavage of APP inactivates this functional APP domain promoting exc

148 nal fragments derived from BACE1 cleavage of APP, or endogenous Abeta levels.

149 evels and enhanced amyloidogenic cleavage of APP, selectively in AD-vulnerable brain regions.

150 nd substantially reduced premature deaths of APP/PS1-Tg mice at a dose lowering brain 24S-hydroxychol

151 s mimics and largely occludes the effects of APP family inactivation.

152 ADAM17 negatively controls the expression of APP.

153 us beta-cleaved carboxy-terminal fragment of APP (APP-betaCTF).

154 he beta cleaved carboxy terminal fragment of APP (APP-betaCTF, C99).

155 ropose that the 99-aa C-terminal fragment of APP (C99), when delivered to the ER for cleavage by gamm

156 However, the biological function of APP is poorly understood.

157 holine chloride) in two generations (Gen) of APP/PS1 mice.

158 of TrkB 1-486 fragment in the hippocampus of APP/PS1 mice facilitates amyloid pathology and mitigates

159 ere we report that selective inactivation of APP family members in excitatory neurons of the postnata

160 ns as shown by pharmacological inhibition of APP processing or by intraneuronal infusion of an antibo

161 Also, knockdown of APP expression or blocking ZIKV-APP interactions enhance

162 35 up-regulation by reducing total levels of APP and results in a significant decrease in its metabol

163 Levels of APP and Tau in brain tissue correlated with the abundanc

164 perhaps by increasing steady state levels of APP, while they also provide support for a fundamental r

165 Mislocalization of APP can promote iron retention, thus we hypothesized tha

166 aberrant posttranslational modifications of APP can alter APP processing and increase Abeta generati

167 eaves TrkB and blunts its phosphorylation of APP, facilitating AD pathogenesis.

168 2DM promotes the amyloidogenic processing of APP and hyperphosphorylation of tau.

169 preferential non-amyloidogenic processing of APP at the cell surface promotes ferroportin stabilizati

170 asing alpha-secretase-mediated processing of APP at the plasma membrane.

171 (flAPP), indicative of reduced processing of APP by BACE1.

172 that endocytotic amyloidogenic processing of APP impairs iron export by destabilizing ferroportin on

173 on increases the amyloidogenic processing of APP leading to intracellular accumulation of newly produ

174 Given that processing of APP to Abeta and soluble APP alpha (sAPPalpha) contribut

175 merges where the amyloidogenic processing of APP, combined with age-dependent iron elevation in the t

176 el to evaluate the therapeutic properties of APP-103, a polyoxalate-based copolymer molecule containi

177 -298 resulted in nonsignificant reduction of APP, BACE1, and tau in mice.

178 al process that depends on the regulation of APP metabolism.

179 We identified miR-298 as a repressor of APP, BACE1, and the two primary forms of Abeta (Abeta40

180 The inferred deleterious role of APP and DR6 is confirmed in vitro in models of ALS.

181 Despite its importance, the role of APP family in neuronal function and survival remains unc

182 eristics by normalizing the transcriptome of APP/PSEN1 mice and repressing the induction of genes inv

183 The Akt-HTT pathway and axonal transport of APP thus regulate APP presynaptic levels and synapse hom

184 quired for efficient post-Golgi transport of APP to endosomes.

185 TT decreased axonal anterograde transport of APP, reduced presynaptic APP levels, and increased synap

186 n's disease, regulates neuritic transport of APP, we used a microfluidic corticocortical neuronal net

187 to the removal from neurons and transport of APP-derived neurotoxic peptides.

188 Rhizolutin treatment of APP/PS1 double transgenic mice with AD significantly dis

189 Treatment of APP/PS1 mice with miRCD33 vector at an early age (2 mont

190 hus, miR-346 plays a role in upregulation of APP in the CNS and participates in maintaining APP regul

191 ripheral inflammation by examining levels of APPs, and their contribution to disease burden and progr

192 Levels of APPs, including soluble CD14 (sCD14), lipopolysaccharide

193 ired learning and memory ability of 9-mo-old APP/PS1 mice (P = 0.001), which was completely rescued b

194 Chronic treatment of 10 month-old APP/PS1 mice with 5i (2 mg/kg, i.p., 3 times per week, 4

195 ue deposition in 6, 12, and 18-22 months old APP/PS1 mice in the prefrontal (PFC), somatosensory (SS2

196 These opposite effects on APP beta/alpha-processing suggest that protection from a

197 the functional impact of miRNAs and genes on APP metabolism and the signaling pathways involved.

198 horylation in APPPS1 mice, which overexpress APP, reduced presynaptic APP levels, restored synapse nu

199 shes its neurotrophic activity, decreasing p-APP Y687 and altering its subcellular trafficking.

200 kably, BDNF stimulates TrkB to phosphorylate APP Y687 residue that accumulates APP in the TGN (Trans-

201 t the TrkB receptor binds and phosphorylates APP, reducing amyloid-beta production, which are abrogat

202 , with those containing apple pomace powder (APP) showing the greatest difference to the control (SC1

203 ograde transport of APP, reduced presynaptic APP levels, and increased synaptic density.

204 , which overexpress APP, reduced presynaptic APP levels, restored synapse number and improved learnin

205 e secretase machinery is actively processing APP in EVs isolated from the brains of wild-type and APP

206 are produced from amyloid precursor protein (APP) along the endocytic pathway of living cells.

207 up-regulation of amyloid precursor protein (APP) and Abeta (40 and 42) in astrocytes.

208 strocyte-released amyloid precursor protein (APP) and death receptor-6 (DR6) on MNs as the top predic

209 ion by modulating amyloid precursor protein (APP) and gamma-secretase levels in lipid rafts.

210 xtra gene copy of amyloid precursor protein (APP) and is specifically mediated by the beta cleaved ca

211 cleavages of the amyloid precursor protein (APP) and mediates a synergistic effect, when combined wi

212 mutations in the amyloid precursor protein (APP) and presenilin (PSEN1 and PSEN2) genes.

213 ng levels of amyloid beta precursor protein (APP) and presenilin 1 (PS1) with AD mutations, we show t

214 redistribution of amyloid precursor protein (APP) and Tau to lipid rafts and increased the abundance

215 n of amyloid beta (Abeta) precursor protein (APP) beyond its role in Alzheimer's disease is emerging.

216 sed from the amyloid-beta precursor protein (APP) by beta-site APP-cleaving enzyme 1 (BACE1) and the

217 e cleavage of the amyloid precursor protein (APP) by the beta and gamma secretases.

218 Processing of amyloid precursor protein (APP) by the beta-secretase BACE1 is the initial step of

219 ) mutations alter amyloid precursor protein (APP) cleavage by gamma-secretase, increasing the proport

220 terase, beta-site amyloid precursor protein (APP) cleaving enzyme-1 (BACE-1), and Abeta42 and tau agg

221 Amyloid precursor protein (APP) is associated with both familial and sporadic forms

222 Amyloid-beta precursor protein (APP) is overshadowed by its degradation product, the Alz

223 Amyloid precursor protein (APP) is predominantly expressed in brains and implicated

224 ale wild-type and amyloid precursor protein (APP) knock-out (KO) mice to assess the effects of Abetao

225 as those encoding amyloid precursor protein (APP) or presenilins (PSEN1 or PSEN2) carrying mutations

226 ions by promoting amyloid precursor protein (APP) processing.

227 ve suggested that amyloid precursor protein (APP) regulates synaptic homeostasis, but the evidence ha

228 a is derived from amyloid precursor protein (APP) through sequential proteolytic cleavage by BACE1 an

229 cleavage of beta-amyloid precursor protein (APP) to form the amyloid beta (Abeta) peptide is related

230 ed from preplaque amyloid precursor protein (APP) transgenic rats were found to produce a variety of

231 ted from the amyloid-beta precursor protein (APP) via cleavages by beta- and gamma-secretase.

232 iosis in the male amyloid precursor protein (APP)(SWE) /presenilin 1 (PS1)(DeltaE9) transgenic model

233 ge product of the amyloid precursor protein (APP), and aberrant posttranslational modifications of AP

234 d cleavage of the amyloid precursor protein (APP), and how this relationship relates to Alzheimer's d

235 because the amyloid-beta precursor protein (APP), APP metabolites, and key APP cleaving enzymes were

236 e upregulation of amyloid precursor protein (APP), BACE-1, a trending increase in beta-amyloid Abeta(

237 lated-Tau (pTau), amyloid precursor protein (APP), GFAP, Iba1, alphaII-spectrin, and spectrin breakdo

238 nt forms of human amyloid precursor protein (APP), producing high levels of amyloid beta (Abeta) and

239 derived from the amyloid precursor protein (APP).

240 r's disease gene, amyloid precursor protein (APP).

241 derived from the Amyloid Precursor Protein (APP).

242 proteins (amylin, amyloid precursor protein [APP], and amyloid-beta [Abeta]) and amyloid, as well as

243 to levels of neonatal acute phase proteins (APPs), key components of innate immune function, measure

244 Acute phase proteins (APPs), plasma proteins synthesized in the liver, are inc

245 Although advanced practice providers (APPs) can expand access to cirrhosis-related care, their

246 fferent Abeta mouse models (APP/PS1, PS2APP, APP-SL70, App (NL-G-F) , and APPswe) together with 136 1

247 Immunohistochemistry for pTau, APP, GFAP, and Iba1 was performed.

248 ay and axonal transport of APP thus regulate APP presynaptic levels and synapse homeostasis.

249 , these results suggest that Cav-1 regulates APP metabolism, and that depletion of Cav-1 in T2DM prom

250 ylation by the Ser/Thr kinase Akt, regulates APP transport in axons but not dendrites.

251 shown that cholesterol metabolism regulates APP processing to Abeta, the mechanism is not well under

252 The reverse APP processing shift occurs in App(s) rats.

253 tile compounds were identified in the SC100, APP and oligofructose (OLIGO) sponge cakes by olfactomet

254 Several APP mutations cause familial Alzheimer's disease (AD), w

255 id-beta precursor protein (APP) by beta-site APP-cleaving enzyme 1 (BACE1) and the gamma-secretase co

256 that processing of APP to Abeta and soluble APP alpha (sAPPalpha) contributes to disease phenotypes,

257 t assay (ELISA), for Human Abeta and soluble APP, and Western analysis, for full length APP, betaCTF

258 To study APP protective/pathogenic mechanisms, we generated knock

259 in two independent transgenic lines, termed APP(SWE)/PS1(DeltaE9) and APPPS1-21, leads to a reductio

260 e found that CTNNB1, IL1A, IL1B, TNF, TGFB1, APP, and IL6 had the higher activity in G12V mice than i

261 These findings demonstrate that APP family is not required for neuronal survival and sug

262 Mechanistically, we demonstrate that APP-103 exerts protective effects by specifically target

263 Here, we report that APP is processed by endogenous alpha-secretase at the tr

264 We show that APP-103 is safe, and that it effectively promotes kidney

265 uired for neuronal survival and suggest that APP family may regulate neuronal excitability through Kv

266 Taken together, these findings suggest that APP is a restriction factor that protects against ZIKV b

267 Our findings suggest that APP-Ser-675 phosphorylation alters the balance of APP pr

268 observed in APP KO neurons, suggesting that APP expression is required.

269 now find a role for the APP family in neuronal excitability, synaptic plasticity

270 s, was lower in the dorsal CA1 region in the APP/PS1 mouse model of Abeta pathology, relative to cont

271 s molecular and behavioral phenotypes in the APP/PS1 mouse model of Alzheimer's disease.

272 The abundance of the APP processing enzymes Adam9 and Psen1 mRNA, which code

273 imaging data to determine the impact of the APP/PS1 genotype and a Hfd on capillary stalling and CBF

274 f miR-346: specifically, that it targets the APP mRNA 5'-UTR to upregulate APP translation and Abeta

275 and iPSCs from the same participant with the APP V717I mutation.

276 These APPs were not elevated in sera of patients with Alzheime

277 This APP domain contains the sites cleaved by beta- and alpha

278 exhibited by knockout mice lacking all three APP family members.

279 ibution of Abeta plaques across age in three APP-overexpression mouse lines (APP/PS1, Tg2576, and hAP

280 on, 13 rats (5 wild type and 8 McGill-R-Thy1-APP transgenic (Tg)) were examined.

281 ACE1 are dependent on cholesterol binding to APP.

282 Our results also suggest that subsequent to APP cleavage two pools of Abetaos are produced.

283 rmed on a 1 T MRI scanner using a transgenic APP/PSEN1 mouse model of Alzheimer's disease.

284 accumulate spontaneously in aged transgenic APP(swe)/PS1(DeltaE9) mice.

285 ABCB1 induction in the brains of PCN-treated APP/PS1-21 mice with a concomitant decrease in Abeta lev

286 is mouse model of AD (P = 0.007 to untreated APP/PS1).

287 OLT1177 fed to mice (P = 0.008 to untreated APP/PS1).

288 it targets the APP mRNA 5'-UTR to upregulate APP translation and Abeta production.

289 AD-linked APPswe mutant variant upregulates APP, APP carboxyl terminal fragments, and Abeta levels.

290 roved spatial reference memory compared with APP/PS1 aged-matched littermates.

291 tio on tau pathology are also confirmed with APP transmembrane domain (TMD) mutant hNPCs, which displ

292 Moreover, naive hNPCs co-cultured with APP TMD I45F (high Abeta42/40) cells, not with I47F cell

293 here we identified protein interaction with APP tail-1 (PAT1) as a potential direct adapter between

294 We found that FERMT2 directly interacts with APP to modulate its metabolism, and that FERMT2 underexp

295 We have found that ZIKV interacts with APP, and viral infection increases APP expression via en

296 ith patients without APP care, patients with APP care had higher rates of HCC screening (adjusted odd

297 We observed that aging brain tissues with APP had protective effects on ZIKV infection by reducing

298 ding to the GABA(B)R1a binding region within APP suppressed in vivo spontaneous neuronal activity in

299 Compared with patients without APP care, patients with APP care had higher rates of HCC

300 ruption of MEC grid cells emerged in younger APP-KI mice, although the spatial memory and CA1 remappi

301 The zebrafish APP orthologue, Appb, is strongly expressed during early

302 knockdown of APP expression or blocking ZIKV-APP interactions enhanced ZIKV replication in human neur