ライフサイエンスコーパス: APP

1 APP binds the HIV-1 Gag polyprotein, retains it in lipid

2 APP-KO mice displayed a shorter APTT, but not PT, when m

3 APP-KO mice presented a higher number of circulating pla

4 n in amyloid precursor protein/presenilin 1 (APP/PS1) double-transgenic 3-mo-old mice after the occur

5 the amyloid precursor protein/presenilin 1 (APP/PS1) mouse model of AD amyloidosis on a Clu(+/+) or

6 achieved using 2-aminophenyl-1H-pyrazole (2-APP) as a new directing group.

7 n axonal transport, which induce an abnormal APP metabolism with important implications in neurodegen

8 M/G ratio increased in the order ADM - ACC - APP.

9 coupled with cognitive improvements in an AD APP/PS1 transgenic mouse model.

10 nes that promote beta-amyloidogenesis in AD (APP, PSEN1/2, and APOE4) have primary effects on ELN fun

11 s post-translational modifications affecting APP accumulation, ubiquitination of cytodomain lysines m

12 re treated once with brain extract from aged APP tg mice and the culture medium was continuously supp

13 We also found that the brain of aged APP/PS1 mice was not insulin resistant, contrary to the

14 ynaptic and postsynaptic localization of all APP family members and could show that heterologous expr

15 loid beta precursor protein (APP) gene alter APP processing, either causing familial Alzheimer's dise

16 BACE inhibitors), those strategies may alter APP/APLP physiological function.

17 ntial role of sAPPalpha or other non-amyloid APP fragments as acute modulators of mitochondrial metab

18 k5 and BACE-1, and accelerates amyloidogenic APP processing.

19 ffect on BACE-1 activation and amyloidogenic APP processing.

20 her hand, blocks Egr-1-induced amyloidogenic APP processing but does not affect tau phosphorylation.

21 An APP mutant lacking all C-terminal lysines underwent the

22 mary, this study identifies matriptase as an APP-cleaving enzyme, an activity that could have importa

23 lactate levels and memory performance in an APP/PS1 mouse model of AD, which progressively accumulat

24 The mAPP(-/-) mice crossed to an APP/PS1 transgenic mouse line demonstrated reduced micro

25 neuronal and glial proliferation by using an APP/PS1 transgenic model and in vitro assays.

26 There were 625 SOC, 148; ST, 278; and APP, 199.

27 ort regulates BACE1 trafficking in axons and APP processing at presynaptic terminals.

28 We further demonstrate that matriptase and APP directly interact with each other and that matriptas

29 the intraneuronal accumulation of oAbeta and APP-CTFs and resultant lysosomal pathology at early stag

30 nic mice with this inhibitor reduces tau and APP cleavage, ameliorates synapse loss and augments long

31 sion also increased mRNA levels for TP53 and APP, effectors of TSPYL5 Furthermore, DNMT3L overexpress

32 gy-mediated regulation of BACE1 turnover and APP processing, thus building a foundation for future de

33 Both US9 and APP processing machinery rely on their ability to shuttl

34 Artificial APP ubiquitination with rapalog-mediated proximity induc

35 V mutation, the only recessive AD-associated APP mutation, shifted the preferential beta-cleavage sit

36 he neurotransmitter receptor GluA2, and beta-APP.

37 dentified a novel direct interaction between APP and the alpha2A-adrenergic receptor (alpha2AAR) that

38 Both APP and ST-when completed-increased the use of penicilli

39 peptidase (AEP), simultaneously cleaves both APP and tau, controlling the onset of pathogenesis of Al

40 ponse, this novel regulation of alpha2AAR by APP may have an impact on modulation of noradrenergic ac

41 A lack of APP C-terminal lysines caused APP redistribution from endosomal intraluminal vesicles

42 flow restriction in the inferior vena cava, APP-KO mice, as well as chimeric mice with selective def

43 arance, and the pathologic effect of certain APP metabolites on ELN functions.

44 a-site APP cleaving enzyme 1 (BACE1) cleaves APP at minor Asp(1) site to generate C99 for amyloid bet

45 with each other and that matriptase cleaves APP at a specific arginine residue (Arg-102) both in vit

46 sines may represent a key signal controlling APP endosomal sorting.

47 M344 increases sAPPalpha and CTFalpha APP metabolite production, both cleavage products of ADA

48 ble mutant (S226A) into 5XFAD mice decreases APP and tau proteolytic cleavage, attenuates AD patholog

49 nduced neurons effectively rescued defective APP processing, demonstrating the functional importance

50 Different APP mutations have diverse effects on the levels of APP

51 man AD In this review, we evaluate different APP mouse models of AD, and review recent studies using

52 PP C-terminal lysines with arginine disrupts APP ubiquitination and that an increase in the number of

53 nd should stimulate new studies to elucidate APP-related targets suitable for pharmacological manipul

54 ble, shed matriptase form cleaves endogenous APP in SH-SY5Y cells and that this cleavage significantl

55 ther, these results suggest that endothelial APP functions as a vascular niche signal that negatively

56 n-canonical MAP kinase cascade that enhances APP transcription and amyloid-beta synthesis.

57 viously screened as negative for established APP, PSEN1, and PSEN2 causal variants.

58 gly recognized as an important crossroad for APP and these secretases, with major implications for AP

59 hese secretases, with major implications for APP processing and amyloidogenesis.

60 Our findings indicate a role for APP in AD pathogenesis beyond the generation of Abeta an

61 umulation of APP carboxylterminal fragments (APP-CTFs) and oligomeric amyloid beta (oAbeta) but no hi

62 the retromer in the production of Abeta from APP.

63 ver, we demonstrated that soluble Abeta from APP/PS1 mice impairs neuronal cell proliferation using n

64 enetic approach to remove the Nrf2 gene from APP/PS1 mice, a widely used animal model of AD.

65 scriptional profiles of adult microglia from APP/PS1 mice and identified a role for RIPK1 in regulati

66 Particularly, whether and how APP may regulate functions of cell surface receptors, in

67 genic mice overexpressing in neurons a human APP gene harboring the APP(E693Q) (Dutch) mutation have

68 ing, in rodent neuroglial cultures and human APP-expressing Chinese hamster ovary cells.

69 s at the synapses of AD-related mutant human APP (hAPP) transgenic (Tg) mice and patient brains.

70 Inducing autophagy in mutant human APP neurons augments autophagic retention of BACE1 in di

71 of Alzheimer's disease-related mutant human APP transgenic neurons and mouse brains.

72 T2 and FE65, both shown to increase immature APP in the early secretory pathway.

73 M344 also increases levels of immature APP, supporting an effect on APP trafficking, concurrent

74 ne to valine substitution at position 673 in APP (A673V), or position 2 of the amyloid-beta (Abeta) s

75 hondrial biogenesis and synaptic activity in APP mice; and that SS31 may confer protective effects ag

76 ranslocation of p53 in cultured cells and in APP/PS1 mice.

77 preferential beta-cleavage site of BACE1 in APP from the Glu(11) site to the Asp(1) site both in mal

78 he ability to ameliorate nesting behavior in APP/PS1 mice.

79 ting membrane, with a subsequent decrease in APP C-terminal fragment (CTF) content in secreted exosom

80 p62 expression rescues cognitive deficits in APP/PS1 mice, a widely used animal model of AD.

81 nificantly exacerbates cognitive deficits in APP/PS1, without altering gross motor function.

82 II transmembrane serine protease family, in APP processing.

83 tor XIa (FXIa), but not FXIIa, was higher in APP-KO mice compared with controls.

84 A in relation to the effects of mutations in APP as the APP proteolytic system has not been investiga

85 r's disease are associated with mutations in APP that increase toxic amyloidogenic cleavage of APP an

86 Mutations in APP, PSEN1, and PSEN2 lead to early-onset Alzheimer dise

87 nts reported from AD-associated mutations in APP.

88 n induced by several agonists were normal in APP-deficient platelets, but the number of circulating p

89 y loss and anxiety-like behavior observed in APP/PS1 mice.

90 gnificantly altered the amyloid pathology in APP mice.

91 to show decreased Abeta levels in plasma in APP A673T carriers and thus provides evidence that lower

92 tion of axonal transport and specifically in APP dynamics, which might link tau isoform imbalances wi

93 nst mitochondrial and synaptic toxicities in APP transgenic mice.

94 whereas lactate levels remained unaltered in APP/PS1 mice from 3 to 12 months of age.

95 ber of substituted lysines tends to increase APP metabolism.

96 e endocytic retention of BACE1 and increased APP processing at presynaptic sites.

97 Furthermore, DNMT3L overexpression increased APP and PSD95 expression in differentiating neurons, whe

98 unction further supports a need to integrate APP and ELN relationships, including the role of amyloid

99 The level of the 25-kDa APP-CTF was evaluated in three independent CSF sample se

100 cts as a neurotrophic factor and full-length APP forming trans-cellular dimers.

101 ite the several-fold increase in CAA levels, APP/PS1;Clu(-/-) mice had significantly less hemorrhage

102 Here we show that all mammalian APP family members (APP, APLP1, and APLP2) exhibit synap

103 tion, indicative of increased BACE1-mediated APP processing, in rodent neuroglial cultures and human

104 cleavage site abolished matriptase-mediated APP processing.

105 show that all mammalian APP family members (APP, APLP1, and APLP2) exhibit synaptogenic activity, in

106 , we administered SS31 to an AD mouse model (APP) over a period of 6 weeks, beginning when the APP mi

107 Moreover, APP/APLPs all bind to synaptic-signaling molecules, such

108 analysis revealed reduced full-length mutant APP and soluble/insoluble Abeta levels in the SS31-treat

109 Abeta levels and immunoreactivity of mutant APP and Abeta levels and (4) mitochondrial function by m

110 nced the lysosomal degradation of the mutant APP, and inhibited gamma-secretase cleavage of the mutan

111 nced the lysosomal degradation of the mutant APP, and inhibited gamma-secretase cleavage of the mutan

112 the effects of increased levels of neuronal APP or Abeta on mitochondrial metabolism and gene expres

113 DS and in Ts65DN mice; however, normalizing APP gene copy number in Ts65Dn mice fails to rescue plas

114 taCTF-APPL1 interactions constitutes a novel APP-dependent pathogenic pathway in AD.

115 tic, with the discovery of a number of novel APP secretases (including delta- and eta-secretases, alt

116 calizing to synapses and genetic ablation of APP prevents both Abeta binding and Abeta-mediated synap

117 time was normal, and in vivo, the absence of APP did not alter thrombus formation in the femoral arte

118 have intraneuronal lysosomal accumulation of APP carboxylterminal fragments (APP-CTFs) and oligomeric

119 ) to reduce apoE expression in the brains of APP/PS1-21 mice homozygous for the APOE-epsilon4 or APOE

120 ease in CAA within the cerebrovasculature of APP/PS1;Clu(-/-) mice.

121 hat increase toxic amyloidogenic cleavage of APP and produce amyloid beta (Abeta) at the expense of s

122 1 distribution in axons and beta cleavage of APP at synapses remain largely unknown.

123 ragment beta (C99), generated by cleavage of APP by beta-site APP cleaving enzyme 1 (BACE-1), is the

124 Gag promotes secretase-dependent cleavage of APP, resulting in the overproduction of toxic Abeta isof

125 axons, leading to enhanced beta-cleavage of APP.

126 cular domains served to characterize CTFs of APP in human CSF.

127 s chimeric mice with selective deficiency of APP in blood cells, developed much larger thrombi than c

128 They further suggest that disruption of APP endosomal sorting reduces its sequestration in ILVs

129 Interfering with HIV-1's evasion of APP-mediated restriction also suppresses HIV-1 spread, o

130 xic effects of Abeta depend on expression of APP and that the Abeta-mediated impairment of synaptic p

131 ke of oAbeta and oTau requires expression of APP.

132 gates to synapses requires the expression of APP.

133 roposes that a small amphipathic fragment of APP, the amyloid beta-protein (Abeta), self-associates t

134 s is known about the physiologic function of APP outside of AD.

135 ficantly improves the cognitive functions of APP/presenilin-1 (PS1) transgenic mice.

136 repeat expansions and a copy number gain of APP, were found in 61 brains.

137 Two homologs of APP exist in mammals: the APP like proteins APLP1 and AP

138 Our results emphasize the importance of APP in AD and should stimulate new studies to elucidate

139 A lack of APP C-terminal lysines caused APP redistribution from en

140 , where APP is highly expressed, the lack of APP leads to a dramatic increase in plasma membrane recr

141 he ACH, PSH and AMA in relation to levels of APP proteolytic fragments reported from AD-associated mu

142 ations have diverse effects on the levels of APP proteolytic fragments.

143 halose decreases the lysosomal metabolism of APP by altering its endocytic vesicular transport.

144 eneration of Abeta and suggest modulation of APP expression as a therapy for AD.SIGNIFICANCE STATEMEN

145 f 3R tau favored the anterograde movement of APP vesicles, increasing anterograde run lengths and red

146 This effect closely mimics the phenotype of APP A673T, a recently discovered mutation that protects

147 SEN2-mediated processing of a larger pool of APP-CTF on the endosomal membrane.

148 Consequently, the presence of APP attenuates alpha2AAR internalization and desensitiza

149 BACE1 expression, as well as processing of APP and other neuronal substrates, was unaltered in 4CA

150 that indirectly modulate BACE processing of APP but spare other BACE substrates and achieve therapeu

151 gesting that non-amyloidogenic processing of APP may be responsible for mitochondrial changes.

152 Increased non-amyloidogenic processing of APP, but not Abeta, profoundly decreased respiration and

153 the sequential gamma-secretase processing of APP.

154 to preferentially govern the proteostasis of APP-C99.

155 ation 1), an important negative regulator of APP translation and oligomerogenesis in the post-synapti

156 In this study, we investigated the role of APP in hemostasis and thrombosis, using APP knockout (KO

157 Further in vivo studies on the role of APP in regulating NSC number in the SVZ clearly demonstr

158 avage sites, suggesting that the sequence of APP and possibly other cleaved TM helices may be designe

159 eevec induces formation of a specific set of APP C-terminal fragments, also observed in cells express

160 ain-located lysines for endosomal sorting of APP.

161 o report the results of a treatment study of APP/PS1 mice with RD2.

162 Here, we show that substitution of APP C-terminal lysines with arginine disrupts APP ubiqui

163 functions that partly overlap with those of APP.

164 evidence suggests that the accepted view of APP proteolysis by the canonical alpha-, beta-, and gamm

165 l lysosomal counts in brain of 12-months-old APP(E693Q) as compared with age-matched non-transgenic l

166 little is known about the impact of DAPK1 on APP metabolism and Abeta generation.

167 els of immature APP, supporting an effect on APP trafficking, concurrent with the observed increase i

168 ecreted exosomes, but had minimal effects on APP lysosomal degradation.

169 activity, DV2-103, exerts similar effects on APP metabolism.

170 e-rich diet, which increases serum 27OHC, or APP ablation, abrogated this response in vivo.

171 on, by using anti-murine Abeta antibodies or APP knock-out mice, prevents the cGMP-dependent enhancem

172 , mutant amyloid precursor protein (APP), or APP and presenilin (PS).

173 vo AICD expression, ex vivo AICD delivery or APP knock-down by in utero electroporation of shRNAs wit

174 rk presents a unifying model for how PSEN or APP mutations enhance amyloidogenic Abeta production, su

175 Remarkably, pathogenic PSEN or APP mutations further destabilize labile E-S complexes a

176 es to membrane microdomains where pathologic APP-processing is thought to occur.

177 Alginate from Padina pavonica (APP) had the highest molecular weight (Mw) with 147,000g

178 These results indicate that platelet APP limits venous thromboembolism through a negative reg

179 (S226D) in young 3xTg mice strongly promotes APP and tau fragmentation and facilitates amyloid plaque

180 Carriers of protective APP A673T variant had, on average, 28% lower levels of A

181 ions of the human amyloid precursor protein (APP mice) and WT mice.

182 Amyloid precursor protein (APP) and its extracellular domain, soluble APP alpha (sA

183 tases, cleave the amyloid precursor protein (APP) and modulate beta-amyloid (Abeta) peptide productio

184 that cleaves both amyloid precursor protein (APP) and tau, mediating the amyloid-beta and tau patholo

185 approximation of amyloid precursor protein (APP) and the beta-site APP cleaving enzyme 1.

186 scription of amyloid-beta precursor protein (APP) and thereby increases amyloid-beta levels.

187 ents (CTF) of the amyloid precursor protein (APP) are present in cerebrospinal fluid (CSF) and their

188 from cleavage of amyloid precursor protein (APP) by beta- and gamma-secretases.

189 l cleavage of the amyloid precursor protein (APP) by beta-secretase (BACE) and gamma-secretase.

190 l cleavage of the amyloid precursor protein (APP) by beta-site APP cleaving enzyme 1 (BACE1) and gamm

191 g of amyloid-beta (Abeta) precursor protein (APP) by gamma-secretase produces multiple species of Abe

192 tic processing of amyloid precursor protein (APP) C-terminal fragments (CTFs) by gamma-secretase unde

193 beta-site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1) is the major neuronal bet

194 beta-Site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1) is the major neuronal bet

195 ATEMENT beta-Site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1) trafficking and synaptic

196 he requirement of amyloid precursor protein (APP) for these effects.

197 Mutations in amyloid beta precursor protein (APP) gene alter APP processing, either causing familial

198 The amyloid precursor protein (APP) harbors physiological roles at synapses and is cent

199 The amyloid precursor protein (APP) has long been appreciated for its role in Alzheimer

200 e function of the amyloid precursor protein (APP) in brain health remains unclear.

201 processing of the amyloid precursor protein (APP) into Abeta peptides, which have been implicated as

202 suggests that the amyloid precursor protein (APP) intracellular C-terminal fragment beta (C99), gener

203 disease (AD), the amyloid precursor protein (APP) is cleaved by beta-secretase to generate a 99-aa C-

204 mbrane-associated amyloid precursor protein (APP) is highly expressed in macrophages and microglia, a

205 lites of the amyloid-beta-precursor protein (APP) is neurotoxic.

206 s occurring while amyloid precursor protein (APP) is trafficking through the early secretory pathway.

207 ns (PSEN) and the amyloid precursor protein (APP) lead to production of longer amyloidogenic Abeta pe

208 ypotheses and the amyloid precursor protein (APP) matrix approach (AMA), of which the ACH has held a

209 nd BACE-1-cleaved amyloid precursor protein (APP) metabolites (secreted APPbeta, C99, Abeta40, and Ab

210 and lysosomes in amyloid precursor protein (APP) processing and clearance, and the pathologic effect

211 e exhibit altered amyloid precursor protein (APP) processing, abnormally increased production of amyl

212 ponse and altered amyloid precursor protein (APP) processing.

213 this site of amyloid beta precursor protein (APP) reduced C99 generation and decreased the C99/C89 ra

214 vidence links the amyloid precursor protein (APP) to Alzheimer's disease (AD) and several theories ha

215 roinflammation in amyloid precursor protein (APP) transgenic mice are worsened by astroglial NF-kappa

216 e dynamics of the amyloid precursor protein (APP) were significantly impaired.

217 The amyloid precursor protein (APP), a key player in Alzheimer's disease, belongs to th

218 s disease-related amyloid precursor protein (APP), although neuronal morphology was normal.

219 roteolysis of the amyloid precursor protein (APP), first by the action of beta-secretase, generating

220 ntial cleavage of amyloid precursor protein (APP), is a critical step in the pathogenesis of Alzheime

221 AD (FAD), mutant amyloid precursor protein (APP), or APP and presenilin (PS).

222 tic processing of amyloid precursor protein (APP), play a central role in AD pathogenesis.

223 The amyloid precursor protein (APP), primarily known as the precursor of amyloid peptid

224 mice that express amyloid precursor protein (APP), which is duplicated in DS and in Ts65DN mice; howe

225 oTau can bind to amyloid precursor protein (APP).

226 e TM helix of the amyloid precursor protein (APP).

227 with that of the amyloid precursor protein (APP).

228 eavage of the Alzheimer's precursor protein (APP).

229 Using the amyloid precursor protein (APP)/presenilin 1 (PS1) transgenic mouse model, we found

230 scovered that, in amyloid precursor protein (APP)/presenilin-1 (PS1) mice (age 3-4 mo), a prominent m

231 e-bound beta-site amyloid precursor protein-(APP) cleaving enzyme (BACE1) from the endolysosomal path

232 and that this cleavage significantly reduces APP processing to Abeta40.

233 This molecular mechanism also regulates APP transcription in mice in vivo.

234 he results demonstrate that APP673 regulates APP processing and the BACE1 cleavage site selection is

235 he results demonstrate that APP673 regulates APP processing, and the BACE1 cleavage site selection is

236 It renders APP less susceptible to proteolysis by BACE without inhi

237 The resulting APP/PS1-rTg4510 mice had a threefold increase in tau see

238 functions are mediated by both the secreted APP ectodomain that acts as a neurotrophic factor and fu

239 Similarly, APP transgenic mice treated with NIR showed a significan

240 n memory and LTP is dependent upon APP since APP-KO mice were resistant to oAbeta- and oTau-induced d

241 ), generated by cleavage of APP by beta-site APP cleaving enzyme 1 (BACE-1), is the primary cause of

242 amyloid precursor protein (APP) by beta-site APP cleaving enzyme 1 (BACE1) and gamma-secretase.

243 Under normal conditions, beta-site APP cleaving enzyme 1 (BACE1) cleaves APP at minor Asp(1

244 development.SIGNIFICANCE STATEMENT beta-site APP cleaving enzyme 1 (BACE1) is essential for amyloid b

245 beta-Site APP cleaving enzyme 1 (BACE1), the transmembrane asparty

246 Assessing BACE1 (beta-site APP cleaving enzyme 1) knockout mice for general health

247 id precursor protein (APP) and the beta-site APP cleaving enzyme 1.

248 2alpha and enhanced translation of beta-site APP cleaving enzyme-1 (BACE1).

249 (APP) and its extracellular domain, soluble APP alpha (sAPPalpha) play important physiological and n

250 Moreover, specific APP isoforms contain Kunitz protease-inhibitory domains,

251 guideline application with decision support (APP).

252 ncovers a new pathway that controls synaptic APP processing by enhancing axonal BACE1 trafficking, th

253 whether axonal transport regulates synaptic APP processing.

254 ecause some therapeutic interventions target APP processing (e.g., BACE inhibitors), those strategies

255 We demonstrate that APP-CTFs are detectable in human CSF, being the most abu

256 Our study provided the first evidence that APP fine tunes GPCR signaling and trafficking.

257 Our data suggest that APP-CTF could be a potential diagnostic biomarker for AD

258 Evidence suggests that APP intracellular domain (AICD) could regulate synapse f

259 The APP interaction with alpha2AAR is promoted by agonist st

260 tanding of the roles these fragments and the APP proteolytic system as a whole in normal aging and di

261 on to the effects of mutations in APP as the APP proteolytic system has not been investigated systema

262 rotective signaling pathway initiated by the APP transcriptionally active intracellular domain (AICD)

263 e this effect, we combined mice carrying the APP/PS1 transgene array that develop plaques with rTg451

264 ments, also observed in cells expressing the APP protective mutation and in cells exposed to a conven

265 ng in neurons a human APP gene harboring the APP(E693Q) (Dutch) mutation have intraneuronal lysosomal

266 ave described a novel C-to-T mutation in the APP gene that corresponds to an alanine to valine substi

267 nicillin or cephalosporin use overall in the APP period (aOR, 1.8; 95% CI, 1.1-2.9) and in a per-prot

268 In the APP period, there were 292 unique Web site views; 112 us

269 d that neurogenesis is affected early in the APP/PS1 hippocampus, as evidenced by a significant decre

270 enhances Abeta production by increasing the APP/BACE-1 convergence in endolysosomal compartments.

271 Two homologs of APP exist in mammals: the APP like proteins APLP1 and APLP2, exhibiting functions

272 pable of accommodating the complexity of the APP proteolytic system is required to integrate availabl

273 ereas DNMT3LshRNA could partially rescue the APP and PSD95 up-regulation in DS cells.

274 driver that targets functional cargos to the APP machinery and can be used as a tool to study the con

275 over a period of 6 weeks, beginning when the APP mice were 12 months of age.

276 Thus, APP might serve as a common therapeutic target against A

277 Using the McGill-R-Thy1-APP transgenic rat as a model of selective Abeta patholo

278 Compared to APP, APLP1 exhibits increased trans-cellular binding and

279 Notably, the core genes were connected to APP (encoding amyloid beta precursor protein), a major p

280 ting axons of cocultured neurons, similar to APP and other SAMs.

281 ostnatal Abeta precursor protein transgenic (APP tg) mice, Abeta deposition emerged in HSCs when cult

282 function was maintained in the SS31-treated APP mice over the 6 weeks of SS31 treatment compared wit

283 iogenesis and synaptic genes in SS31-treated APP mice relative to SS31-untreated APP mice.

284 ced soluble Abeta levels in the SS31-treated APP mice relative to the untreated APP mice.

285 e/insoluble Abeta levels in the SS31-treated APP mice.

286 er dimerization between mutant and wild-type APP, enhanced the lysosomal degradation of the mutant AP

287 er dimerization between mutant and wild-type APP, enhanced the lysosomal degradation of the mutant AP

288 -treated APP mice relative to SS31-untreated APP mice.

289 with mitochondrial function in the untreated APP mice.

290 1-treated APP mice relative to the untreated APP mice.

291 and oTau on memory and LTP is dependent upon APP since APP-KO mice were resistant to oAbeta- and oTau

292 An RNA interference screen using APP-CTF [99-residue CTF (C99)]- and Notch-specific gamma

293 e of APP in hemostasis and thrombosis, using APP knockout (KO) mice.

294 zheimer's disease (AD)-related rare variants APP A673T and ABCA7 rs200538373-C with the levels of bet

295 IV-associated neurocognitive disorders where APP misprocessing to amyloid beta formation has been obs

296 mitochondrial perturbations in models where APP is overexpressed, and a potential role of sAPPalpha

297 ry superior cervical ganglion neurons, where APP is highly expressed, the lack of APP leads to a dram

298 which might link tau isoform imbalances with APP abnormal metabolism in neurodegenerative processes.

299 nesis but also as the essential partner with APP and its metabolites that drive the development of AD

300 tological measures of tau pathology in young APP/PS1-rTg4510 mice and an increase in high-molecular-w