ライフサイエンスコーパス: Abeta

1 ing can result in formation of beta-amyloid (Abeta).

2 loidogenic pathway to generate amyloid-beta (Abeta).

3 l fluid (CSF) or plasma in MCI Abeta+ and AD Abeta+.

4 s degradation product, the Alzheimer protein Abeta.

5 ntibody for monomeric and fibrillar forms of Abeta.

6 e maturation of multiple substrates, such as Abeta.

7 tion may contribute to impaired clearance of Abeta.

8 er mimic the oligomers formed by full-length Abeta.

9 bear "tails" derived from the N-terminus of Abeta.

10 tein (App) gene was mutated to produce human Abeta.

11 C) to 5hmC are responsive to the presence of Abeta.

12 ess, calcium overload, oxidative stress, and Abeta 1-42 oligomers toxicity.

13 we report that the soluble, nonfibrillizing Abeta (1-30) peptide recapitulates full-length Abeta ste

14 Moreover, we found that Abeta (1-30) uptake is also dependent on PrP(C) expressi

15 hat underlies the stereoselective binding of Abeta (1-30).

16 during the synthesis to append residues from Abeta(1-14) to the parent macrocyclic beta-hairpin pepti

17 erein parallel and anti-parallel variants of Abeta(1-40) dimers were designed and synthesized, and th

18 n of binary and ternary complexes among TTR, Abeta(1-42) peptide, and TTR stabilizers using isotherma

19 Notably, Abeta(1-42) tetramers and octamers inserted into lipid b

20 crocyclic beta-hairpin peptides derived from Abeta(16-22) and Abeta(30-36), capable of forming hexame

21 clic beta-hairpin peptide 1, which comprises Abeta(16-22) and Abeta(30-36).

22 ynthesized macrocyclic peptides derived from Abeta(17-23) and Abeta(30-36) that fold to form beta-hai

23 ing to the abnormal (+)/normal (-) status of Abeta ((18)F-florbetapir or (18)F-florbetaben) positron

24 of functional gap junctions indicating that Abeta(25-35) causes rapid internalization of Cx43 gap ju

25 We show that Abeta(25-35) impairs functional gap junction coupling ye

26 how that interruption of Cx43 endocytosis in Abeta(25-35)-exposed astrocytes resulted in their retent

27 lready reached the Golgi was not affected in Abeta(25-35)-exposed astrocytes.

28 yclic peptides derived from Abeta(17-23) and Abeta(30-36) that fold to form beta-hairpins and assembl

29 irpin peptides derived from Abeta(16-22) and Abeta(30-36), capable of forming hexamers that can be ob

30 peptide 1, which comprises Abeta(16-22) and Abeta(30-36).

31 -bead-one compound (OBOC) library to inhibit Abeta(40) aggregation, we investigated eight (8) analogu

32 detection of ultra-low concentrations of the Abeta-40 peptides.

33 Furthermore, Abeta(42) colocalized with HSV-1 latency-associated tran

34 e abundance of these proteins, as well as of Abeta(42) ExNef further potentiated phosphorylation of T

35 g microglial response to Abeta peptide 1-42 (Abeta(42)) stimulation in vitro, in aging-associated mic

36 arch demonstrated that soluble amyloid-beta (Abeta)(42), elicits presynaptic glutamate release.

37 TTR against cellular toxicity of pathogenic Abeta, a protein associated with Alzheimer's disease.

38 the deposition, processing, and toxicity of Abeta (Abeta) peptides.

39 of APP, BACE1, and the two primary forms of Abeta (Abeta40 and Abeta42) in a primary human cell cult

40 d C-terminal regions, with the N-terminus of Abeta accommodated by the oligomers as an unstructured t

41 ospective biomarkers of the speed with which Abeta accumulates over time.

42 Abeta accumulation affects mitochondrial redox balance,

43 neurodegenerative process, including reduced Abeta accumulation as well as tau hyperphosphorylation,

44 containing phospho-deficient PS1 show severe Abeta accumulation in microglia as well as the postsynap

45 g early therapeutic option for prevention of Abeta accumulation in the brain.

46 line to model the impact of human APP (hAPP)/Abeta accumulation on tauopathy in the entorhinal cortex

47 , and improves cognition in a mouse model of Abeta accumulation.

48 Amyloid-beta peptide (Abeta) accumulation in the brain is a hallmark of Alzhei

49 ured platelets and decreased the adhesion of Abeta-activated platelets to injured carotid arteries in

50 PES of Abeta-ADCRP is a valid biomarker of underlying amyloid p

51 pression scores (PESs) of the (18)F-FDG- and Abeta-ADCRP were compared with Braak tangle stage and Th

52 as only negligible improvement compared with Abeta-ADCRP.

53 However, the mechanisms by which Abeta affects sleep are unknown.

54 its high specific affinity for beta-amyloid (Abeta) aggregates, leading to the successful PET imaging

55 tinct effects of IAPP peptides in modulating Abeta aggregation and toxicity and provide new insight i

56 vel the mechanistic consequences of delaying Abeta aggregation via weak metal-ion binding, quantitati

57 been proposed as indicative of beta-amyloid (Abeta) aggregation and thus potential biomarkers for Alz

58 understanding the complex interplay between Abeta, aging, and neurodegeneration within the most vuln

59 thesized that accumulation and deposition of Abeta altered glutamatergic neurotransmission in a tempo

60 TTR binds Abeta, alters its aggregation, and inhibits its toxicity

61 the ABX cocktail significantly reduced brain Abeta amyloidosis compared to vehicle-treated animals.

62 KO mice produced normal levels of endogenous Abeta and exhibited normal electrophysiological response

63 croscopy we found that the co-aggregation of Abeta and ferritin resulted in the conversion of ferriti

64 Since the interaction between Abeta and fibrinogen increases CAA and plays an importan

65 independent of its ability to interact with Abeta and form heterocomplexes; suggesting mediation by

66 k by decreasing the response of microglia to Abeta and its local toxicity.

67 ith or without antivirals, were assessed for Abeta and p-tau expression over 7 days postinfection.

68 Given that processing of APP to Abeta and soluble APP alpha (sAPPalpha) contributes to d

69 unction, it has been typically presumed that Abeta and tau act independently and in the absence of sp

70 In NCI, proNGF correlated with cerebral Abeta and tau deposition and to cognitive performance.

71 a herein support a synergistic role for both Abeta and tau in driving neuronal dysfunction seen in AD

72 is specific for AD, correlates with cerebral Abeta and tau pathology, and predicts future cognitive d

73 review recent data regarding biomarkers for Abeta and tau pathology, neurodegeneration, synaptic dys

74 w these elements relate to findings based on Abeta and tau PET scintigraphy.

75 ur data suggest that therapies downstream of Abeta and tau together are more suitable to combat AD th

76 ate the metabolism of ApoE and beta-amyloid (Abeta) and are potential therapeutic targets for Alzheim

77 of the AD-associated proteins beta-amyloid (Abeta) and hyper-phosphorylated tau (p-tau) in Vero and

78 erized by amyloid plaques with amyloid beta (Abeta) and neurofibrillary tangles with tau accumulation

79 n cerebrospinal fluid (CSF) or plasma in MCI Abeta+ and AD Abeta+.

80 contained intracellular amylin, APP, and/or Abeta, and amyloid.

81 TDP-43 induced inflammation, interacted with Abeta, and exacerbated AD-like pathology.

82 d clearance of CNS waste products, including Abeta, and for understanding how neuronal activity can m

83 understanding how melatonin protects against Abeta, and that choice of chain perdeuteration is an imp

84 Lesion load correlated with lower Aalpha-, Abeta-, and Adelta-fiber but not with C-fiber function i

85 IgG1 Fc domain (hFc) or to the amyloid-beta (Abeta) antibody bapineuzumab (Bapi).

86 of Alzheimer's disease pathogenesis in which Abeta appears early, followed by deposition of abnormal

87 Naturally secreted soluble Abeta applied onto the healthy brain increases Ca(2+) co

88 ccumulated that implicates the N-terminus of Abeta as a region that may initiate the formation of dam

89 mplicating the intraneuronal accumulation of Abeta as a significant immunological component in the AD

90 nated, native, mouse and human brain-derived Abeta assemblies.

91 Therefore, we investigated Abeta asymmetries in Abeta mouse models examined by Abet

92 ing fragments that dramatically improves the Abeta-binding affinity and lipophilicity for favorable b

93 cting fragments further improves the in vivo Abeta-binding specificity and brain uptake of the corres

94 deltaC reduces the later-stage extracellular Abeta burden and cognitive impairment, suggesting that p

95 Increased brain Abeta burden by amylin and pramlintide was associated wi

96 Thus, we reveal the Abeta-burdened neuron as a primary proinflammatory agent

97 identified an inflammatory profile unique to Abeta-burdened neurons, since neighboring glial cells di

98 o recordings revealed a strong role for hAPP/Abeta, but not tau, in the emergence of EC neuronal hype

99 nally, this segment also inhibits seeding of Abeta catalyzed by Abeta fibrils extracted from the brai

100 rden of tau (Braak score, P = 1.0 x 10(-5)), Abeta (CERAD score, P = 1.8 x 10(-5)), and cognitive dia

101 An important mechanism of Abeta clearance in the brain is uptake and degradation b

102 pite the presence of mechanisms dedicated to Abeta clearance is still lacking.

103 this issue of the JCI, Roy et al. show that Abeta complexed with nucleic acids triggers an antiviral

104 g with 5xFAD mouse analysis, we determine 15 Abeta-correlated proteins (e.g., MDK, NTN1, SMOC1, SLIT2

105 portions of Abeta-preventing (Abeta1-19) and Abeta-degradation products (Abeta1-20 and Abeta1-34).

106 d inflammation as well as enhanced the brain Abeta deposition and cognitive impairment in Tg-SwDI mic

107 the PFC region is selectively susceptible to Abeta deposition and less responsive to the attenuating

108 ssion of CD36 in the brain may contribute to Abeta deposition and neuroinflammation in AD.

109 eir ability to neutralize Abeta seeds before Abeta deposition becomes detectable in Abeta precursor p

110 , M1 and SS2 regions plateau with respect to Abeta deposition by 12 months of age and are susceptible

111 ry to expectation, the LLD group showed less Abeta deposition than the ND group and Abeta deposition

112 less Abeta deposition than the ND group and Abeta deposition was not associated with depression hist

113 ose relationship between vascular and plaque Abeta deposition, several factors favour one or the othe

114 l amyloid angiopathy (CAA) and beta-amyloid (Abeta) deposition in the brain parenchyma are hallmarks

115 Amyloid-beta (Abeta) deposition occurs years before cognitive symptoms

116 myloid angiopathy (CAA), where beta-amyloid (Abeta) deposits around cerebral blood vessels, is a majo

117 re affected by the presence of beta-Amyloid (Abeta) deposits, hallmark lesions of Alzheimer's disease

118 a mutation to further stabilize oligomers of Abeta-derived peptides that contain more of the native s

119 reclinical and clinical studies suggest that Abeta drives neurite and synapse degeneration through an

120 and humans causally modulates beta-amyloid (Abeta) dynamics (e.g., [1-3]).

121 Striatal lesion core and globus pallidus of Abeta + ET1 rats showed extensive degeneration of neuron

122 excessive neuronal demise in the striatum of Abeta + ET1 rats.

123 Deposition of amyloid-beta (Abeta) fibers in the extracellular matrix of the brain i

124 eta fibril induced by EGCG and inhibition of Abeta fibril and oligomer formation, as manifested by th

125 nsor data are consistent with degradation of Abeta fibril induced by EGCG and inhibition of Abeta fib

126 In this study, we develop a minimal model of Abeta fibrillization to investigate the onset of AD over

127 in short timescales, an understanding of how Abeta fibrillization usually starts to dominate at a lon

128 eric Abeta peptide and efficiently modulates Abeta fibrillization.

129 herical oligomers and perturbs amyloid-beta (Abeta) fibrillization.

130 also inhibits seeding of Abeta catalyzed by Abeta fibrils extracted from the brain of an Alzheimer's

131 mitations of current tools to size and count Abeta fibrils in real time.

132 ide monomers can be catalyzed by preexisting Abeta fibrils.

133 Biomarkers such as beta-amyloid (Abeta) fibrils and Tau tangles in Alzheimer's disease ar

134 amage in AD, we investigated the role of the Abeta-fibrinogen interaction in HCAA pathology.

135 up to a 50-fold stronger binding affinity of Abeta for fibrinogen.

136 Yet Abeta formation itself may not be pathogenic.

137 roach to directly detect oligomeric forms of Abeta formed in solution.

138 ind specifically to the N-terminal region of Abeta, forming a dynamic, partially compact complex.

139 receptor component 1 (Pgrmc1), while longer Abeta forms induce sleep through a pharmacologically tra

140 d signatures for Abeta43, Abeta38, and short Abeta fragments.

141 ments without impacting normal physiological Abeta functions.

142 ease but plasma p-tau181 is increased if CSF Abeta has already changed prior to Abeta PET changes.

143 Human Abeta has higher propensity to form toxic Abeta species,

144 (TTR) on cellular toxicity of beta-amyloid (Abeta) has been previously reported.

145 terise the different types and morphology of Abeta-hIAPP heterocomplexes and determine if formation o

146 ght into the potential pathogenic effects of Abeta-IAPP hetero-oligomerization and development of IAP

147 ostaining that parallels the accumulation of Abeta in 5xFAD mice was not affected by PD except for a

148 protecting against the pathologic actions of Abeta in AD.SIGNIFICANCE STATEMENT Elevated levels of be

149 show that statins are effective at reducing Abeta in human neurons from nondemented control subjects

150 beta-site cleaving enzyme (BACE1), APP, and Abeta in human primary astrocytes (HPAs) exposed to Tat.

151 Such findings strongly implicate Abeta in the altered iron handling and increased oxidati

152 gomers mostly colocalized with intracellular Abeta in the brain of AD patients.

153 dies of immunity to pathogenic amyloid-beta (Abeta) in LOAD are lacking.

154 E STATEMENT Elevated levels of beta-amyloid (Abeta) in the brain are thought to contribute to the cog

155 A new Abeta-independent hypothesis emerges where the amyloidog

156 whether this phenomenon represents an early, Abeta-independent pathway that facilitates dementia path

157 of AT and PM FTP, but not EC, were driven by Abeta+ individuals.

158 rIAPP exhibited reductions in Abeta induced neuronal cell death that was independent o

159 ation; and potential rescue of amyloid-beta (Abeta) induced synaptic impairment.

160 In vitro, rhizolutin substantially decreased Abeta-induced apoptosis and inflammation in neuronal and

161 eviously demonstrated implicated in blocking Abeta-induced cytotoxicity in neuronal cell cultures.

162 s were used to analyse annexin A5 effects on Abeta-induced cytotoxicity.

163 that tau suppression did not protect against Abeta-induced damage of long-term synaptic plasticity an

164 Several compounds inhibit Abeta-induced Fyn kinase activation and decrease pTau le

165 of several transmembrane proteins, restored Abeta-induced impaired gap junction coupling between ast

166 to choroid plexus cell cultures restored the Abeta-induced impairments on autophagy flux and apoptosi

167 expression in these animals protects against Abeta-induced impairments without impacting normal physi

168 olecular factors that control sensitivity to Abeta-induced impairments, and suggest that inhibiting P

169 ME-1 and LCMT-1 in regulating sensitivity to Abeta-induced impairments, and suggest that inhibition o

170 , LCMT-1, altered the sensitivity of mice to Abeta-induced impairments, suggesting that PME-1 inhibit

171 However, Abeta-induced inactivation of the eukaryotic initiation

172 protect dendritic spines and processes from Abeta-induced injury.

173 o demonstrated that APN deficiency increased Abeta-induced microglia activation and neuroinflammatory

174 we cautiously conclude that ligand 1 reduces Abeta-induced mitochondrial and synaptic toxicities, and

175 he sensitizing nAChRs, linked to early-stage Abeta-induced neurotoxicity, which may represent novel t

176 These results unveil a novel mechanism of Abeta-induced synaptic dysfunction in AD patients, and i

177 acers between the Cu-chelating group and the Abeta-interacting fragments further improves the in vivo

178 proach uses a bifunctional chelator with two Abeta-interacting fragments that dramatically improves t

179 d, suggesting that the microglial packing of Abeta into dense plaque is an important neuroprotective

180 Abeta is derived from amyloid precursor protein (APP) th

181 h the self-assembly of amyloid-beta peptide (Abeta) is a causative process in Alzheimer's disease, ha

182 Amyloid-beta (Abeta) is a macromolecular structure of great interest b

183 a and is not associated with increased human-Abeta levels and AD pathology.

184 h associated with a significant reduction in Abeta levels and deposition and tau phosphorylation.

185 Although Abeta levels become abnormal long before severe cognitiv

186 o inhibit abnormal APP processing and reduce Abeta levels in AD neurons.

187 ions in APP metabolism rather than simply on Abeta levels.

188 surrogate of learning and memory, but normal Abeta levels.

189 Amyloid-beta (Abeta) likely plays a primary role in Alzheimer's diseas

190 hitecture of heteromerization between 4F and Abeta(M1-42) discovered in this study provides evidence

191 These data support Abeta mechanistic tenets in a human physiological model

192 e unknown mechanisms are triggered to resist Abeta-mediated detrimental events.

193 the therapeutic interventions that may alter Abeta metabolism in humans.

194 ew, the authors describe the determinants of Abeta metabolism, summarize the effects of Abeta on athe

195 nuclear receptors involved in beta-amyloid (Abeta) metabolism and progression of Alzheimer's disease

196 ronal damage, underlying mechanisms by which Abeta modulates Cx43 in astrocytes remain elusive.

197 t links the microscopic metal-ion binding to Abeta monomers to its macroscopic impact on the peptide

198 of Abeta PET and TSPO PET in 4 investigated Abeta mouse models (APP/PS1: R = 0.593, P = 0.001; PS2AP

199 refore, we investigated Abeta asymmetries in Abeta mouse models examined by Abeta small-animal PET an

200 We demonstrate that hIAPP promotes Abeta oligomerization and formation of small oligomer an

201 e brain in vivo and the inability to degrade Abeta oligomers due to a phagolysosome dysfunction.

202 key insight has been an increase in soluble Abeta oligomers in early AD that is causally linked to n

203 Genetic disruptions revealed that short Abeta oligomers induce acute wakefulness through Adrener

204 istent with a model in which the assembly of Abeta oligomers is driven by hydrogen bonding and hydrop

205 eta40 ratio and amount of soluble, fibrillar Abeta oligomers were elevated in Trem2-deficient brains.

206 insights into the structure and assembly of Abeta oligomers, our laboratory has previously designed

207 al. elucidate the first atomic structures of Abeta oligomers, which reveal how they form lipid-stabil

208 Amyloid-beta (Abeta) oligomers are implicated in Alzheimer disease (AD

209 f Abeta metabolism, summarize the effects of Abeta on atherothrombosis and cardiac dysfunction, discu

210 PA, leaving unopposed the harmful effects of Abeta on the synapse.

211 amined the effect of increased beta-amyloid (Abeta) on Cx43 expression and function leading to neuron

212 mouse models diminishes ApoE expression and Abeta pathologies, whereas overexpression of C/EBPbeta a

213 ASO treatment led to decreased Abeta pathology and improved spatial learning and memory

214 c and mitochondrial function, independent of Abeta pathology.

215 ived ROS in mediating microglial response to Abeta peptide 1-42 (Abeta(42)) stimulation in vitro, in

216 y to divalent metal ions, binds to monomeric Abeta peptide and efficiently modulates Abeta fibrilliza

217 The nucleation of Alzheimer-associated Abeta peptide monomers can be catalyzed by preexisting A

218 e the chemical components of cocoa hindering Abeta peptide on-pathway aggregation and toxicity in a h

219 of the molecular pathways for amyloid-beta (Abeta) peptide aggregation from monomers into amyloid fi

220 l form of CAA in which mutations within the (Abeta) peptide cause an increase in vascular deposits.

221 rsor protein (APP) to form the amyloid beta (Abeta) peptide is related to the pathogenesis of Alzheim

222 The amyloid-beta (Abeta) peptide, a key pathogenic factor in Alzheimer's d

223 this method in the case of the amyloid beta (Abeta) peptide, whose oligomers are associated with Alzh

224 could be an initial source of amyloid beta (Abeta) peptide-containing amyloid plaque development.

225 the accumulation of misfolded amyloid-beta (Abeta) peptide.

226 plaques primarily comprising amyloid- beta (Abeta) peptide.

227 cessing, resulting in increased secretion of Abeta peptides and an increased Abeta38 to Abeta40 and A

228 s, for example post-translationally modified Abeta peptides with a pyroglutamate at the N-terminus (p

229 plaques composed of fibrillar amyloid beta (Abeta) peptides and intracellular neurofibrillary tangle

230 ofibrillary tangles, formed by amyloid beta (Abeta) peptides and phosphor-tau, respectively, in the c

231 of amyloid plaques composed of amyloid beta (Abeta) peptides and the cerebrospinal fluid concentratio

232 Preventing aggregation of amyloid beta (Abeta) peptides is a promising strategy for the treatmen

233 Specific forms of amyloid beta (Abeta) peptides, for example post-translationally modifi

234 ortion of longer amyloidogenic amyloid-beta (Abeta) peptides.

235 position, processing, and toxicity of Abeta (Abeta) peptides.

236 was a significant correlation between AIs of Abeta PET and TSPO PET in 4 investigated Abeta mouse mod

237 ed if CSF Abeta has already changed prior to Abeta PET changes.

238 lassified as AD dementia but having negative Abeta PET scans show little increase but plasma p-tau181

239 AIs of Abeta PET were analyzed in correlation with TSPO PET AIs

240 (+) ) synthesis, and reversed the defects in Abeta phagocytosis.

241 inflammatory response may precede insoluble Abeta plaque and tau tangle formation.

242 g studies in patients with AD, indicate that Abeta plaque deposition precedes cortical tau pathology.

243 barrier and provides excellent contrast for Abeta plaques and cerebral amyloid angiopathy.

244 aspects that contribute to the formation of Abeta plaques are well addressed at the intra- and inter

245 The deposition of amyloid beta (Abeta) plaques and fibrils in the brain parenchyma is a

246 resent with both extracellular amyloid-beta (Abeta) plaques and intracellular tau-containing neurofib

247 terized by the accumulation of amyloid-beta (Abeta) plaques and tau neurofibrillary tangles in the br

248 body-based removal of cerebral amyloid beta (Abeta) plaques may possibly clear tau tangles and modest

249 of brain metabolic wastes and amyloid-beta (Abeta) plaques, perivascular reactive astrogliosis, and

250 Oligomers of the beta-amyloid peptide, Abeta, play a central role in the pathogenesis and progr

251 but a mechanistic understanding of the role Abeta plays in AD has remained unclear.

252 n-3-gallate (EGCG), found in green tea, with Abeta polypeptides, using a combination of in vitro immu

253 effectively reducing the available monomeric Abeta pool for incorporation into fibrils.

254 hods and labeled most elderly individuals as Abeta-positive.

255 significantly predicted progression time to Abeta positivity (ADNI memory factor composite was trend

256 ciated with increased odds of progression to Abeta positivity.

257 of AD pathogenesis has been that changes in Abeta precipitate the disease process and initiate a del

258 efore Abeta deposition becomes detectable in Abeta precursor protein-transgenic mice.

259 1 organoids secrete increased proportions of Abeta-preventing (Abeta1-19) and Abeta-degradation produ

260 tes the non-amyloidogenic pathway preventing Abeta production.

261 Abeta protofibrils accumulate at the exterior of senile

262 e a viable therapeutic avenue for preventing Abeta-related impairments in Alzheimer's disease.

263 re attractive antibody targets, due to pGlu3-Abeta's neo-epitope character and its propensity to form

264 investigated the effects of mutations on the Abeta secretome in human neurons generated in 2D and 3D.

265 s that therapeutically targetable pathogenic Abeta seeds already exist during the lag phase of protei

266 s antibodies for their ability to neutralize Abeta seeds before Abeta deposition becomes detectable i

267 Moreover, AD Abeta+ showed a significant association between the redu

268 symmetries in Abeta mouse models examined by Abeta small-animal PET and tested if such asymmetries ha

269 an Abeta has higher propensity to form toxic Abeta species, which are considered the main pathogenic

270 The relationship between amyloid-beta (Abeta) species and tau pathology in Alzheimer's disease

271 However, the main beta-amyloid (Abeta) species and what imbues the aggregates with such

272 eta (1-30) peptide recapitulates full-length Abeta stereoselective cellular uptake, allowing us to de

273 cal responses to picomolar concentrations of Abeta, suggesting that reduced PME-1 expression in these

274 changes may begin early, potentially before Abeta surpasses the threshold for abnormality.

275 preclinical studies, we describe ADx-001, an Abeta-targeted liposomal macrocyclic gadolinium (Gd) ima

276 mer's disease pathogenesis, but longitudinal Abeta, tau, and neurodegeneration (A/T/N) measurements i

277 Further, these changes occurred in the Abeta;tau transgenic animals at greater levels than worm

278 herefore identify a specific sequence within Abeta that is responsible for the recognition of the pep

279 thogenic entity in AD, as compared to rodent Abeta, the rat Amyloid Precursor Protein (App) gene was

280 previously been explored as a potential anti-Abeta therapeutics.

281 ic interactions of metal ions with monomeric Abeta to their effects on bulk aggregation.

282 r overlapping mechanism between ischemia and Abeta toxicity are lacking.

283 rmone that has been shown to protect against Abeta toxicity in cellular and animal studies, but the m

284 we investigated the effects of annexin A5 on Abeta toxicity in choroid plexus.

285 oconstrictive endothelin-1 (ET-1) along with Abeta toxicity on CNS pathogenesis; driven by the anatom

286 omical units in the brain after ischemia and Abeta toxicity will help in the design of effective and

287 dditive association between the infarcts and Abeta toxicity.

288 ified apparent changes in gene expression on Abeta treatment in the presence of the sensitizing nAChR

289 Genes up-regulated with Abeta treatment were associated with calcium signaling a

290 Mechanistically, LRP4 promotes Abeta uptake by astrocytes likely by interacting with Ap

291 SORL1 and TREM2 mutations also impaired hMGL Abeta uptake in an APOE-dependent manner in vitro and at

292 POE-dependent manner in vitro and attenuated Abeta uptake/clearance in mouse AD brain xenotransplants

293 When utilizing Abeta variants with different critical oligomer concentr

294 To better mimic oligomers of full length Abeta, we use an orthogonal protecting group strategy du

295 al fluid phosphorylated tau and subthreshold Abeta were associated with increased odds of progression

296 increasing levels of soluble and oligomeric Abeta, which are known to be the most toxic amyloid spec

297 d from the central and C-terminal regions of Abeta, which bear "tails" derived from the N-terminus of

298 he recovery of the amide-I band of monomeric Abeta, which is red-shifted by 26 cm(-1) when compared t

299 s to be affected by EC tau in the absence of Abeta, which may be less clinically consequential.

300 rease the interaction between fibrinogen and Abeta, which might be central to cerebrovascular patholo