ライフサイエンスコーパス: beta-amyloid

1 sitron emission tomography imaging for brain beta-amyloid.

2 inhibited by elevated levels of full-length beta-amyloid.

3 onformers with structures similar to that of beta-amyloid.

4 id peptide ("T30") which has homologies with beta-amyloid.

5 -terminal peptide to modulate the potency of beta-amyloid.

6 regation of the Alzheimer's-related peptide, beta-amyloid.

7 sment, laboratory analyses of CSF, including beta amyloid 1-42 (Abeta 42), total tau (t-tau), phospho

8 amily, is up-regulated in neurons upon toxic beta-amyloid 1-42 (Abeta(1-42)) exposure both in vitro a

9 Furthermore, we showed that beta-amyloid 1-42 (Abeta(1-42)) oligomers, but not monom

10 ply florbetapir)-PET scan and at least 1 CSF beta-amyloid 1-42 (Abeta1-42) sample obtained within 30

11 tal tau (t-tau), phosphorylated tau (p-tau), beta-amyloid 1-42 (Abeta42), neurofilament light chain (

12 Hg for P-tau alone vs 60.1 [16.4] mm Hg for beta-amyloid 1-42 alone vs 56.6 [14.5] mm Hg for negativ

13 al fluid levels of orexin, tau proteins, and beta-amyloid 1-42 and polysomnographic assessment of sle

14 in those exhibiting both P-tau elevation and beta-amyloid 1-42 reduction vs either biomarkers alone (

15 rmal looking neurons expressing p-tau and in beta-amyloid 1-42-plaque positive regions.

16 spinal fluid phosphorylated tau (P-tau) and beta-amyloid 1-42.

17 Levels of orexin, tau proteins, and beta-amyloid 1-42; macrostructural variables of nocturna

18 Serial CSF samples were analyzed for beta-amyloid 40 (Abeta40), Abeta42, total tau, tau phosp

19 ipoprotein E gene, and CSF concentrations of beta-amyloid 42 (Abeta42) and tau (biomarkers of Alzheim

20 nted microglial proinflammatory response and beta-amyloid 42 (Abeta42) neurotoxicity independent of t

21 nsities (WMH), lacunes, microbleeds with CSF beta-amyloid 42 (Abeta42), total tau, and tau phosphoryl

22 odulates cerebrospinal fluid (CSF) levels of beta-amyloid 42 (Abeta42).

23 eimer disease biomarker (cerebrospinal fluid beta-amyloid 42 and total tau)-by-VEGF interactions eval

24 ar endothelial growth factor interacted with beta-amyloid 42 in predicting longitudinal memory declin

25 d 42, suggesting that phosphorylated tau 181/beta-amyloid 42 levels modulate age-related changes in m

26 in water fraction and phosphorylated tau 181/beta-amyloid 42, suggesting that phosphorylated tau 181/

27 set AD (LOAD) also results from dysregulated beta-amyloid 42, the clinical phenotypes of ADAD and LOA

28 (CSF) biomarkers of AD pathology, including beta-amyloid 42, total tau protein, phosphorylated tau 1

29 e mutations that result in overproduction of beta-amyloid 42.

30 In vivo imaging of brain beta-amyloid, a hallmark of Alzheimer disease, may assis

31 l industry has put a large emphasis on brain beta amyloid (Abeta) either through its removal via anti

32 Aggregates of tau and beta amyloid (Abeta) plaques constitute the histopatholo

33 Beta amyloid (Abeta) triggers the elimination of excitat

34 itro binding to alpha synuclein (alpha-syn), beta amyloid (Abeta), and tau fibrils.

35 immunoassays have been developed to measure beta-amyloid (Abeta) 42 in cerebrospinal fluid (CSF).

36 M2 deficiency and haploinsufficiency augment beta-amyloid (Abeta) accumulation due to a dysfunctional

37 amyloid precursor protein) processing causes beta-amyloid (Abeta) accumulation in autosomal dominant

38 beta-amyloid (Abeta) accumulation in the brain is 1 of 2

39 ledge about spatial and temporal patterns of beta-amyloid (Abeta) accumulation is essential for under

40 beta-amyloid (Abeta) accumulation leads to reduced and f

41 The effect of beta-amyloid (Abeta) accumulation on regional structural

42 as a long preclinical stage characterized by beta-amyloid (Abeta) accumulation without symptoms.

43 n SVD and altered production or clearance of beta-amyloid (Abeta) affecting its cleavage products.

44 fluorescence probe for specific detection of beta-amyloid (Abeta) aggregates.

45 sgenic 3-mo-old mice after the occurrence of beta-amyloid (Abeta) aggregation and the hyperphosphoryl

46 beta-Amyloid (Abeta) aggregation is thought to initiate

47 Comparisons of total beta-amyloid (Abeta) and Abeta peptides 38, 40, and 42 i

48 autoradiography and immunocytochemistry for beta-amyloid (Abeta) and beta-amyloid precursor protein

49 hallmarks of AD--extracellular deposition of beta-amyloid (Abeta) and intraneuronal hyperphosphorylat

50 T and ABCA7 rs200538373-C with the levels of beta-amyloid (Abeta) and parameters of metabolic and car

51 odic memory and also with aggregation of the beta-amyloid (Abeta) and tau proteins and atrophy of med

52 mong putative downstream synaptic targets of beta-amyloid (Abeta) are signaling molecules involved in

53 uantitative output value for PET measures of beta-amyloid (Abeta) binding across tracers and methods

54 beta-amyloid (Abeta) binds to lipoproteins and this comp

55 ntially affecting the diagnostic efficacy of beta-amyloid (Abeta) brain PET imaging.

56 s to inflammation-related processes, such as beta-amyloid (Abeta) burdening.

57 The accurate measurement of beta-amyloid (Abeta) change using amyloid PET imaging is

58 eceptor 3 (CR3) in the regulation of soluble beta-amyloid (Abeta) clearance independent of phagocytos

59 We studied whether brain Mg(2+) can decrease beta-amyloid (Abeta) deposition and ameliorate the cogni

60 Follow-up of beta-amyloid (Abeta) deposition in transgenic mouse mode

61 Recent studies show that cerebral beta-amyloid (Abeta) deposition is associated with blood

62 The amyloid hypothesis suggests that beta-amyloid (Abeta) deposition leads to alterations in

63 poroparietal hypometabolism, and neocortical beta-amyloid (Abeta) deposition, are included in the rec

64 nical practice can reliably predict cortical beta-amyloid (Abeta) deposition.

65 Although the formation of beta-amyloid (Abeta) deposits in the brain is a hallmark

66 n cleaved by gamma-secretase to generate the beta-amyloid (Abeta) found in senile plaques.

67 We assessed the clinical utility of beta-amyloid (Abeta) imaging with (18)F-florbetaben (FBB

68 ltransferase activity co-occurs with greater beta-amyloid (Abeta) in Alzheimer's disease (AD).

69 Accumulation of beta-amyloid (Abeta) in the brain is associated with mem

70 D) is characterized by chronic deposition of beta-amyloid (Abeta) in the brain, progressive neurodege

71 hogenic feature of AD is the accumulation of beta-amyloid (Abeta) in the brain.

72 Quantification of beta-amyloid (Abeta) in vivo is often accomplished using

73 Abnormal accumulation of beta-amyloid (Abeta) is the major neuropathological hall

74 , it was shown that high Hcy increases brain beta-amyloid (Abeta) levels in amyloid precursor protein

75 Although beta-amyloid (Abeta) may be the primary driver of Alzhei

76 beta-amyloid (Abeta) oligomers have been closely implica

77 s necessary for the toxic effects of soluble beta-amyloid (Abeta) oligomers on synapses and hippocamp

78 e exhibit a greater than twofold increase in beta-amyloid (Abeta) pathology.

79 ort the observation that accumulation of the beta-amyloid (Abeta) peptide in the brain plays a centra

80 Alzheimer's disease (AD) include deposits of beta-amyloid (Abeta) peptide in the brain, loss of synap

81 he accumulation and deposition of plaques of beta-amyloid (Abeta) peptide in the brain.

82 s characterized by the aberrant formation of beta-amyloid (Abeta) peptide oligomers and fibrils.

83 amyloid precursor protein (APP) and modulate beta-amyloid (Abeta) peptide production.

84 e findings that neural activity may modulate beta-amyloid (Abeta) peptide secretion and experimental

85 beta-amyloid (Abeta) peptide, accumulation of which is a

86 ucose, as found in MetS/T2DM, and oligomeric beta-amyloid (Abeta) peptide, thought to be a key mediat

87 on the membrane-mediated aggregation of the beta-amyloid (Abeta) peptide.

88 ide, significantly reduced the generation of beta-amyloid (Abeta) peptides by primary neuron cultures

89 Cellular membrane disruption induced by beta-amyloid (Abeta) peptides has been considered one of

90 ach with results from the aggregation of the beta-amyloid (Abeta) peptides measured using thioflavin

91 AD), constituting, together with accumulated beta-amyloid (Abeta) peptides, a hallmark of the disease

92 The accumulation of beta-amyloid (Abeta) peptides, a pathological hallmark o

93 The accumulation of beta-amyloid (Abeta) peptides, a pathological hallmark o

94 he amyloid precursor protein (APP) generates beta-amyloid (Abeta) peptides.

95 's disease (AD), harbor an increased load of beta-amyloid (Abeta) plaque burden that is felt to be a

96 to be a powerful strategy for investigating beta-amyloid (Abeta) plaque-associated neuronal lipids a

97 Alzheimer disease (AD) is characterized by beta-amyloid (Abeta) plaques and tau neurofibrillary tan

98 Abeta.SIGNIFICANCE STATEMENT Tau tangles and beta-amyloid (Abeta) plaques are key lesions in Alzheime

99 In Alzheimer's disease (AD), beta-amyloid (Abeta) plaques are tightly enveloped by mi

100 butyrylcholinesterase accumulate with brain beta-amyloid (Abeta) plaques in Alzheimer disease (AD).

101 se (AD) because reactive astrocytes surround beta-amyloid (Abeta) plaques in autopsy brain tissue.

102 ed severity of other AD hallmarks, including beta-amyloid (Abeta) plaques, tau neurofibrillary tangle

103 Amyloid precursor protein (APP) derivative beta-amyloid (Abeta) plays an important role in the path

104 D) are caused by mutations in genes encoding beta-amyloid (Abeta) precursor protein (APP), presenilin

105 e gene, has been shown to reduce Alzheimer's beta-amyloid (Abeta) production and tau phosphorylation.

106 e study also demonstrates that modulation of beta-amyloid (Abeta) release can occur at both axonal an

107 Because deposition of cerebral beta-amyloid (Abeta) seems to be a key initiating event

108 While beta-amyloid (Abeta), a classic hallmark of Alzheimer's

109 Amyloid plaques, consisting of deposited beta-amyloid (Abeta), are a neuropathological hallmark o

110 known to increase the deleterious effect of beta-amyloid (Abeta), contributing to early cognitive im

111 in turn, chronically elevates levels of CSF beta-amyloid (Abeta), exacerbating ongoing AD pathogenes

112 Fibrinogen interacts with beta-amyloid (Abeta), forming plasmin-resistant abnormal

113 from multiple neurotoxic stimuli, including beta-amyloid (Abeta), glutamate and staurosporine.

114 e histone deacetylase inhibitor M344 reduces beta-amyloid (Abeta), reduces tau Ser(396) phosphorylati

115 sk factor in AD, as it specifically binds to beta-amyloid (Abeta), thereby altering fibrin clot struc

116 A previous study found an effect of sleep on beta-amyloid (Abeta), which is a key protein in Alzheime

117 tau, and cholinergic pathologies as well as beta-amyloid (Abeta)-induced epileptiform activity, some

118 disease (AD) resulted in an amelioration of beta-amyloid (Abeta)-induced synaptic depression and cog

119 e (AD) and in microglia surrounding neuritic beta-amyloid (Abeta)-plaques in the brains of people wit

120 episodic memory has largely been limited to beta-amyloid (Abeta).

121 nd worsening of cognition is associated with beta-amyloid (Abeta).

122 au with modest selectivity versus aggregated beta-amyloid (Abeta).

123 or model denoting the presence or absence of beta-amyloid (Abeta+/-) and neurodegeneration (ND+/-).

124 gy (SNAP), defined as biomarker negative for beta-amyloid (Abeta-) but positive for neurodegeneration

125 logic processes (accumulation of neocortical beta-amyloid [Abeta] and tau) provides an important oppo

126 Remarkably, beta-amyloid (Abeta1-40/42) peptide levels were as follo

127 nthesis in C2C12 myotubes induced to express beta-amyloid (Abeta42).

128 oprotein activity may contribute to cerebral beta-amyloid accumulation in AD.

129 for P-glycoprotein in clearance of cerebral beta-amyloid across the blood-brain barrier (BBB).

130 transfer (PeT) probe (1) to directly locate beta-amyloid aggregates (Abeta plaques) in the brain wit

131 Filamentous beta-amyloid aggregates are crucial for the pathology of

132 can be exploited for screening of potential beta-amyloid aggregation inhibitors, whereas some of the

133 with prior work showing that proSAAS blocks beta-amyloid aggregation into fibrils, this study suppor

134 ipheral anionic site of AChE, preventing the beta-amyloid aggregation promoted by AChE.

135 id, and are involved in sterol transport and beta-amyloid aggregation, it would be interesting to inv

136 (TR-LRET) was developed for the detection of beta-amyloid aggregation.

137 er tauopathy brains or to lesions containing beta-amyloid, alpha-synuclein, or TDP-43.

138 lied for the first time for the detection of beta amyloid and ApoE at clinical relevant levels in cer

139 nsgenic AD (3xTg-AD) mice, with no change in beta amyloid and phospho-tau levels.

140 e also applied immunohistochemistry to study beta-amyloid and activated microglia in the mouse brain

141 PFRAP and ICA), inhibitory property against beta-amyloid and alpha-synuclein fibril formation and pr

142 mical analyses showed significant amounts of beta-amyloid and amyloid precursor protein (APP) aggrega

143 r initial scans, had abnormal levels of both beta-amyloid and brain injury biomarkers.

144 ore protective isoform accumulate less brain beta-amyloid and have a lower LOAD risk.

145 two clinically-relevant markers of dementia, beta-amyloid and PHF-tau, were profiled in formalin-fixe

146 in a buildup of abnormal proteins, including beta-amyloid and phospho-Tau.

147 The universal presence of beta-amyloid and tau in Alzheimer's disease (AD) has fac

148 e kinase-3beta (GSK-3beta) by attacking both beta-amyloid and tau protein cascades has been identifie

149 The accumulation of aggregated beta-amyloid and tau proteins into plaques and tangles i

150 and had normal cerebrospinal fluid levels of beta-amyloid and tau proteins.

151 rs measured in plasma and CSF, distinct from beta-amyloid and tau, could prove useful in predicting m

152 rs measured in plasma and CSF, distinct from beta-amyloid and tau, could prove useful in predicting m

153 al regions required the presence of cortical beta-amyloid and was associated with decline in global c

154 ntisera, methoxy-X04 staining for fibrillary beta-amyloid, and ex vivo autoradiography served as term

155 Rather, our results suggest that beta-amyloid- and tau-related pathological processes may

156 uld be rescued by immunotherapy with an anti-beta-amyloid antibody.

157 tivities and altered microglial responses to beta-amyloid are associated with increased AD risk.

158 Beta-amyloid (beta-A) peptides are potential biomarkers

159 el-based approaches to the quantification of beta-amyloid binding in the brain from dynamic PET data.

160 c modifiers of the relation between cortical beta-amyloid burden (measured using [(18)F]Florbetapir-P

161 o the complexity of the relationship between beta-amyloid burden and AD-related cognitive impairment.

162 Here we show that beta-amyloid burden in medial prefrontal cortex (mPFC) c

163 development of PET radiotracers for imaging beta-amyloid burden in the brain of individuals at risk

164 or protein processing or extracellular Abeta/beta-amyloid burden.

165 s and classified as positive or negative for beta-amyloid by 5 readers who were blind to patient info

166 induction or activation to increase cerebral beta-amyloid clearance could constitute a novel preventi

167 How the CD33m isoform increases beta-amyloid clearance remains unknown.

168 iminishing the amount of CD33M and enhancing beta-amyloid clearance.

169 in inflammatory cell populations involved in beta-amyloid clearance.SIGNIFICANCE STATEMENT Mounting e

170 d as versatile intermediates to a variety of beta-amyloid cleaving enzyme-1 (BACE1) inhibitors.

171 odies against TfR and beta-secretase (BACE1 [beta-amyloid cleaving enzyme-1]) traverse the blood-brai

172 mmary, pyroGlu-3 Abeta is a major species of beta-amyloid deposited early in diffuse and focal plaque

173 The lack of strong association between brain beta-amyloid deposition and cognitive impairment has bee

174 of AD, we evaluated the association between beta-amyloid deposition and neuroinflammation in AD.

175 A clear positive correlation between beta-amyloid deposition and neuroinflammation was detect

176 To monitor the longitudinal changes in beta-amyloid deposition and neuroinflammation, we used i

177 o cerebral amyloid angiopathy, the result of beta-amyloid deposition in cerebral vessels.

178 ject, we also observed similar rs73069071-by-beta-amyloid deposition interaction effect on global cog

179 All PCA subjects showed beta-amyloid deposition on PET scanning.

180 DLB, compared to AD, and its relationship to beta-amyloid deposition on PET.

181 mal aging in relation to age, cognition, and beta-amyloid deposition.

182 ks of age, long before memory impairments or beta-amyloid deposition.

183 on observed in this population is not due to beta-amyloid deposition.

184 tes was observed from the earliest stages of beta-amyloid deposition.

185 PC simple spike activity prior to cerebellar beta-amyloid deposition.

186 port, our results suggest that extracellular beta-amyloid deposits cause a local impairment in the re

187 found within dystrophic neurites surrounding beta-amyloid deposits in AD mouse models but the patholo

188 Analysis of beta-amyloid deposits, tau phosphorylation, and inflamma

189 e that is associated with aging and not with beta-amyloid deposits.

190 T30 peptide and beta-amyloid each have toxic effects on PC12 cells, comp

191 ns, among which we analyzed paths related to beta-amyloid, estrogen, and nicotine pathways.

192 A critical step of beta-amyloid fibril formation is fibril elongation in wh

193 monly characterized by the presence of cross-beta amyloid fibrils as well as the loss of neuronal or

194 which subsequently aggregates to form cross-beta amyloid fibrils that are a hallmark of Alzheimer's

195 a functional N-terminal domain exists within beta-amyloid for its agonist-like activity.

196 The activity of the N-terminal beta-amyloid fragment appears to reside largely in a seq

197 In addition, the N-terminal beta-amyloid fragment augmented theta burst-induced post

198 following bilateral injection of N-terminal beta-amyloid fragment into the dorsal hippocampi of inta

199 ike full-length beta-amyloid, the N-terminal beta-amyloid fragment is monomeric and nontoxic.

200 The N-terminal beta-amyloid fragment is present in the brains and CSF o

201 These findings suggest that the N-terminal beta-amyloid fragment may serve as a potent and effectiv

202 olated mouse nerve terminals, the N-terminal beta-amyloid fragment proved to be highly potent and mor

203 ar phagocytes can be enlisted to clear Abeta/beta-amyloid from the brain.

204 Soluble beta-amyloid has been shown to regulate presynaptic Ca(2

205 The amyloid hypothesis posits that disrupted beta-amyloid homeostasis initiates the pathological proc

206 Multivariate analysis showed beta-amyloid imaging as the single variable most strongl

207 e aimed to determine the prognostic value of beta-amyloid imaging, alone and in combination with memo

208 Using postmortem beta-amyloid immunohistochemistry data from 243 AD parti

209 a peptide competing with the aggregation of beta-amyloid in Alzheimer's disease.

210 y potent and more effective than full-length beta-amyloid in its agonist-like action on nicotinic rec

211 dissociation of WMHs and cerebrospinal fluid beta-amyloid in relation to regional glucose metabolism

212 hich the use of PPIs increased the levels of beta-amyloid in the brains of mice.

213 (>/=500x) in vitro selectivity for tau over beta-amyloid, in comparison with the benchmark compound

214 beta-Amyloid interacts with hippocampal and cortical tau

215 Although beta-amyloid is necessary for the pathologic diagnosis o

216 However, rmTBIs did not increase beta-amyloid levels or tau phosphorylation in the 3xTg-A

217 familial AD mutations and develop increased beta-amyloid levels, plaque deposition, and memory defic

218 not plasma apoE levels, correlated with CSF beta-amyloid levels.

219 xplored the effect of synaptic activation on beta-amyloid, little is known about Tau protein.

220 ciations of bace-1 promoter methylation with beta-amyloid load among persons with AD dementia, and PH

221 Validation based on beta-amyloid load by immunocytochemistry, and replicatio

222 Age and beta-amyloid (measured using PiB PET) were differentiall

223 aque levels determined; 25 brains (37%) were beta-amyloid negative; and 43 brains (63%) were beta-amy

224 tability develops in a common mouse model of beta-amyloid neuropathology - Tg2576 mice.

225 PrP(C) and mGluR5 are co-receptors also for beta-amyloid oligomers (AbetaOs) and have been shown to

226 s have not identified an association between beta-amyloid or tau and rates of hippocampal atrophy in

227 of mitochondrial ATP synthase), glypican 5, beta-amyloid, P-tau] were reduced almost to control leve

228 s revealed that the association between mPFC beta-amyloid pathology and impaired hippocampus-dependen

229 th microglial C3a receptor (C3aR) to mediate beta-amyloid pathology and neuroinflammation in AD mouse

230 ption as a mechanistic pathway through which beta-amyloid pathology may contribute to hippocampus-dep

231 However, whether the influence of beta-amyloid pathology on hippocampus-dependent memory i

232 Indirect evidence of beta-amyloid pathology promoting alpha-synuclein fibrill

233 Independent evidence associates beta-amyloid pathology with both non-rapid eye movement

234 By linking beta-amyloid pathology with impaired NREM SWA, these dat

235 D model, downregulating membralin results in beta-amyloid pathology, neuronal death, and exacerbates

236 result of the extracellular accumulation of beta-amyloid peptide (Abeta) and intracellular accumulat

237 ggregation in two different amyloid systems, beta-amyloid peptide (Abeta) and transthyretin, by these

238 Elevated levels of the beta-amyloid peptide (Abeta) are thought to contribute t

239 It has been widely reported that beta-amyloid peptide (Abeta) blocks long-term potentiati

240 the cytotoxicity of the Alzheimer's disease beta-amyloid peptide (Abeta) by remodeling seeding-compe

241 beta-Amyloid peptide (Abeta) plaques are a cardinal neur

242 The applicability of beta-amyloid peptide (Abeta) positron emission tomograph

243 In Alzheimer's disease, aggregation of the beta-amyloid peptide (Abeta) results in the formation of

244 (AD) is characterized by accumulation of the beta-amyloid peptide (Abeta), which is generated through

245 (AD) is characterized by accumulation of the beta-amyloid peptide (Abeta), which likely contributes t

246 s, or similarly advanced in individuals with beta-amyloid peptide (Abeta)-negative (Abeta-) suspected

247 om the central and C-terminal regions of the beta-amyloid peptide (Abeta).

248 ers of a family of peptides derived from the beta-amyloid peptide (Abeta).

249 plaques composed of aggregated forms of the beta-amyloid peptide (Abeta).

250 onstrated by following the fibrillization of beta-amyloid peptide 1-42 (Abeta42) as a function of tim

251 lution structures of oligomers formed by the beta-amyloid peptide Abeta are needed to understand the

252 Oligomers of the beta-amyloid peptide Abeta have emerged as important con

253 tructure and inhibits the aggregation of the beta-Amyloid Peptide Abeta42 and transthyretin.

254 Without decreasing beta-amyloid peptide load in the brain, alpha-MSH improv

255 TgCRND8 mice with established beta-amyloid peptide pathology and nontransgenic litterm

256 beta-sheet containing residues 16-22 of the beta-amyloid peptide, Abeta.

257 The pathological beta-amyloid peptide, involved in Alzheimer's disease, d

258 ta-secretase site to initiate the release of beta-amyloid peptide.

259 Beta amyloid peptides (Abeta) are known risk factors inv

260 tia, is characterized by the accumulation of beta-amyloid peptides (Abeta) in senile plaques in the b

261 beta-Amyloid peptides (Abeta), derived from proteolytic

262 ) was originally identified as the source of beta-amyloid peptides that accumulate in Alzheimer's dis

263 e via the production and deposition of toxic beta-amyloid peptides.

264 In vivo detection of brain beta-amyloid plaque density may increase diagnostic accu

265 tantly, the beneficial effects of decreasing beta-amyloid plaques and neurodegeneration by Delta(9)-T

266 is end, we analyzed the LCO-stained cores of beta-amyloid plaques in postmortem tissue sections from

267 Pathognomonic accumulation of cerebral beta-amyloid plaques likely results from imbalanced prod

268 in the activated microglia that surround the beta-amyloid plaques.

269 a-amyloid negative; and 43 brains (63%) were beta-amyloid positive.

270 atrophy factor compositions were inferred in beta-amyloid-positive (Abeta+) mild cognitively impaired

271 ytochemistry, and replication with fibrillar beta-amyloid positron emission tomographic imaging with

272 beta-Amyloid precursor protein (APP) and its cleaved pro

273 ted previously that the Alzheimer-associated beta-amyloid precursor protein (APP) facilitates neurona

274 The beta-amyloid precursor protein (APP) is involved in Alzh

275 The beta-amyloid precursor protein (APP) plays a central rol

276 amyloid-beta generation from its precursor, beta-amyloid precursor protein (APP), in a competitive m

277 transcriptomic changes in control and mutant beta-amyloid precursor protein (APPSw,Ind) transgenic mi

278 n SH-SY5Y neuroblastoma cells expressing the beta-amyloid precursor protein (betaAPP) harboring the f

279 Sarm1(-/-) mice developed fewer beta-amyloid precursor protein aggregates in axons of th

280 Here we report that FAD mutations in beta-amyloid precursor protein and presenilin 1 are able

281 cytochemistry; white matter showed Abeta and beta-amyloid precursor protein by immunocytochemistry, b

282 n pathway represses the transcription of the beta-amyloid precursor protein cleaving enzyme (BACE1) v

283 e that over-express the Swedish mutant human beta-amyloid precursor protein gene with G protein-coupl

284 We examined [3H]PiB binding and Abeta and beta-amyloid precursor protein immunocytochemistry in au

285 nocytochemistry for beta-amyloid (Abeta) and beta-amyloid precursor protein in brain tissue were obta

286 eavage of the Alzheimer's disease-associated beta-amyloid precursor protein in vitro and in human emb

287 ) and decreased beta-secretase processing of beta-amyloid precursor protein.

288 beta-carboxyl-terminal fragment (betaCTF) of beta-amyloid precursor protein.

289 In addition, PIs induced beta-amyloid production, indicative of increased BACE1-m

290 iomarker strategy for the early detection of beta-amyloid-related abnormalities.

291 Subtle memory impairment with a positive beta-amyloid scan identifies healthy individuals at high

292 triggers that range from oxidized lipids to beta-amyloid seem to stimulate autophagosome formation p

293 frontotemporal lobar degeneration, including beta-amyloid senile plaques, tau neurofibrillary tangles

294 Amyloid-beta amyloid status (negative or positive) and neurodege

295 this segment is prone to self-associate into beta-amyloids, suggesting that sites involved in fibrili

296 Unlike full-length beta-amyloid, the N-terminal beta-amyloid fragment is mo

297 ous studies showing that resveratrol reduces beta-amyloid toxicity they also give evidence of a promi

298 ons with severe CAA suggests a difference in beta-amyloid trafficking.

299 In particular, picomolar beta-amyloid was found to have an agonist-like action on

300 Although neprilysin is known to degrade beta-amyloid, we observed no increased amyloid depositio