ライフサイエンスコーパス: beta-amyloid

1 ppocampus and increased levels of neurotoxic beta-amyloid.

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

3 o lower cognitive performance independent of beta-amyloid.

4 71 years +/- 6; 13 women) were positive for beta-amyloid.

5 le for the observed hIAPP cross-seeding with beta-amyloid.

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

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

8 .53 to 0.69); in the few direct comparisons, beta-amyloid 42 (Abeta42)/phosphorylated tau (p-tau) rat

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

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

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

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

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

14 cognitively unimpaired subcohort (n = 330), beta-amyloid(42) and tau were quantified in cerebrospina

15 globulin gene whose antibodies interact with beta-amyloid, a long non-coding RNA AC099552.4 (p = 1.2

16 BB) in promoting the clearance of neurotoxic beta-amyloid (AB) peptides from the brain into the blood

17 rotein (APP), BACE-1, a trending increase in beta-amyloid Abeta(42/40) ratio and hyperphosphorylated

18 reatic islet amyloid polypeptide (hIAPP) and beta amyloid (Abeta) can accumulate in Type 2 diabetes (

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

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

21 Beta amyloid (Abeta) triggers the elimination of excitat

22 eceptors (nAChRs), high-affinity targets for beta amyloid (Abeta).

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

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

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

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

27 However, growing evidence suggests that beta-amyloid (Abeta) accumulation, that initiates LOAD-r

28 one of the first responses to extracellular beta-amyloid (Abeta) accumulation.

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

30 take and exhibits high specific affinity for beta-amyloid (Abeta) aggregates, leading to the successf

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

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

33 ts in DS have been proposed as indicative of beta-amyloid (Abeta) aggregation and thus potential biom

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

35 shown to regulate the metabolism of ApoE and beta-amyloid (Abeta) and are potential therapeutic targe

36 e accumulation of the AD-associated proteins beta-amyloid (Abeta) and hyper-phosphorylated tau (p-tau

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

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

39 he two stages.SIGNIFICANCE STATEMENT Tau and beta-amyloid (Abeta) are hallmarks of Alzheimer's diseas

40 ng (APP-cleaving) enzyme 1 (BACE1), APP, and beta-amyloid (Abeta) are linked with vascular disease de

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

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

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

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

45 idated measure of systemic vascular risk and beta-amyloid (Abeta) burden have an interactive associat

46 of memory abilities and its relationship to beta-amyloid (Abeta) burden in a large cohort (N = 1,070

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

48 under debate, as potential triggers such as beta-amyloid (Abeta) can vary in size, configuration and

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

50 Cerebral amyloid angiopathy (CAA) and beta-amyloid (Abeta) deposition in the brain parenchyma

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

52 Cerebral amyloid angiopathy (CAA), where beta-amyloid (Abeta) deposits around cerebral blood vess

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

54 As such, we have assessed whether tau and beta-amyloid (Abeta) deposits might be present in pancre

55 se functions are affected by the presence of beta-Amyloid (Abeta) deposits, hallmark lesions of Alzhe

56 ion in rodents and humans causally modulates beta-amyloid (Abeta) dynamics (e.g., [1-3]).

57 with normal aging, and that the presence of beta-amyloid (Abeta) facilitates its spread to neocortex

58 Biomarkers such as beta-amyloid (Abeta) fibrils and Tau tangles in Alzheime

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

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

61 AD.SIGNIFICANCE STATEMENT Elevated levels of beta-amyloid (Abeta) in the brain are thought to contrib

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

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

64 Accumulation of beta-amyloid (Abeta) is one of the hallmarks of Alzheime

65 Beta-amyloid (Abeta) is thought to play a critical role

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

67 a modulator of nuclear receptors involved in beta-amyloid (Abeta) metabolism and progression of Alzhe

68 Targeting toxicity associated with beta-amyloid (Abeta) misfolding and aggregation is a pro

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

70 tudies have examined the effect of increased beta-amyloid (Abeta) on Cx43 expression and function lea

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

72 cally characterized by the deposition of the beta-amyloid (Abeta) peptide in senile plaques in the br

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

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

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

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

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

78 In Alzheimer's disease (AD), beta-amyloid (Abeta) peptides accumulate extracellularly

79 matinib mesylate, 1a, inhibits production of beta-amyloid (Abeta) peptides both in cells and in anima

80 that truncated apolipoprotein fragments and beta-amyloid (Abeta) peptides coexist as neurotoxic hete

81 r (BBB) in promoting clearance of neurotoxic beta-amyloid (Abeta) peptides from the brain into the bl

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

83 Extracellular deposition of beta-amyloid (Abeta) peptides in the brain is a hallmark

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

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

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

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

88 e (AD) brains are senile plaques, comprising beta-amyloid (Abeta) peptides, and neuronal inclusions f

89 rder characterized by abnormal deposition of beta-amyloid (Abeta) peptides.

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

91 plexes exhibit effective in vitro binding to beta-amyloid (Abeta) plaques and fibrils, inhibit Abeta

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

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

94 The structural polymorphism in beta-amyloid (Abeta) plaques from Alzheimer disease (AD)

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

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

97 sly we have reported that SYK also regulates beta-amyloid (Abeta) production and hyperphosphorylation

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

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

100 However, the main beta-amyloid (Abeta) species and what imbues the aggrega

101 ISF) and cerebrospinal fluid (CSF) levels of beta-amyloid (Abeta) that accumulates in Alzheimer's dis

102 e co-morbid concurrence of large infarct and beta-amyloid (Abeta) toxicity can precipitate the early

103 Combination of ischemia and beta-amyloid (Abeta) toxicity has been shown to simultan

104 nvestigate the interaction of the AD peptide beta-amyloid (Abeta) with the iron storage protein ferri

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

106 o interfere with AChE-induced aggregation of beta-amyloid (Abeta), and Abeta self-aggregation was ass

107 Digital measures of tau, beta-amyloid (Abeta), and SYN histopathology in neocorti

108 Paravascular drainage of solutes, including beta-amyloid (Abeta), appears to be an important process

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

110 isease (AD) therapies predominantly focus on beta-amyloid (Abeta), but Abeta effects may be maximal b

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

112 n central norepinephrine metabolism, tau and beta-amyloid (Abeta), inflammation, BBB-dysfunction, neu

113 way by the beta-secretase, BACE1, generating beta-amyloid (Abeta), or along the nonamyloidogenic path

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

115 Tau and beta-amyloid (Abeta), the primary pathological features

116 beta-amyloid (Abeta)-dependent neuronal hyperactivity is

117 beta-amyloid (Abeta)-moderated sex differences in tau si

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

119 whose processing can result in formation of beta-amyloid (Abeta).

120 eatures of Alzheimer's disease (AD): tau and beta-amyloid (Abeta).

121 ing, and inversely correlated with levels of beta-amyloid (Abeta).

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

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

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

125 AD pathology, including the accumulation of beta-amyloid (Abeta).

126 Moreover, while the pathogenic AD peptide beta-amyloid (Abeta)42 cleaves HK and induces a dramatic

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

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

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

130 d with worse impact of primary AD pathology (beta-amyloid, Abeta) on neurodegeneration and cognitive

131 during lifetime, caused by an extra copy of beta-amyloid-(Abeta)-precursor-protein gene.

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

133 The 42-amino-acid beta-amyloid (Abeta42) is a critical causative agent in

134 ve in the context of a secondary insult like beta-amyloid accumulation or stroke.

135 MRI and PET how cerebral iron together with beta-amyloid affects cognition among cognitively normal

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

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

138 beta-Amyloid aggregates found in brain plaques are viewe

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

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

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

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

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

144 No clusters showed associations between beta-amyloid and global cognition.

145 rain iron content negatively correlated with beta-amyloid and global cognitive scores (eg, in the fro

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

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

148 several small series have demonstrated both beta-amyloid and tau aggregation, including neurofibrill

149 Although both beta-amyloid and tau are biomarkers of cognitive aging a

150 beta-amyloid and tau burden were measured at autopsy.

151 ing domestic cats spontaneously develop both beta-amyloid and tau pathology similar, but not identica

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

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

154 etection of AD biomarkers such as aggregated beta-amyloid and tau proteins.

155 ion of toxic AD proteinaceous species (i.e., beta-amyloid and tau).

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

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

158 ic amyloids from lung endothelium, including beta amyloid, and tau.

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

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

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

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

163 lusion: These PVEC results indicate that the beta-amyloid buildup curve does not plateau at an early

164 It was hypothesized that the brain beta-amyloid buildup curve plateaus at an early symptoma

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

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

167 Inflammation increases beta-amyloid burden and is thought to drive Alzheimer's

168 nd Alzheimer disease pathology, particularly beta-amyloid burden and tau tangle density.

169 rticipants with even modestly elevated brain beta-amyloid burden at study entry, suggesting plasma NT

170 Neuropathologic examination assessed beta-amyloid burden, tau tangle density, neocortical Lew

171 f Alzheimer's disease dementia by increasing beta-amyloid burden.

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

173 % CI: -0.56, -0.12; P = .003) independent of beta-amyloid burden.

174 MS pathobiology retards the accumulation of beta-amyloid but not the accumulation of tau.

175 The potential benefit of beta-amyloid clearance from the circulation via CR1-medi

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

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

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

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

180 scopic protein aggregates comprising a cross-beta amyloid core and are associated with deadly human d

181 investigated the effect on the shape of the beta-amyloid curve in AD when PVE correction (PVEC) is a

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

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

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

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

186 The presence of extracellular beta-amyloid deposition as neuritic plaques and intracel

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

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

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

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

191 omarkers of cognitive aging and AD, cortical beta-amyloid deposition was lower in MS than age-matched

192 This inflammation and beta-amyloid deposition were associated with reactive mi

193 uid (CSF) levels of beta-amyloid peptide (A, beta-amyloid deposition), phosphorylated tau (T, patholo

194 metry performance did not predict concurrent beta-amyloid deposition, small vessel disease or Alzheim

195 s, but no evidence that it predicted in vivo beta-amyloid deposition, white matter hyperintensity vol

196 neurodegenerative pathologies resulting from beta-amyloid deposition.

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

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

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

200 croglia as the only myeloid cells present at beta-amyloid deposits.

201 zheimer pathology in the brain, particularly beta-amyloid (estimated increase [+/-SE] in beta-amyloid

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

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

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

205 ch do not share the characteristics of cross-beta amyloid fibrils.

206 ed as a potent inhibitor and reducer of both beta-amyloid fibrils (the main component of "plaques") a

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

208 rgets involved in the "cholinergic" and the "beta-amyloid" hypothesis.

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

210 to Rab5(+), clathrin(+) endosomes containing beta-amyloid in a process of LC3-associated endocytosis

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

212 s to increased intracellular accumulation of beta-amyloid in early-onset Alzheimer's disease.

213 n association with neurons, tau tangles, and beta-amyloid in specimens from the brains of individuals

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

215 (>/=500x) in vitro selectivity for tau over beta-amyloid, in comparison with the benchmark compound

216 beta-Amyloid interacts with hippocampal and cortical tau

217 dementia, elevated brain iron together with beta-amyloid is associated with lower cognitive function

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

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

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

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

222 ments did not correlate with amelioration of beta amyloid load or hippocampal adult neurogenesis rate

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

224 ted the associations between tissue iron and beta-amyloid load and their relationship to cognitive pe

225 nd research suggests that both alpha-syn and beta-amyloid may also form strains.

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

227 recursor VGF in 5xFAD mice partially rescued beta-amyloid-mediated memory impairment and neuropatholo

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

229 RC death by subretinally injected oligomeric beta-amyloid (OAbeta) and observed that ELVs administrat

230 tein (PrP(C)) is a key neuronal receptor for beta-amyloid oligomers (AbetaO), mediating their neuroto

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

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

233 ssociated with cognition related to elevated beta-amyloid (p <= 0.01) and/or tau burden (p <= 0.03).

234 as found to be significantly associated with beta-amyloid (p value = 3.44 x 10(-8)) which was driven

235 significant increases on select measures of beta-amyloid pathology after exposure to WD.

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

237 their cross-sectional relationship with age, beta-amyloid pathology, and mild cognitive impairment or

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

239 d sleep deprivation has been associated with beta amyloid peptide (Abeta) aggregation, which is a maj

240 g on the cerebrospinal fluid (CSF) levels of beta-amyloid peptide (A, beta-amyloid deposition), phosp

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

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

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

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

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

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

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

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

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

250 -normalized NDE levels of usually pathologic beta-amyloid peptide 1-42 (1.6-fold, P < 0.0001), P-T181

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

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

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

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

255 Soluble oligomers of the beta-amyloid peptide, Abeta, are thought to be the synap

256 Oligomers of the beta-amyloid peptide, Abeta, play a central role in the

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

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

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

260 Clinical trials targeting beta-amyloid peptides (Abeta) for Alzheimer disease (AD)

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 Interactions of beta-amyloid peptides with an elevated level of their no

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

265 beta-amyloid (estimated increase [+/-SE] in beta-amyloid per 1-unit increase in scam score, 0.22 +/-

266 ritical microglial cellular function such as beta-Amyloid phagocytosis.

267 in a mouse model of AD, before deposition of beta amyloid plaques.

268 ty at all dose levels for in vivo imaging of beta amyloid plaques.

269 not without (Spearman rho = 0.15; P = .33), beta-amyloid plaques in cohort 1.

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

271 axis, culminating in an impaired response to beta-amyloid plaques in vivo.

272 The deposition of beta-amyloid plaques is likely to start years in advance

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

274 ease characterized by the presence of Abeta (beta-amyloid) plaques and tau neural fibrillary tangles

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

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

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

278 The proteolytic cleavage of beta-amyloid precursor protein (APP) to form the amyloid

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

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

281 Intramembrane cleavage of the beta-amyloid precursor protein C99 substrate by gamma-se

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

283 ing APPSwDI transgenic mice expressing human beta-amyloid precursor protein Swedish (Tg-SwDI), a mode

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

285 disease both demonstrate the accumulation of beta-amyloid protein containing "plaques" and tau protei

286 ally, S100 protein, neuron-specific enolase, beta-amyloid protein, tau protein and phospho-tau were d

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

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

289 o explore the pathological effects of stable beta-amyloid-sheet oligomers compared with those of fibr

290 We found beta-amyloid staining, predominantly in Cortical Layers

291 More recently, the discovery of the cross-beta amyloid state revealed that deeper energy minima ex

292 s demonstrate patterns reflective of a cross-beta amyloid structure.

293 cortical tissue is strongly associated with beta-amyloid, tau-related neuropathology, and the rate o

294 firmed that PS2 generates more intracellular beta-amyloid than does PS1.

295 In contrast to canonical cross-beta amyloids, these aggregates retain high degrees of i

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

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

298 positive correlations between brain iron and beta-amyloid were observed in the PET subgroup, revealin

299 (BACE1) is a key enzyme in the generation of beta-amyloid, which is accumulated in the brain of Alzhe

300 A majority underwent PET to measure cerebral beta-amyloid within 30 days of MRI.