ライフサイエンスコーパス: amyloid beta

1 tivity, thereby increasing the production of amyloid-beta.

2 usceptible to phosphorylated tau (Ptau) than amyloid-beta.

3 which inflammation affects the generation of amyloid-beta.

4 deficits in Alzheimer's mice overexpressing amyloid-beta.

5 role of tau protein and its interaction with amyloid-beta.

6 rate that similar mechanisms are involved in amyloid-beta 1-42 (Abeta42) aggregation.

7 Notably, the conformation used by amyloid-beta(1-40) and amyloid-beta(1-42) when interacti

8 Amyloid-beta(1-40) was less prone to adopt the alpha-hel

9 The alpha-helix structure was observed for amyloid-beta(1-42) fragments that were closer to the lip

10 conformation used by amyloid-beta(1-40) and amyloid-beta(1-42) when interacting directly with or nex

11 esigned and synthesized to detect the target amyloid beta-40 sequence (Abeta-40).

12 IFICANCE STATEMENT High levels of oligomeric amyloid-beta(42) (oAbeta(42)) induce synaptic dysfunctio

13 rimarily driven by brain accumulation of the amyloid-beta-42 (Abeta42) peptide generated from the amy

14 d its associated neurotoxic cleavage product amyloid-beta*56.

15 ol to study the aggregation mechanism of the Amyloid beta (Abeta) 42 peptide, whose aggregation inter

16 viduals, the LLD group exhibited less global amyloid beta (Abeta) accumulation (p = .05).

17 While the link between amyloid beta (Abeta) accumulation and synaptic degradati

18 In mouse models of amyloid beta (Abeta) accumulation, defective TREM2 funct

19 Inflammation and amyloidosis from amyloid beta (Abeta) aggregates are implicated in neuron

20 gy due to the sequestration into cytoplasmic amyloid beta (Abeta) aggregates, supporting the feature

21 ology, characterized by amyloid plaques with amyloid beta (Abeta) and neurofibrillary tangles with ta

22 malfunction triggered by the accumulation of amyloid beta (Abeta) and Tau protein.

23 signaling increases synaptic sensitivity to amyloid beta (Abeta) and tau.

24 Amyloid beta (Abeta) causes cytosolic Ca(2+) overload, b

25 Evidence linking amyloid beta (Abeta) cellular uptake and toxicity has bu

26 found that in humans with cognitive decline, amyloid beta (Abeta) constricts brain capillaries at per

27 al cortex, histopathologically hallmarked by amyloid beta (Abeta) extracellular plaques and intracell

28 The fibrils show a remarkable resemblance to amyloid beta (Abeta) fibrils associated with Alzheimer's

29 vels of CD33 inhibit uptake and clearance of amyloid beta (Abeta) in microglial cell cultures.

30 e that plays a key role in the production of amyloid beta (Abeta) in the brain and has been extensive

31 Amyloid beta (Abeta) is a major component of amyloid pla

32 ion (LTP) impairments without altering brain amyloid beta (Abeta) pathology.

33 y model of AD using soluble oligomers of the amyloid beta (Abeta) peptide (AbetaOs).

34 The amyloid beta (Abeta) peptide and its shorter variants, i

35 athy (CAA) and Alzheimer's disease (AD), the amyloid beta (Abeta) peptide deposits along the vascular

36 nges on the predominant clinical role of the amyloid beta (Abeta) peptide in propagating neurofibrill

37 -amyloid precursor protein (APP) to form the amyloid beta (Abeta) peptide is related to the pathogene

38 We illustrate this method in the case of the amyloid beta (Abeta) peptide, whose oligomers are associ

39 SV-1 infection could be an initial source of amyloid beta (Abeta) peptide-containing amyloid plaque d

40 llular amyloid plaques composed of fibrillar amyloid beta (Abeta) peptides and intracellular neurofib

41 aques and neurofibrillary tangles, formed by amyloid beta (Abeta) peptides and phosphor-tau, respecti

42 al deposition of amyloid plaques composed of amyloid beta (Abeta) peptides and the cerebrospinal flui

43 Preventing aggregation of amyloid beta (Abeta) peptides is a promising strategy fo

44 Specific forms of amyloid beta (Abeta) peptides, for example post-translat

45 to regional differences in susceptibility to amyloid beta (Abeta) plaque deposition in cortical regio

46 The deposition of amyloid beta (Abeta) plaques and fibrils in the brain pa

47 gest that antibody-based removal of cerebral amyloid beta (Abeta) plaques may possibly clear tau tang

48 Amyloid beta (Abeta) plays a crucial role in Alzheimer's

49 whether there is a discrepancy in detecting amyloid beta (Abeta) positivity between 18F-florbetaben

50 Understanding the biological function of amyloid beta (Abeta) precursor protein (APP) beyond its

51 d luminal regions and easily aggregates like amyloid beta (Abeta) protein.

52 cence probe ADLumin-1 as a turn-on probe for amyloid beta (Abeta) species.

53 Using this system to target Bace1 suppressed amyloid beta (Abeta)-associated pathologies and cognitiv

54 stages of AD.SIGNIFICANCE STATEMENT Soluble amyloid beta (Abeta)-induced synaptic dysfunction is an

55 Soluble amyloid beta (Abeta)-induced synaptic dysfunction is an

56 d extracellular plaques primarily comprising amyloid- beta (Abeta) peptide.

57 ickness, cerebrospinal fluid (CSF) levels of amyloid-beta (Abeta(42) ), tau, and ptau(181) , and the

58 00B, glial fibrillary acidic protein (GFAP), amyloid-beta (Abeta) 40 and Abeta42, total tau (t-tau) a

59 tau (t-tau), phosphorylated tau (p-tau) and amyloid-beta (Abeta) 42 levels in cerebrospinal fluid (C

60 Amyloid-beta (Abeta) accumulation in the brain is a card

61 commonly associated with increased levels of amyloid-beta (Abeta) and contribute to cognitive deficit

62 (AD) is characterized by plaques containing amyloid-beta (Abeta) and neurofibrillary tangles compose

63 ts deleterious effects mainly by influencing amyloid-beta (Abeta) and Tau (neurofibrillary tangles, N

64 ron emission tomography (PET) biomarkers for amyloid-beta (Abeta) and tau pathologies are accurate fo

65 ks of AD; in particular, the accumulation of amyloid-beta (Abeta) and tau.

66 ed to a human IgG1 Fc domain (hFc) or to the amyloid-beta (Abeta) antibody bapineuzumab (Bapi).

67 Aggregates of amyloid-beta (Abeta) are characteristic of Alzheimer's d

68 Genetic evidence points to deposition of amyloid-beta (Abeta) as a causal factor for Alzheimer's

69 Asymmetries of amyloid-beta (Abeta) burden are well known in Alzheimer

70 The shared role of amyloid-beta (Abeta) deposition in cerebral amyloid angi

71 o the prevailing amyloid cascade hypothesis, amyloid-beta (Abeta) deposition in the brain is the init

72 Amyloid-beta (Abeta) deposition occurs years before cogn

73 Amyloid-beta (Abeta) deposits are a relatively late cons

74 velopment of parenchymal and cerebrovascular amyloid-beta (Abeta) deposits by 40-50%, which is mediat

75 ical hallmark of Alzheimer's disease (AD) is amyloid-beta (Abeta) deposits in the brain, which largel

76 In Alzheimer's disease (AD) amyloid-beta (Abeta) deposits may cause impairments in c

77 nitive decline, raising the possibility that amyloid-beta (Abeta) disrupts hypothalamic neurons criti

78 Deposition of amyloid-beta (Abeta) fibers in the extracellular matrix

79 DP-43 forms spherical oligomers and perturbs amyloid-beta (Abeta) fibrillization.

80 Apolipoprotein E (apoE) colocalizes with amyloid-beta (Abeta) in Alzheimer disease (AD) plaques a

81 Long-term studies of immunity to pathogenic amyloid-beta (Abeta) in LOAD are lacking.

82 ugh AMPK activation; and potential rescue of amyloid-beta (Abeta) induced synaptic impairment.

83 Amyloid-beta (Abeta) is a macromolecular structure of gr

84 Amyloid-beta (Abeta) likely plays a primary role in Alzh

85 Formation of amyloid-beta (Abeta) oligomer pores in the membrane of n

86 Amyloid-beta (Abeta) oligomers are implicated in Alzheim

87 rger values as the size and concentration of amyloid-beta (Abeta) oligomers increase.

88 (TREM2) impairs the response of microglia to amyloid-beta (Abeta) pathology in Alzheimer's disease (A

89 understanding of the molecular pathways for amyloid-beta (Abeta) peptide aggregation from monomers i

90 High levels of the amyloid-beta (Abeta) peptide have been shown to disrupt

91 mer's disease (AD) is the formation of toxic amyloid-beta (Abeta) peptide polymers and the aggregatio

92 The amyloid-beta (Abeta) peptide, a key pathogenic factor in

93 isease (AD) is the accumulation of misfolded amyloid-beta (Abeta) peptide.

94 Amyloid-beta (Abeta) peptides are the major drivers of A

95 f a label-free approach for the detection of amyloid-beta (Abeta) peptides by highly selective aptame

96 amyloid accumulation.SIGNIFICANCE STATEMENT Amyloid-beta (Abeta) peptides have profound neurovascula

97 rimental and clinical evidence suggests that amyloid-beta (Abeta) peptides may function as a link amo

98 asing the proportion of longer amyloidogenic amyloid-beta (Abeta) peptides.

99 PET (30 AD, 6 MCI, 2 cognitively normal) and amyloid-beta (Abeta) PET (17 AD, 3 MCI, 2 cognitively no

100 s evidence to suggest that quantification of amyloid-beta (Abeta) PET images may reduce interreader v

101 stained microglial activation in response to amyloid-beta (Abeta) plaque deposits and cell death.

102 ed gut microbiome is associated with reduced amyloid-beta (Abeta) plaque pathology and astrogliosis i

103 disease (AD) present with both extracellular amyloid-beta (Abeta) plaques and intracellular tau-conta

104 logy is characterized by the accumulation of amyloid-beta (Abeta) plaques and tau neurofibrillary tan

105 this novel compound was found to dissociate amyloid-beta (Abeta) plaques and tau tangles, which are

106 AD), we generated TgAD/GSS mice that develop amyloid-beta (Abeta) plaques of AD and PrP (specifically

107 nces, build-up of brain metabolic wastes and amyloid-beta (Abeta) plaques, perivascular reactive astr

108 Alzheimer's disease continuum is defined as amyloid-beta (Abeta) positive but cognitively normal.

109 itiates the amyloidogenic cascade leading to Amyloid-beta (Abeta) production.

110 The amyloid hypothesis posits that the amyloid-beta (Abeta) protein precedes and requires micro

111 PET neuroimaging of amyloid-beta (Abeta) provides an in vivo biomarker for p

112 The relationship between amyloid-beta (Abeta) species and tau pathology in Alzhei

113 ed wakefulness exacerbates the production of amyloid-beta (Abeta) species, a major driver of AD progr

114 ubjects who were further classified based on amyloid-beta (Abeta) status as positive or negative (Abe

115 amyloid deposits, physically interacts with amyloid-beta (Abeta) via its N-terminal Abeta binding do

116 previous research demonstrated that soluble amyloid-beta (Abeta)(42), elicits presynaptic glutamate

117 ion of the intrinsically disordered peptide, amyloid-beta (Abeta), involve transitions from the disor

118 The link between brain amyloid-beta (Abeta), metabolism, and dementia symptoms

119 protecting SH-SY5Y neuroblastoma cells from amyloid-beta (Abeta)-induced cytotoxicity.

120 ApoE, receptor binding, and interaction with amyloid-beta (Abeta).

121 the neuronal membrane is a target for toxic amyloid-beta (Abeta).

122 on with the N-terminal histidine residues of amyloid-beta (Abeta).

123 tep of the amyloidogenic pathway to generate amyloid-beta (Abeta).

124 amylin, amyloid precursor protein [APP], and amyloid-beta [Abeta]) and amyloid, as well as extracellu

125 Amyloid-beta accumulates in the brain across the lifespa

126 virus vector-based knockdown of CD33 reduced amyloid beta accumulation and neuroinflammation.

127 between cerebral microhemorrhages (MHs) and amyloid beta accumulation in Alzheimer disease (AD), but

128 significant associations between the rate of amyloid-beta accumulation and APOE epsilon4 positivity,

129 ger amyloid-beta-positive individuals, while amyloid-beta accumulation is greater in APOE epsilon4 ca

130 tivity during successful memory encoding and amyloid-beta accumulation with PiB-positron emission tom

131 -florbetapir (pattern expression score of an amyloid-beta AD conversion-related pattern, constructed

132 enic transmission only exists for prions and amyloid beta after systemic injections of contaminated g

133 a relationship between iron accumulation and amyloid-beta aggregation.

134 = .008) and parietal (rho = 0.31; P = .005) amyloid beta and parietal tau load (rho = 0.31; P = .005

135 CSF and PET biomarkers of amyloid beta and tau accurately detect Alzheimer's disea

136 d immunohistochemistry was performed against amyloid-beta and GFAP.

137 284; n2 = 553) with harmonized CSF assays of amyloid-beta and hyperphosphorylated tau (pTau), and lon

138 vide insights into the pathways linking tau, amyloid-beta and neurodegeneration, and may facilitate c

139 glymphatic-lymphatic system in clearance of amyloid-beta and other proteins.

140 ssible interactions between tau proteins and amyloid-beta and study the resulting coupled behavior be

141 disease is characterized by the presence of amyloid-beta and tau deposition in the brain, hippocampa

142 accumulation that frequently associates with amyloid-beta and tau fibrils, the hallmarks of Alzheimer

143 ar aggregation of misfolded proteins such as amyloid-beta and tau in Alzheimer disease, alpha-synucle

144 Stratification of subjects by CSF amyloid-beta and tau levels revealed that CSF sTREM2 con

145 tments targeting vascular health, as well as amyloid-beta and tau levels, may preserve cognitive func

146 We examined these pathways, as well as amyloid-beta and tau pathologies in the hippocampus and

147 osis, cholesterol transport, ubiquitination, amyloid-beta and tau processing).

148 Our analysis reveals ways in which amyloid-beta and tau proteins may conspire with each oth

149 rs; 115 females) were stratified by elevated amyloid-beta and tau status based on 11C-Pittsburgh comp

150 in non-carriers, even after controlling for amyloid-beta and tau status, and were correlated with in

151 learance pathway for protein species such as amyloid-beta and tau, which accumulate in the brain in A

152 ses the cerebrospinal fluid concentration of amyloid-beta and tau.

153 that mediates the converging effects of APOE-amyloid-beta and TMEM106B on TDP-43 aggregation in older

154 ease molecular pathology, with levels of CSF amyloid-beta and total tau contributing independently to

155 e associated with appearance of pathological amyloid-beta and/or tau.

156 related to the pathological hallmarks of AD, amyloid-beta, and tau deposits.

157 nation treatments targeting vascular health, amyloid-beta, and tau levels may more effectively preser

158 tal-tau, neurofilament light chain (NfL) and amyloid-beta, are increasingly being used to define and

159 egin with the initial increases in aggregate amyloid-beta as early as two decades before the developm

160 al tau (AUC=83.08-93.11% across cohorts) and amyloid beta (AUC=76.14-88.09% across cohorts) pathologi

161 nson's disease subgroups with a positive CSF amyloid-beta biomarker signature.

162 181 with CSF and PET measures of neocortical amyloid-beta burden and more accurately distinguishes AD

163 ion Tomography (PiB-PET) to assess fibrillar amyloid-beta burden in cortical and subcortical regions,

164 , there is no proof that the transmission of amyloid beta can also lead to Alzheimer's dementia.

165 on of the alphaSyn sequence contains the non-amyloid beta-component (NAC) crucial for aggregation.

166 NK cell depletion did not affect amyloid beta concentrations but enhanced neurogenesis an

167 ibited 2-5-fold increased surface binding to amyloid-beta conformers as well as substantially more ef

168 This work supports in vivo staging of amyloid-beta deposition in both cortical and subcortical

169 Amyloid-beta deposition into plaques is a pathologic hal

170 Although cerebral amyloid-beta deposition occurs on a continuum, dichotomi

171 e amyloid-beta1-42, vascular and parenchymal amyloid-beta deposits, and astrocytosis (31%, 47-80%, an

172 lular domain accumulate in EVs over time and amyloid-beta dimerizes.

173 A long standing hypothesis that amyloid-beta drives Alzheimer's disease has proven the s

174 cipants, we also show that TMEM106B and APOE-amyloid-beta effects converge to alter myelination and l

175 ht-induced Amyloid-beta oligomerization from Amyloid-beta expression alone.

176 or their ability to bind alpha-synuclein and amyloid beta fibrils in vitro.

177 ence emitted by medin aggregates compared to amyloid-beta fibrils, along with the absence of amyloid

178 nhancing resistance to defined pathognomonic amyloid-beta forms.

179 TDP-43, tau and amyloid-beta have all been linked to hippocampal atrophy

180 blem comes from new research suggesting that amyloid beta helps memory consolidation, before it impai

181 -AZD4694 (also known as (18)F-NAV4694) is an amyloid-beta imaging ligand with high affinity for amylo

182 Amyloid-beta immunodepletion alleviated some but not all

183 ased levels of amyloid precursor protein and amyloid beta in PITRM1-knockout neurons.

184 Owing to an early and marked deposition of amyloid-beta in the basal ganglia, autosomal dominant Al

185 a stages, that correlates with deposition of amyloid-beta in the basal ganglia.

186 Oligomeric amyloid-beta induces a divergent response in human versu

187 ruch's membrane thickens but unlike in mice, amyloid beta is absent.

188 of these alterations remains to be defined, amyloid-beta is a likely contributor in the brain as in

189 ce of immune activation on the production of amyloid-beta is unknown(2,3).

190 microglia activity, substantially increased amyloid-beta levels, and impaired cognition, whereas enh

191 P = .004) and frontal (rho = 0.27; P = .005) amyloid beta load and global tau load (rho = 0.31; P = .

192 tions of MH with regional and global tau and amyloid beta load.

193 factors such as APOEepsilon4 and subcortical amyloid-beta may identify participants closest to MCI fo

194 Iatrogenic transmission of amyloid beta might lead to amyloid deposition in the bra

195 also showed that CSF concentrations of pTau/amyloid-beta moderated the observed predictive relations

196 The Hfd led to increases in amyloid-beta monomers and plaques in APP/PS1 mice, as we

197 tinguished Alzheimer's disease dementia from amyloid beta-negative young adults (AUC=99.40%) and cogn

198 continuum, from the lowest concentrations in amyloid beta-negative young adults and cognitively unimp

199 5.7%), respectively, when compared to either amyloid-beta-negative cognitively unimpaired (0.4 +/- 2.

200 disease had accelerated p-tau217 compared to amyloid-beta-negative cognitively unimpaired (beta = 0.5

201 ative cognitively unimpaired (0.4 +/- 2.7%), amyloid-beta-negative mild cognitive impairment (-0.4 +/

202 .001, using linear mixed effects models) and amyloid-beta-negative mild cognitive impairment patients

203 P-tau217 did not change in amyloid-beta-negative participants, or in patients with

204 positive subjects, but were stable by age in amyloid-beta-negative subjects (age x amyloid-beta statu

205 d the hypothesis that the oligomeric form of amyloid-beta (oAbeta(42)), interacting with alpha7-conta

206 siology, Pyk2(-/-) slices are protected from amyloid-beta-oligomer (Abetao)-induced suppression of LT

207 and physical damage caused by light-induced Amyloid-beta oligomerization from Amyloid-beta expressio

208 aptotoxicity is driven, at least in part, by amyloid-beta oligomers (Abetao), but the exact synaptic

209 This pathologic feature is driven by amyloid-beta oligomers (Abetaos) and propagates from neu

210 by the intracerebroventricular injection of amyloid-beta oligomers (oAbeta), we analyzed cellular an

211 The physical damage caused by Amyloid-beta oligomers also recapitulated the catastroph

212 D22 promotes the clearance of myelin debris, amyloid-beta oligomers and alpha-synuclein fibrils in vi

213 the investigation of disease-relevant small amyloid-beta oligomers by mass spectrometry and ion mobi

214 In particular, we can show that amyloid-beta oligomers develop in two distinct arrangeme

215 investigate the consequences of formation of Amyloid-beta oligomers in living tissues, we developed a

216 to the crucial question of how intracellular Amyloid-beta oligomers underlie the pathologies of A.

217 We show that the lifespan deficit induced by Amyloid-beta oligomers was reduced with Li(+) treatment.

218 ar prion protein on neurons bind Alzheimer's amyloid-beta oligomers, causing neurotoxic effects.

219 of the corresponding structure of the first amyloid-beta oligomers.

220 parison with cerebrospinal fluid measures of amyloid-beta (optimal cut point, 1.51 SUVR).

221 cognitive impairment, but is not related to amyloid-beta or tau pathology measured in cerebrospinal

222 Blood p-tau181 can predict tau and amyloid beta pathologies, differentiate Alzheimer's dise

223 As constitute a novel pathway deregulated in amyloid beta pathology, with potential implications for

224 mapping and tau-PET in n = 236 subjects with amyloid-beta pathology (from the Swedish BioFINDER-2 stu

225 sociated with apolipoprotein (APO) APOE4 and amyloid-beta pathology.

226 esidues 31-42) of the 42-residue form of the amyloid beta peptide (Abeta42), a protein fragment whose

227 n proteostasis, influencing clearance of the amyloid beta peptide and phosphorylation of tau, which a

228 of the 42-residue variant of the Alzheimer's amyloid-beta peptide (Abeta(1-42)).

229 gation process of the 42-residue form of the amyloid-beta peptide (Abeta(42)) are key pathogenic agen

230 Amyloid-beta peptide (Abeta) accumulation in the brain i

231 sis, according to which the self-assembly of amyloid-beta peptide (Abeta) is a causative process in A

232 s study, we aimed to identify the effects of amyloid-beta peptide 42 (amyloid-beta42) and phosphoryla

233 nimpaired participants (22 with elevated CSF amyloid-beta peptide 42 levels, 15 with elevated CSF pho

234 The amyloid-beta peptide is correlated with Alzheimer's dise

235 The formation of oligomers of the amyloid-beta peptide plays a key role in the onset of Al

236 eveloped a fluorescently tagged, optogenetic Amyloid-beta peptide that oligomerizes rapidly in the pr

237 l factors influencing the aggregation of the amyloid-beta peptide, the islet amyloid polypeptide, alp

238 odegenerative diseases caused by variants in amyloid-beta peptide.

239 that HSV-1 catalyzes the aggregation of the amyloid beta-peptide (Abeta(42)), a major constituent of

240 ele carrier status; plasma concentrations of amyloid beta peptides 1-42 and 1-40 and their ratio (Abe

241 Amyloid-beta peptides (Abeta) assemble into both rigid a

242 biological effects of soluble and aggregated Amyloid-beta peptides are difficult to separate in vivo.

243 The binding of amyloid-beta peptides of different concentrations to the

244 eating a molecular beacon reporter to detect amyloid-beta peptides, known to be involved in the patho

245 cognitively impaired (n = 65)] who underwent amyloid-beta PET with (18)F-AZD4694, lumbar puncture, st

246 y by age, sex, amyloid status (determined by amyloid-beta PET), APOE epsilon4 genotype, study cohort,

247 asma pTau181 identified individuals who were amyloid beta-PET-positive regardless of clinical diagnos

248 In a similar analysis on longitudinal amyloid-beta-PET (in ADNI subjects only, n = 639), we fo

249 ction in 3xTg-associated phosphorylated tau, amyloid beta plaques, and activated microglia in 3xTg/SP

250 ressing microglia exclusively surrounded NA+ amyloid beta plaques, which accumulated in an age-depend

251 orks and nuclear pores in mammalian cells to amyloid-beta plaques and dendrites in brain tissues and

252 E10 macrophages surrounded brain and retinal amyloid-beta plaques and expressed 3.2-fold higher insul

253 ctive regional vulnerability of the brain to amyloid-beta plaques and tau neurofibrillary tangles.

254 Amyloid-beta plaques are thought to play either a direct

255 d-beta imaging ligand with high affinity for amyloid-beta plaques.

256 in mass and a preponderance of extracellular Amyloid-beta plaques.

257 adults, through higher concentrations in the amyloid beta-positive cognitively unimpaired older adult

258 groups, to the highest concentrations in the amyloid beta-positive MCI and Alzheimer's disease groups

259 mild cognitive impairment (-0.4 +/- 2.3%) or amyloid-beta-positive cognitively unimpaired (1.2 +/- 2.

260 ere required to observe a slope reduction in amyloid-beta-positive cognitively unimpaired (71 partici

261 Preclinical (amyloid-beta-positive cognitively unimpaired, n = 62) an

262 ation rate is greater in females and younger amyloid-beta-positive individuals, while amyloid-beta ac

263 d increase in tau-PET signal was observed in amyloid-beta-positive mild cognitive impairment (3.0 +/-

264 ively unimpaired (71 participants per arm in amyloid-beta-positive mild cognitive impairment).

265 gnitively unimpaired, n = 62) and prodromal (amyloid-beta-positive mild cognitive impairment, n = 49)

266 0-93 years; 47 amyloid-beta-positive) and 20 amyloid-beta-positive patients with mild cognitive impai

267 Tau-PET slopes decreased with age in amyloid-beta-positive subjects, but were stable by age i

268 nitively normal adults (age: 20-93 years; 47 amyloid-beta-positive) and 20 amyloid-beta-positive pati

269 dies have assessed a quantitative cutoff for amyloid-beta positivity using (18)F-AZD4694 PET.

270 epsilon4 positivity, older age and baseline amyloid-beta positivity, but no effect of sex.

271 he currently approved cerebrospinal fluid or amyloid beta positron emission tomography (PET) diagnost

272 r cells (hNPCs) expressing varying levels of amyloid beta precursor protein (APP) and presenilin 1 (P

273 eta is a neurotoxic peptide excised from the amyloid-beta precursor protein (APP) by beta-site APP-cl

274 Amyloid-beta precursor protein (APP) is overshadowed by

275 beta-42 (Abeta42) peptide generated from the amyloid-beta precursor protein (APP) via cleavages by be

276 ut the brain has been considered because the amyloid-beta precursor protein (APP), APP metabolites, a

277 eptor binds and phosphorylates APP, reducing amyloid-beta production, which are abrogated by delta-se

278 d which is used as a surrogate marker of non-amyloid-beta protein aggregation.

279 n of angiotensin-converting enzyme (ACE), an amyloid-beta protein degrading enzyme, to brain resident

280 P) binds to and regulates the translation of amyloid-beta protein precursor (App) mRNA, but the detai

281 Amyloid beta-protein (Abeta) molecules tend to aggregate

282 ave been examined primarily as inhibitors of amyloid beta-protein (Abeta), whereas testing of inhibit

283 ps between the topographical distribution of amyloid-beta removal from the cerebral cortex and tau pa

284 cleft of lysozyme and those produced from an amyloid-beta segment have both uncovered structural info

285 Amyloid beta-sheet secondary structure was detected in c

286 parison with cerebrospinal fluid measures of amyloid-beta, specifically the Abeta(42)/Abeta(40) ratio

287 age in amyloid-beta-negative subjects (age x amyloid-beta status interaction: t = -2.39, P = 0.018).

288 ssure nor change in blood pressure predicted amyloid-beta status or PACC score at 69-71 years of age.

289 the monomeric unfolded conformations of the amyloid-beta symbol (Abeta) peptide but with aggregated

290 the AD spectrum, stratified by using the A (amyloid beta)/T (tau)/N (neurodegeneration) biomarker cl

291 blood-based biomarkers for AD, for example, amyloid-beta, tau, phosphorylated tau and neurofilament

292 he possibility of iatrogenic transmission of amyloid beta through putatively contaminated neurosurgic

293 betapir (AV45) PET was performed to quantify amyloid beta to study associations of MH with regional a

294 w that this response is dysfunctional during amyloid beta toxicity and pathology in the mouse hippoca

295 the link between mitochondrial dynamics and amyloid beta toxicity.

296 to better understand any potential routes of amyloid beta transmission and to clarify whether other s

297 epitopes of 28 monoclonal antibodies against amyloid-beta using immunoselection of random sequences f

298 th expression and induced oligomerization of Amyloid-beta were detrimental to lifespan and healthspan

299 ein previously known to reduce the levels of amyloid-beta, which is critical in the pathogenesis of A

300 heimer's disease brain extracts suggest that amyloid-beta, which migrates on sodium dodecyl sulphate