ライフサイエンスコーパス: amyloid beta

1 id imaging or a cerebrospinal fluid assay of amyloid beta.

2 these populations from the toxic effects of amyloid beta.

3 manised monoclonal antibody directed against amyloid beta.

4 ase, the enzyme involved in the formation of amyloid beta.

5 model of AD, which progressively accumulates amyloid-beta.

6 f Alzheimer disease-associated dysfunctions, amyloid-beta.

7 Western blot or immunofluorescence for AQP4, amyloid-beta 1-42, and glial fibrillary acidic protein.

8 d mouse neuroblastoma cells treated with the amyloid-beta(1-42) peptide also showed a similarly highe

9 imaging and positron emission tomography for amyloid-beta ((11) C-PiB or (18) F-florbetapir) and tau

10 reduction in its steady-state level and less amyloid-beta-40 (Abeta40) peptide uptake.

11 six markers of synaptic subtypes, as well as amyloid beta 42 and paired helical filament tau.

12 fter the final scans, histologic measures of amyloid-beta (4G8), microglia (ionized calcium binding a

13 Beta-amyloid (beta-A) peptides are potential biomarkers to mo

14 he amyloid fibril formation from Alzheimer's amyloid beta (Abeta) (1-40) and on that from D76N beta2-

15 Amyloid beta (Abeta) 42 is an aggregation-prone peptide

16 pid microenvironment, which may occur during amyloid beta (Abeta) accumulation and neuronal degenerat

17 Amyloid beta (Abeta) accumulation is an early event in t

18 Different amyloid beta (Abeta) aggregates can be discriminated by

19 acterized by the progressive accumulation of amyloid beta (Abeta) and microtubule associate protein t

20 f dementia, characterized by accumulation of amyloid beta (Abeta) and neurofibrillary tangles.

21 dysfunction due to the disrupting binding of amyloid beta (Abeta) and tau oligomers is one of the ear

22 Accumulation of amyloid beta (Abeta) and tau represent the two major pat

23 ic amyloidogenic cleavage of APP and produce amyloid beta (Abeta) at the expense of sAPPalpha and oth

24 Blocking toxic amyloid beta (Abeta) could be beneficial for AD and repr

25 We coimmunostained for retinal amyloid beta (Abeta) deposition and melanopsin to locate

26 rring polyphenols have been found to inhibit amyloid beta (Abeta) fibril formation and reduce neuron

27 ursor protein (APP) and its cleavage product amyloid beta (Abeta) have been thoroughly studied in Alz

28 on of dynamin-related protein (Drp1) against amyloid beta (Abeta) induced mitochondrial and synaptic

29 e of Alzheimer's disease (AD), intracellular amyloid beta (Abeta) induces mitochondrial dysfunction a

30 The conversion of the native random coil amyloid beta (Abeta) into amyloid fibers is thought to b

31 mine whether periodontitis is related to the amyloid beta (Abeta) load in blood and the role of any s

32 the production, aggregation, and toxicity of amyloid beta (Abeta) or to promote Abeta clearance.

33 Compelling evidence links amyloid beta (Abeta) peptide accumulation in the brains

34 gents that detect amyloid plaques containing amyloid beta (Abeta) peptide aggregates in the brain of

35 Taking a fibrillar assembly of amyloid beta (Abeta) peptide as the model system, here w

36 There are three specific regions in the Amyloid beta (Abeta) peptide sequence where variations c

37 Alzheimer's disease, are largely composed of amyloid beta (Abeta) peptide, derived from cleavage of a

38 ves of KLVFF, a fragment Abeta(16-20) of the amyloid beta (Abeta) peptide, is investigated and recove

39 sease (AD) is characterized by deposition of amyloid beta (Abeta) peptides into senile plaques in the

40 Self-association of amyloid beta (Abeta) peptides is a hallmark of Alzheimer

41 Aggregation of amyloid beta (Abeta) peptides is a significant event tha

42 a Drosophila model of AD, reducing levels of amyloid beta (Abeta) peptides, reversing locomotor defec

43 en deposits are Alzheimer disease-associated amyloid beta (Abeta) peptides.

44 progression, a vicious cycle revolves around amyloid beta (Abeta) production, aggregation, plaque for

45 mportant transport step in the regulation of amyloid beta (Abeta) production.

46 e also report a functional interplay between amyloid beta (Abeta), beta-adrenergic signaling, and alt

47 chondria-targeted tetra-peptide SS31 against amyloid beta (Abeta)-induced mitochondrial and synaptic

48 on differs by the presence of elevated brain amyloid beta (Abeta); and (3) whether plasma total tau l

49 etamine (METH) and nicotine (NT) can enhance amyloid-beta (Abeta) accumulation in BMEC through Alpha7

50 whether p62 also plays a role in regulating amyloid-beta (Abeta) aggregation and degradation.

51 tein transthyretin (TTR) is known to inhibit amyloid-beta (Abeta) aggregation in vitro and suppress t

52 isease (AD); however, the specific impact of amyloid-beta (Abeta) aggregation on biomarker abnormalit

53 Amyloid-beta (Abeta) and human islet amyloid polypeptide

54 Amyloid-beta (Abeta) and hyperphosphorylated tau (p-tau)

55 with the accumulation of protein aggregates; amyloid-beta (Abeta) and tau in the brain during AD, and

56 Amyloid-beta (Abeta) and tau pathologies are intertwined

57 gnition of monomeric, oligomeric, and fibril amyloid-beta (Abeta) by three homologous antibodies (sol

58 Despite the demonstration that amyloid-beta (Abeta) can trigger increased tau phosphory

59 Impairment of amyloid-beta (Abeta) clearance leads to Abeta accumulati

60 erapy targeting soluble and aggregated brain amyloid-beta (Abeta) continues to dominate clinical rese

61 Accurate measurement of changes in amyloid-beta (Abeta) deposition over time is important i

62 It is not known exactly where amyloid-beta (Abeta) fibrils begin to accumulate in indi

63 cent studies found that the concentration of amyloid-beta (Abeta) fluctuates with the sleep-wake cycl

64 Failure to clear amyloid-beta (Abeta) from the brain is in part responsib

65 P-Cleaving Enzyme 1 (BACE1), a key enzyme in amyloid-beta (Abeta) generation.

66 Low molecular weight oligomers of amyloid-beta (Abeta) have emerged as the primary toxic a

67 Accumulation and aggregation of amyloid-beta (Abeta) in the brain is an initiating step

68 The misfolding and self-assembly of amyloid-beta (Abeta) into oligomers and fibres is fundam

69 Amyloid-beta (Abeta) is a 39-42 residue protein produced

70 plasticity and memory.SIGNIFICANCE STATEMENT Amyloid-beta (Abeta) is a key pathogenetic factor in Alz

71 Whether amyloid-beta (Abeta) is associated with gait speed in el

72 Amyloid-beta (Abeta) is thought to play an essential pat

73 ead changes, we found an increase in soluble amyloid-beta (Abeta) levels that was restricted to the t

74 pite increasing appreciation that oligomeric amyloid-beta (Abeta) may contribute to cognitive decline

75 Amyloid-beta (Abeta) oligomers associate with AVs in AD

76 by shRNA reduces tau phosphorylation, lowers amyloid-beta (Abeta) pathology, and improves cognition i

77 Oligomeric forms of the amyloid-beta (Abeta) peptide are thought to represent th

78 Alzheimer's disease (AD) is characterized by amyloid-beta (Abeta) peptide deposition in brain parench

79 diabetes (T2D), with the Alzheimer's disease amyloid-beta (Abeta) peptide modulates their self-assemb

80 Extracellular deposition of amyloid-beta (Abeta) peptide, a metabolite of sequential

81 Alzheimer's disease are directed against the amyloid-beta (Abeta) peptide.

82 own that apoE, apoE4 in particular, binds to amyloid-beta (Abeta) peptides at residues 12-28 of Abeta

83 llular amyloid plaques chiefly consisting of amyloid-beta (Abeta) peptides in the brain interstitium.

84 Amyloid-beta (Abeta) peptides play a key role in synapti

85 The accumulation of soluble amyloid-beta (Abeta) peptides produces profound neuronal

86 protein (APP) into short, aggregation-prone amyloid-beta (Abeta) peptides, which are centrally impli

87 its of amyloid plaques containing aggregated amyloid-beta (Abeta) peptides.

88 ite matter hyperintensities (WMH) on MRI and amyloid-beta (Abeta) PET.

89 yloidosis is commensurate with reductions in amyloid-beta (Abeta) plaque pathology and plaque-localis

90 sease (AD) is characterized by extracellular amyloid-beta (Abeta) plaques and intracellular tau inclu

91 Amyloid-beta (Abeta) plaques are a key histopathological

92 Tau aggregates and amyloid-beta (Abeta) plaques are key histopathologic fea

93 characterized by the presence of parenchymal amyloid-beta (Abeta) plaques, cerebral amyloid angiopath

94 allmarks of Alzheimer's disease (AD) include amyloid-beta (Abeta) plaques, neurofibrillary tangles, a

95 Amyloid-beta (Abeta) plays a key role in the pathogenesi

96 Processing of amyloid-beta (Abeta) precursor protein (APP) by gamma-se

97 ly influence its beta secretase activity and amyloid-beta (Abeta) production.

98 ealth, synaptic plasticity, dementia-related amyloid-beta (Abeta) protein expression, and hippocampal

99 Accumulation of amyloid-beta (Abeta) protein may cause synapse degenerat

100 Abnormal accumulation of tau and amyloid-beta (Abeta) proteins in the human brain are 2 p

101 ecursor protein mutations falling within the amyloid-beta (Abeta) sequence lead to a wide range of di

102 ion 673 in APP (A673V), or position 2 of the amyloid-beta (Abeta) sequence.

103 led newborn cells), and amyloidosis [soluble amyloid-beta (Abeta) species and Abeta plaque load].

104 s central to AD pathobiology, including tau, amyloid-beta (Abeta), and the Abeta-degrading protease n

105 nked to neurodegenerative disorders, such as amyloid-beta (Abeta), tau, or alpha-synuclein (alphaSyn)

106 Amyloid-beta (Abeta)-induced neuron death is considered

107 which shows antiaggregation activity against amyloid-beta (Abeta)1-42 peptide aggregation.

108 enetic evidence implicate soluble oligomeric amyloid-beta (Abetao) in triggering Alzheimer's disease

109 our understanding of the soluble oligomeric amyloid-beta-Abetao-binding cellular prion protein (PrP(

110 = 19), neurologically normal elderly without amyloid-beta accumulation (normal ageing, n = 13), and n

111 neurologically normal elderly with cortical amyloid-beta accumulation (pathological ageing, n = 15).

112 In particular, intracellular amyloid-beta accumulation and oligomerization are early

113 T quantification is necessary for monitoring amyloid-beta accumulation and response to therapy.

114 ed to a significant reduction in amyloid and amyloid-beta accumulation both in leptomeningeal and bra

115 re, non-local associations linking increased amyloid-beta accumulation rates with increased tau depos

116 hich potentially leads to worsening vascular amyloid-beta accumulation, activation of vascular injury

117 PINK1-deficient mAPP mice augmented cerebral amyloid-beta accumulation, mitochondrial abnormalities,

118 age-related progression of tumor growth and amyloid-beta accumulation.

119 Overall, these data provide evidence that amyloid beta acts to enhance tau pathology by increasing

120 in brain damage and reduced accumulation of amyloid beta aggregates.

121 he molecular and mesoscopic self-assembly of amyloid-beta, alpha synuclein, human islet amyloid polyp

122 amyloidogenic protein metal-complexes (like amyloid-beta, alpha-synuclein and prion-protein).

123 rget mechanisms of epileptogenesis involving amyloid beta and tau.

124 and is similar to the mechanism observed for amyloid-beta and alpha-synuclein.

125 23)I-ABC577 showed high binding affinity for amyloid-beta and desirable pharmacokinetics in the precl

126 d the accumulation of N-terminally truncated amyloid-beta and full-length amyloid-beta, depending on

127 specks released by microglia bind rapidly to amyloid-beta and increase the formation of amyloid-beta

128 sults provide rationale for the targeting of amyloid-beta and lacunes in therapeutic strategies aimed

129 ecursor protein (APP) and tau, mediating the amyloid-beta and tau pathology in Alzheimer's disease (A

130 rtical associations between the maps of Tau, amyloid-beta, and gray matter intensity.

131 This effect was also specific to amyloid-beta, and not total protein, tau, YKL-40, or hyp

132 pathology we found that early intraneuronal amyloid beta build-up is sufficient to unleash a global

133 4 localization was associated with increased amyloid-beta burden (R2 = 0.15; P = .003) and increasing

134 Omega-3 polyunsaturated fatty acids promote amyloid-beta clearance from the brain through mediating

135 Microglia lose their amyloid-beta-clearing capabilities with age and as AD pr

136 nally truncated amyloid-beta and full-length amyloid-beta, depending on disease stage as well as brai

137 e applied to examine the association between amyloid-beta deposition and regional glucose metabolism.

138 Biomarkers of amyloid-beta deposition precede neurodegeneration on mag

139 mer's disease, but little is known about how amyloid-beta deposition relates to longitudinal progress

140 Amyloid-beta deposition, neuroinflammation and tau tangl

141 ecent experiments suggest that variations in amyloid-beta fibril structure in vivo may correlate with

142 ursor proteins that lead to the formation of amyloid beta fibrils implicated in Alzheimer's disease,

143 ed amyloid-beta11-x fibrils than full-length amyloid-beta fibrils.

144 gnitive disorders where APP misprocessing to amyloid beta formation has been observed.

145 E1) is the major neuronal beta-secretase for amyloid-beta generation and is degraded in lysosomes.

146 uptake inhibitor (SSRI) citalopram decreases amyloid-beta generation and plaque load.

147 and structure distinct from the conventional amyloid beta-hairpin and revealed that the nucleating NF

148 ognitive impairment associated with cortical amyloid-beta have a greatly increased risk of progressin

149 CAA-like pathology in patients treated with amyloid-beta immunotherapy for Alzheimer's disease has h

150 ments targeting specific pathologies such as amyloid beta in Alzheimer's disease (AD) have not led to

151 major candidate therapeutic targets to lower amyloid-beta in a preventive mode, i.e., gamma- and beta

152 785 decreased the levels of C99 and secreted amyloid-beta in cellular, zebrafish, and mouse models of

153 igate the sequence of development of tau and amyloid-beta in relationship to age, and to the developm

154 Non-invasive imaging of amyloid-beta in the brain, a hallmark of Alzheimer's dis

155 The frequent presence of amyloid-beta in the brains of cognitively healthy older

156 The genetic evidence implicating amyloid-beta in the initial stage of Alzheimer's disease

157 e to the misaggregation of proteins, such as amyloid-beta, in neurodegenerative conditions such as AD

158 peutic effects of fenamates using a model of amyloid beta induced memory loss and a transgenic mouse

159 cated in neurotrophic factor withdrawal- and amyloid-beta-induced dendritic spine collapse and neuron

160 signalling (OPTN or NDP52) fails to reverse amyloid-beta-induced detrimental effects.

161 Concomitantly with these amyloid-beta-induced disruptions, the AIS/TDB sorting fu

162 eptors (OPTN and NDP52), thereby alleviating amyloid-beta-induced loss of synapses and cognitive decl

163 isoforms differ in axodendritic sorting and amyloid-beta-induced missorting and that the axodendriti

164 Pathomechanistically, amyloid-beta insult caused cofilin activation and F-acti

165 and ELN relationships, including the role of amyloid-beta, into a broader conceptual framework of how

166 ents with Alzheimer's disease, deposition of amyloid-beta is accompanied by activation of the innate

167 The same group also had significantly lower amyloid beta levels and deposition, less tau neuropathol

168 Slow wave activity disruption increases amyloid-beta levels acutely, and poorer sleep quality ov

169 had significantly lower cerebrospinal fluid amyloid-beta levels compared with control individuals (m

170 g neuronal PINK1 function strikingly reduces amyloid-beta levels, amyloid-associated pathology, oxida

171 recursor protein (APP) and thereby increases amyloid-beta levels.

172 of CBF and radiotracer clearance changes on amyloid-beta load estimates was small.

173 promotes the rescue of amyloid pathology and amyloid-beta-mediated mitochondrial and synaptic dysfunc

174 d-beta species and other proteins related to amyloid-beta metabolism or Alzheimer's disease were quan

175 terminal fragments (APP-CTFs) and oligomeric amyloid beta (oAbeta) but no histological evidence of am

176 c doses of soluble oligomeric forms of human amyloid-beta (oAbeta) and Tau (oTau) proteins impairs me

177 have recently demonstrated that pathological Amyloid beta oligomer (Abetao) regulates the association

178 e Osaka (E693Delta) mutation, which promotes amyloid-beta oligomerization.

179 omarkers; novel candidate biomarkers include amyloid beta oligomers and synaptic markers.

180 mainly attributed to synaptotoxicity of the amyloid-beta oligomers (AbetaOs).

181 ttributed to neuronal dysfunction induced by amyloid-beta oligomers (AbetaOs).

182 o amyloid-beta and increase the formation of amyloid-beta oligomers and aggregates, acting as an infl

183 trials of emerging therapies targeting tau, amyloid-beta or alpha synuclein, and to stratify them by

184 not examined which aspect of sleep modulates amyloid-beta or other Alzheimer's disease biomarkers.

185 in the amounts of amyloid precursor protein, amyloid-beta or synaptic proteins.

186 ssion tomography (PET) imaging (API) detects amyloid-beta pathology early in the course of Alzheimer'

187 an anti-ASC antibody blocked the increase in amyloid-beta pathology in APPSwePSEN1dE9 mice.

188 ce failed to induce seeding and spreading of amyloid-beta pathology in ASC-deficient APPSwePSEN1dE9 m

189 ion is connected to seeding and spreading of amyloid-beta pathology in patients with Alzheimer's dise

190 Histology confirmed reduction of amyloid-beta pathology in TG-BACE mice.

191 ction of ASC specks resulted in spreading of amyloid-beta pathology in transgenic double-mutant APPSw

192 great interest and support the idea that the amyloid-beta pathology might have remote effects in dise

193 translational platform, we demonstrated that amyloid-beta pathology recapitulates an Alzheimer-like p

194 ApoE4 increases brain amyloid-beta pathology relative to other ApoE isoforms.

195 of brain metabolism, neuroinflammation, and amyloid-beta pathology were obtained through small-anima

196 In individuals who are positive for amyloid-beta pathology with symptomatic Alzheimer diseas

197 -mediated neurodegeneration independently of amyloid-beta pathology.

198 ing as an inflammation-driven cross-seed for amyloid-beta pathology.

199 ronal dystrophy in TREM2-deficient mice with amyloid-beta pathology.

200 Pyroglutamate-modified amyloid-beta (pEAbeta) has been described as a relevant

201 curs early and promotes the disease-defining amyloid beta peptide (Abeta) and Tau pathologies.

202 The aggregation of the amyloid beta peptide (Abeta) into amyloid fibrils is a d

203 The amyloid beta peptide (Abeta) is a key player in the etio

204 t to be instigated by toxic oligomers of the amyloid beta peptide (AbetaOs).

205 ilized proteins including oxidized LDL, IgG, amyloid beta peptide 1-42, C4b-binding protein, and fact

206 dies have suggested that when the 40-residue amyloid beta peptide is encapsulated in a reverse micell

207 gatively charged and hydrophobic Alzheimer's amyloid beta peptide using weak and stringent selections

208 The accumulation of amyloid beta peptide(1-42) (Abeta(1-42)) in extracellula

209 ads to a number of metabolites including the amyloid beta peptide.

210 The coaggregation of the amyloid-beta peptide (Abeta) and alpha-synuclein is comm

211 samples for systemic and brain inflammation; amyloid-beta peptide (Abeta) and Ser-202-phosphorylated

212 Given that synthetic amyloid-beta peptide (Abeta) has been shown to adopt dis

213 High levels of amyloid-beta peptide (Abeta) have been related to Alzhei

214 Amyloid-beta peptide (Abeta) isoforms of different lengt

215 In Alzheimer's disease the amyloid-beta peptide (Abeta) misfolds into neurotoxic ol

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

217 small peptides, in particular the mammalian amyloid-beta peptide (Abeta).

218 te in the cellular efflux of desmosterol and amyloid-beta peptide (Abeta).

219 he aggregation of the 42-residue form of the amyloid-beta peptide (Abeta42) is a pivotal event in Alz

220 Soluble oligomers of the amyloid-beta peptide (AbetaOs) are thought to be proxima

221 Non-fibrillar soluble oligomeric forms of amyloid-beta peptide (oAbeta) and tau proteins are likel

222 of brain pathologies such as accumulation of amyloid-beta peptide and mitochondrial damage.

223 yloidogenic peptides, such as the well-known amyloid-beta peptide involved in Alzheimer's disease.

224 acts with lipoprotein particles and with the amyloid-beta peptide, and it is associated with increase

225 lzheimer's disease is the aggregation of the amyloid-beta peptide, which was shown to follow differen

226 Neprilysins in particular are the major amyloid-beta peptide-degrading enzymes.

227 igned antibody DesAb-Abeta against the human Amyloid-beta peptide.

228 disease characterized by aggregation of the amyloid-beta peptide.

229 ualitatively different IDP ensembles for the amyloid-beta peptide.

230 ade and peptide-membrane interactions of the amyloid beta-peptide (Abeta) have been implicated as tox

231 synaptotagmin, and synaptophysin, but not of amyloid beta-peptide 42 or P-T181-tau, were correlated s

232 including the mitochondrial poison rotenone, amyloid beta-peptide, hydrogen peroxide, and high levels

233 ment of this clearance step, for example, by amyloid beta peptides, causes feedback inhibition of MPP

234 peptides, including insulin, amylin, and the amyloid beta peptides.

235 Neurotoxic amyloid-beta peptides (Abeta) are major drivers of Alzhe

236 ibrils formed in vitro by 40- and 42-residue amyloid-beta peptides (Abeta40 and Abeta42) are polymorp

237 's disease (AD) is accumulation of misfolded amyloid-beta peptides and hyperphosphorylated tau protei

238 An improved understanding of the ways that amyloid-beta peptides are formed could help efforts to f

239 Aggregation of amyloid-beta peptides into fibrils or other self-assembl

240 Accumulation of amyloid-beta peptides is a dominant feature in the patho

241 se the unfolded protein response and improve amyloid-beta phagocytosis by macrophages of patients wit

242 In addition to amyloid-beta plaque and tau neurofibrillary tangle depos

243 Formation of amyloid-beta plaque cores (APC) is related to interactio

244 ese females exhibited increased formation of amyloid beta plaques and cognitive impairments relative

245 ent neuropathological traits, including tau, amyloid beta plaques, vascular injury and Lewy bodies.

246 his effect is mediated by an accumulation of amyloid beta plaques.

247 ure, which suggests that tau tangles but not amyloid-beta plaques correlate with cognition and clinic

248 and increased annualized change in cortical amyloid-beta plaques measured as florbetapir positron em

249 In a mouse model that exhibits amyloid-beta plaques similar to AD patients, cholinergic

250 Mutations in amyloid beta precursor protein (APP) gene alter APP proc

251 All other mutations at this site of amyloid beta precursor protein (APP) reduced C99 generat

252 sport proteins JNK-interacting protein 1 and amyloid beta precursor protein in the brains and spinal

253 e core genes were connected to APP (encoding amyloid beta precursor protein), a major player in Alzhe

254 NCT and PS1 play important roles in binding amyloid beta precursor proteins and modulating PS1 catal

255 P-1, which in turn enhances transcription of amyloid-beta precursor protein (APP) and thereby increas

256 ntified a caspase-3 cleavage site within the amyloid-beta precursor protein, and a caspase-3 cleavage

257 , including transgenic mice expressing human amyloid-beta precursor protein, presenilin 1, and tau mu

258 aneuronal accumulation of metabolites of the amyloid-beta-precursor protein (APP) is neurotoxic.

259 ain amyloid precursor protein expression and amyloid beta production are associated with the pathophy

260 The aggregation of amyloid beta protein (Abeta) is a fundamental pathogenic

261 APP at minor Asp(1) site to generate C99 for amyloid beta protein (Abeta) production, and predominant

262 P cleaving enzyme 1 (BACE1) is essential for amyloid beta protein production.

263 etase cleavage of the mutant C99 to generate amyloid beta protein, leading to recessively inherited A

264 abilities of amyloid-beta protein (1-42) and amyloid-beta protein (1-40) in their monomeric and oligo

265 nergy landscapes and relative stabilities of amyloid-beta protein (1-42) and amyloid-beta protein (1-

266 While amyloid-beta protein (Abeta) aggregation into insoluble

267 Brain accumulation of the amyloid-beta protein (Abeta) and synapse loss are neurop

268 The amyloid-beta protein (Abeta) protein plays a pivotal rol

269 Amyloid beta-protein (Abeta) assembly is hypothesized to

270 port on the plasticity-disrupting effects of amyloid beta-protein (Abeta) isolated from Alzheimer's d

271 hat a small amphipathic fragment of APP, the amyloid beta-protein (Abeta), self-associates to form so

272 SIGNIFICANCE STATEMENT: Oligomers of amyloid beta-protein (oAbeta) are tought to play an impo

273 Soluble oligomers of amyloid beta-protein (oAbeta) isolated from the brains o

274 However, for the amyloid beta-protein peptide (Abeta), thought to be the

275 haracterized by the self-assembly of tau and amyloid beta proteins into oligomers and fibrils.

276 nhancing mitochondrial proteostasis to delay amyloid-beta proteotoxic diseases, such as Alzheimer's d

277 onse signature present in diseases involving amyloid-beta proteotoxicity in human, mouse and Caenorha

278 Using a worm model of amyloid-beta proteotoxicity, GMC101, we recapitulated mi

279 (PET) tracer known as (18)F-AV-1451; and (2) amyloid-beta, quantified with (11)C-PiB PET.

280 ed to assess regional differences in age and amyloid-beta-related changes in glucose metabolism.

281 regions that showed both age-invariance and amyloid-beta-related increases in glucose metabolism.

282 The characteristic 2D IR features of amyloid beta-sheet secondary structure are created by as

283 ontained inclusions specifically enriched in amyloid beta-sheets.

284 ase; however, it is not clear how individual amyloid-beta species accumulate and affect other neuropa

285 loid-beta42 accumulation than those of other amyloid-beta species across brain areas and disease stag

286 To this end, the amounts of amyloid-beta species and other proteins related to amylo

287 These truncated amyloid-beta species could play critical roles in the di

288 prion protein (PrP(C)) mediates toxicity of amyloid-beta species linked to Alzheimer's disease was i

289 well as brain area, and determined how these amyloid-beta species respectively correlate with clinico

290 ctions between PrP(C) and disease-associated amyloid-beta species will require experimental medicine

291 on this article.Sleep deprivation increases amyloid-beta, suggesting that chronically disrupted slee

292 cascade that enhances APP transcription and amyloid-beta synthesis.

293 Similarly, other proteins, including amyloid-beta, tau, alpha-synuclein, and serum amyloid A,

294 Amyloid-beta, tau, and alpha-synuclein, or more specific

295 ion the following morning for measurement of amyloid-beta, tau, total protein, YKL-40, and hypocretin

296 clearance of interstitial solutes, including amyloid-beta, through the brainwide network of perivascu

297 sites regulates its biology and ameliorates amyloid beta toxicity in vivo.

298 alterations were associated with ameliorated amyloid beta toxicity.

299 ials of compounds that inhibit PrP-dependent amyloid-beta toxicity are commencing in humans, and alth

300 The 12-28 fragment of amyloid beta was used to show that as the charge state w

301 , it is unlikely that treatments directed at amyloid-beta will have major clinical effects in the lat