ライフサイエンスコーパス: amyloid plaque

1 l imaging sessions, and always surrounded an amyloid plaque.

2 stsynaptic structures within the vicinity of amyloid plaques.

3 self-assembly of the proteins comprising the amyloid plaques.

4 nature and are not directly associated with amyloid plaques.

5 to the presence of Abeta fibrils observed in amyloid plaques.

6 ed AD mouse model substantially reduces beta-amyloid plaques.

7 or in APP/PS1 mice prior to the formation of amyloid plaques.

8 revention in presymptomatic subjects bearing amyloid plaques.

9 axonal swellings at Alzheimer's disease (AD) amyloid plaques.

10 llings that resemble the dystrophic axons at amyloid plaques.

11 other species that prevent the formation of amyloid plaques.

12 onfirmed neurodegeneration in the absence of amyloid plaques.

13 upregulated in microglial cells surrounding amyloid plaques.

14 and many do not robustly remove pre-existing amyloid plaques.

15 intra- and extracellular inclusions, such as amyloid plaques.

16 s were translated to increased deposition of amyloid plaques.

17 8 nor the bigenic mice develop extracellular amyloid plaques.

18 ofibrillary tangles (NFTs) and extracellular amyloid plaques.

19 res of AD, including its colocalization with amyloid plaques.

20 loid (Abeta) and its massive accumulation in amyloid plaques.

21 eta (Abeta) peptide deposition into cerebral amyloid plaques.

22 PP(E693Q) X PS1Delta9 bigenic mice developed amyloid plaques.

23 ity, and for furthering their aggregation in amyloid plaques.

24 istics of human dementia, such as tangles or amyloid plaques.

25 strophic neurites (DNs) in areas surrounding amyloid plaques.

26 to wild type in hippocampus areas devoid of amyloid plaques.

27 anumab to the brain resulted in clearance of amyloid plaques.

28 on of the synaptic pathology associated with amyloid plaques.

29 CASP4, more microglia were clustered around amyloid plaques.

30 in axonal dystrophy and synaptic loss around amyloid plaques.

31 e activated microglia that surround the beta-amyloid plaques.

32 d clearance of Abeta, the major component of amyloid plaques.

33 ns, restored synaptic integrity, and reduced amyloid plaques.

34 ion is more pronounced in patients with more amyloid plaques (a marker of AD severity).

35 Amyloid plaques, a neuropathological hallmark of Alzheim

36 Selective detection and staining of toxic amyloid plaques, a potential biomarker present in the Al

37 and accumulates fibrillar Abeta amyloid and amyloid plaques accompanied by neuritic dystrophy and be

38 neurodegenerative dementia characterized by amyloid plaque accumulation, synapse/dendrite loss, and

39 ssociated with the presence of extracellular amyloid plaques adjacent to beta cells and intracellular

40 In addition to protein fibrils, amyloid plaques also contain non-proteinaceous component

41 (AD), characterized by neurodegeneration and amyloid plaque and neurofibrillary pathologies.

42 ely 2 million years ago served to reduce the amyloid plaque and vascular burden of APOE varepsilon4,

43 ve shown associations between PET imaging of amyloid plaques and amyloid-beta pathology measured at a

44 default mode network fails before measurable amyloid plaques and appears to initiate a connectivity c

45 n of neural activity prevents the buildup of amyloid plaques and associated neural pathologies remain

46 e patients presenting cerebellar damage with amyloid plaques and ataxia with unclear pathophysiology.

47 The molecular interplay between parenchymal amyloid plaques and CAA is unclear.

48 mulation and exacerbated Abeta deposition as amyloid plaques and CAA without affecting Abeta producti

49 isease, can occur in the form of parenchymal amyloid plaques and cerebral amyloid angiopathy (CAA).

50 rest in degenerative brain diseases, such as amyloid plaques and changes in cortical layers and subco

51 henotype of APP/Abca1(ko) mice in regards to amyloid plaques and cognitive deficits.

52 and endogenous monocytes, homed to cerebral amyloid plaques and directly engulfed amyloid-beta; thei

53 matched non-demented cases were examined for amyloid plaques and Dkk-1 expression and subjected to du

54 accumulation of lysosome-like organelles at amyloid plaques and establish that the majority of these

55 transgenic mouse model that develop typical amyloid plaques and followed the progression of patholog

56 Glycosaminoglycans (GAGs) bind all known amyloid plaques and help store protein hormones in (acid

57 vations are consistent with the reduction in amyloid plaques and improvement of cognitive function in

58 The data for amyloid plaques and insoluble amyloid-beta (Abeta) also

59 lasses of abnormal structures, extracellular amyloid plaques and intraneuronal neurofibrillary tangle

60 expressed in reactive astrocytes surrounding amyloid plaques and may contribute to Abeta degradation.

61 y, the beneficial effects of decreasing beta-amyloid plaques and neurodegeneration by Delta(9)-THC in

62 Besides the hallmark pathology of amyloid plaques and neurofibrillary tangles (NFTs), it h

63 his is the only mouse model that co-develops amyloid plaques and neurofibrillary tangles but also bec

64 Amyloid plaques and neurofibrillary tangles co-occur in

65 which is defined pathologically by abundant amyloid plaques and neurofibrillary tangles concurrent w

66 Further, the development of amyloid plaques and neurofibrillary tangles contributes

67 tive disease pathologically characterized by amyloid plaques and neurofibrillary tangles in the brain

68 Amyloid plaques and neurofibrillary tangles simultaneous

69 Determining the relative contribution of amyloid plaques and neurofibrillary tangles to brain dys

70 yloid pathway and the tau pathway-leading to amyloid plaques and neurofibrillary tangles, respectivel

71 PET images, used for in vivo imaging of beta-amyloid plaques and neurofibrillary tangles, were obtain

72 with the frequently associated pathology of amyloid plaques and neurofibrillary tangles.

73 between the axonal lysosome accumulations at amyloid plaques and neuronal lysosomes of the wild-type

74 that chronically disrupted sleep may promote amyloid plaques and other downstream Alzheimer's disease

75 nositol (GPI) anchoring and the abundance of amyloid plaques and protease-resistant PrP(Sc) (PrP(Res)

76 gy, sAPP-alpha overexpression decreases beta-amyloid plaques and soluble Abeta.

77 ameliorated the amyloid pathology, including amyloid plaques and soluble amyloid.

78 dromal phase between the first appearance of amyloid plaques and tangles and the manifestation of dem

79 Amyloid plaques and tau tangles are common pathological

80 is understood to involve the accumulation of amyloid plaques and tau tangles in the brain.

81 ge 0-92) and (3) Alzheimer's neuropathology (amyloid plaques and tau tangles) using a postmortem samp

82 HFD significantly increased amyloid plaques and worsened cognitive performance compa

83 nt deposits containing by the Abeta peptide (amyloid plaques) and the tau protein (neurofibrillary ta

84 DCP-LA, effectively prevents synaptic loss, amyloid plaques, and cognitive deficits (also prevented

85 gomers, greater synaptic density surrounding amyloid plaques, and increased expression of presynaptic

86 P are the major constituent of AD-associated amyloid plaques, and mutations or duplications of the ge

87 is characterized by neurofibrillary tangles, amyloid plaques, and neurodegeneration.

88 dentification of substructures within single amyloid plaques, and the quantification of rCBF.

89 ected away from traditional targets, such as amyloid plaques, and towards characterization of early o

90 Amyloid plaques are a key pathological hallmark of Alzhe

91 Larger non-toxic amyloid plaques are also present in tissues of eosinophi

92 mmature neurons, challenging the notion that amyloid plaques are necessary for neurodegeneration.

93 ebate in Alzheimer's disease (AD) is whether amyloid plaques are pathogenic, causing overt physical d

94 Amyloid plaques are primarily composed of aggregated amy

95 ith the development of cortical PiB-positive amyloid plaques (area under receiver operating character

96 for only 14 d also decreased the density of amyloid plaques assessed postmortem.

97 The amyloid plaques associated with Alzheimer's disease (AD)

98 (Abeta) is the main protein component of the amyloid plaques associated with Alzheimer's disease.

99 The APP(E693Q) mice did not develop amyloid plaques at any age studied, up to 30 months.

100 The amyloid beta peptide aggregates into amyloid plaques at presymptomatic stages of Alzheimer's

101 s present at sites of inflammation including amyloid plaques, atherosclerotic lesions, and arthritic

102 40 using surface plasmon resonance and their amyloid plaque binding ability in AD mouse brain section

103 le-aged individuals before the appearance of amyloid plaques, biomarker studies in living individuals

104 nerative conditions and show that regions of amyloid plaque buildup in brain tissue of Alzheimer's pa

105 B as a potential long-term therapy to reduce amyloid plaque burden and improve cognitive performance.

106 d AbetaPP/PS1 mice have significantly higher amyloid plaque burden at 12 months than outcrossed Abeta

107 eta levels were translated into an increased amyloid plaque burden both in the cortex (54%, p < 0.01)

108 and BACE1, consequently leading to increased amyloid plaque burden in the brain.

109 y occlusion, we observed a rapid increase in amyloid plaque burden in the region surrounding the infa

110 The amyloid plaque burden was decreased by roughly 50% in th

111 brain levels of insoluble Abeta42 as well as amyloid plaque burden were markedly reduced in APP(Swe)/

112 tration is effective in reducing the Abeta42 amyloid plaque burden, reversing cholinergic neuron abno

113 ffect is largely mediated by an individual's amyloid plaque burden.

114 ments in older APP/PS1 mice with significant amyloid plaque burden.

115 shown to colocalize with regions marked with amyloid plaques burden suggesting a strong link between

116 ndings indicate that early-onset parenchymal amyloid plaques can serve as a scaffold to capture CAA m

117 ion protein in the form of frequent cortical amyloid plaques, cerebral amyloid angiopathy, and tauopa

118 r's disease is the presence of extracellular amyloid plaques chiefly consisting of amyloid-beta (Abet

119 -SwDI mice, but exhibited larger parenchymal amyloid plaques compared with Tg-5xFAD mice.

120 me 4q25, encodes the collagen-like Alzheimer amyloid plaque component precursor, a type II transmembr

121 ative disease, is the deposition of neuritic amyloid plaques composed of aggregated forms of the beta

122 The presence of amyloid plaques composed of amyloid beta (Abeta) fibrils

123 oincides with the formation of extracellular amyloid plaques composed of the amyloid-beta (Abeta) pep

124 Amyloid plaques comprised of insoluble, fibrillar amyloi

125 Amyloid plaques comprising misfolded proteins are the ha

126 Amyloid plaques, consisting of deposited beta-amyloid (A

127 ociated with extracellular brain deposits of amyloid plaques containing aggregated amyloid-beta (Abet

128 tomography (PET) imaging agents that detect amyloid plaques containing amyloid beta (Abeta) peptide

129 howed that synthetic Abeta40 prions produced amyloid plaques containing both Abeta40 and Abeta42 in t

130 the detection of substructures within single amyloid plaques correlating with amyloid deposition dens

131 In vivo detection of brain beta-amyloid plaque density may increase diagnostic accuracy

132 ith postmortem beta-amyloid burden, neuritic amyloid plaque density, and neuropathological diagnosis

133 ced the levels of BACE1, soluble Abeta40/42, amyloid plaque density, and rescued cognitive deficits o

134 m of Abeta peptide, which is dominant in the amyloid plaques deposited in the brains of AD patients.

135 lure of this clearance system contributes to amyloid plaque deposition and Alzheimer's disease progre

136 m status, results in significantly decreased amyloid plaque deposition and microglial activation.

137 he absence of mutant protein overexpression, amyloid plaque deposition and synaptic degradation.

138 sly shown to exhibit behavioral deficits and amyloid plaque deposition between 4-9 months of age.

139 e regional dependency between metabolism and amyloid plaque deposition have arrived at conflicting re

140 to attenuate Abeta generation and attenuate amyloid plaque deposition in AD.

141 ulation of amyloid-beta (Abeta) peptides and amyloid plaque deposition in brain is postulated as a ca

142 how this results in a distinctive pattern of amyloid plaque deposition in default mode network region

143 ally coupled with Abeta1-42 peptide to image amyloid plaque deposition in the mouse brain.

144 Whether the decline in FC precedes amyloid plaque deposition or is a consequence thereof is

145 A striking increase in amyloid plaque deposition was observed in prion-infected

146 these findings suggest that animal behavior, amyloid plaque deposition, and AbetaPP processing are se

147 Before amyloid plaque deposition, the amnesia in these mice is

148 d inflammatory dysregulation, and subsequent amyloid plaque deposition.

149 eceptor in the brain that strongly regulates amyloid plaque deposition.

150 such as episodic memory decline and neuritic amyloid plaque deposition.

151 ves elevated brain Abeta levels and eventual amyloid plaque deposition.

152 es APP and tau fragmentation and facilitates amyloid plaque deposits and neurofibrillary tangle (NFT)

153 ical areas increased drastically even before amyloid plaque deposits became evident.

154 ed by prominent ataxia and extracellular PrP amyloid plaque deposits in brain.

155 The amyloid plaques detected by T2*-weighted muMRI were conf

156 ate that USPIO-PEG-Abeta1-42 can be used for amyloid plaque detection in vivo by intravenous injectio

157 , but there was no significant difference in amyloid plaque distribution between the two groups.

158 2 injected AD transgenic correlated with the amyloid plaque distribution histologically.

159 he six CR animal (16.7%) did not express any amyloid plaques, five of seven Controls (71.4%) and four

160 m unilateral vibrissal deprivation decreased amyloid plaque formation and growth.

161 identified to have AD-type dementia without amyloid plaque formation but with extensive intraneurona

162 Abeta-peptide generation and thereby reduce amyloid plaque formation in the brain, a neuropathologic

163 ha-syn, yet the precise role of alpha-syn in amyloid plaque formation remains elusive.

164 e found that 3-month-old Tg2576 mice, before amyloid plaque formation, exhibit decreased weight with

165 We analyzed brain exosome content, amyloid plaque formation, neuronal degeneration, sphingo

166 ded Abeta42 peptide is sufficient to promote amyloid plaque formation.

167 ntribute to both neurofibrillary tangles and amyloid plaque formation.

168 upt several behaviors independent of visible amyloid plaque formation.

169 complexes in blood and partly colocalize in amyloid plaques from Alzheimer disease patients.

170 to distinguish individuals with no or sparse amyloid plaques from those with moderate to frequent pla

171 es leading to an updated hypothesis in which amyloid plaques give way to amyloid oligomers as the dri

172 t observe any alteration in the formation of amyloid plaques, gliosis, synaptic loss, or cognitive be

173 based proteomic technologies for analysis of amyloid plaques has transformed the way amyloidosis is d

174 ve astrocytes are intimately associated with amyloid plaques; however, their role in AD pathogenesis

175 Given the wide-spread distribution of amyloid plaques, if the canonical cascade hypothesis wer

176 we investigated how early-onset parenchymal amyloid plaques impact the development of microvascular

177 trocytes and activated microglia surrounding amyloid plaques, implicating their role in disease patho

178 was observed to enter the CNS and bind beta-amyloid plaques in a transgenic mouse model of Alzheimer

179 d in AD, is neurotoxic, and colocalizes with amyloid plaques in AD animal models and human brains.

180 peptides, which are a main component of the amyloid plaques in AD brains, affected Ptc1-Gli1 signali

181 ons of fibrillar Abeta, a major component of amyloid plaques in AD brains.

182 also correlates with their associations with amyloid plaques in Alzheimer's brains: RTN3, but not RTN

183 ortant pathological features associated with amyloid plaques in Alzheimer's disease (AD) and age-depe

184 beta peptides (Abeta(1-40/42)) form neuritic amyloid plaques in Alzheimer's disease (AD) patients and

185 the patterns of neurofibrillary tangles and amyloid plaques in Alzheimer's disease suggested a hiera

186 ow that a murine analog of aducanumab clears amyloid plaques in an acute setting and restores calcium

187 As a test case, we examined amyloid plaques in an Alzheimer's disease (AD) mouse mod

188 ce, as well as within astrocytes surrounding amyloid plaques in APP/PS1 mice.

189 r ER inclusion is found in areas surrounding amyloid plaques in biopsy samples from Alzheimer's disea

190 Remarkably, IAPP colocalized with amyloid plaques in brain parenchymal deposits, suggestin

191 f PAR-4 and ceramide, astrocytes surrounding amyloid plaques in brain sections of the 5xFAD mouse (an

192 negative correlation between plasma HDL and amyloid plaques in brain, suggesting that plasma lipopro

193 d, we analyzed the LCO-stained cores of beta-amyloid plaques in postmortem tissue sections from front

194 on and adjacent to pre-existing parenchymal amyloid plaques in Tg-5xFAD mice.

195 The detection of amyloid plaques in the brain is important for the diagno

196 WST CWD produced PrP(Sc) amyloid plaques in the brain of the SGH that were partia

197 D, high-resolution images of individual beta-amyloid plaques in the brain parenchyma and vasculature

198 rP-A116V, and a near-complete absence of PrP amyloid plaques in the brain.

199 ssing donors spontaneously home to compacted amyloid plaques in the brain.

200 Moreover, the Abeta amyloid plaques in the brains of bigenic mice inoculated

201 g in vivo leads to a significant decrease in amyloid plaques in the cortex and hippocampus of neurolo

202 een demonstrated to precede its formation as amyloid plaques in the extracellular space in Alzheimer'

203 of Alzheimer disease is the accumulation of amyloid plaques in the extracellular space in the brain.

204 usion reduced the number of Abeta42-positive amyloid plaques in the hippocampus and cerebral cortex o

205 ced the Abeta(1-42) levels and the number of amyloid plaques in the hippocampus.

206 d with a reduction of the number and size of amyloid plaques in the MR imaging-guided focused ultraso

207 lzheimer's disease through their presence in amyloid plaques in the nervous systems of affected indiv

208 teins delays the age-dependent production of amyloid plaques in transgenic mouse models of AD.

209 Activated microglia are associated with amyloid plaques in transgenic mouse models of cerebral a

210 omising and non-invasive method to visualize amyloid plaques in vivo because of its acceptable depth

211 for cellular imaging, (ii) visualization of amyloid plaques in vivo in a mouse model of Alzheimer's

212 developed several contrast agents to detect amyloid plaques in vivo using magnetic resonance microim

213 ound intracellularly, and extracellularly as amyloid plaques, in Alzheimer's disease and in dementia

214 Since amyloid plaque is present in the human brain for years p

215 lation of aggregated amyloid-beta (Abeta) in amyloid plaques is a neuropathological hallmark of Alzhe

216 Ubiquitin accumulation in amyloid plaques is a pathological marker observed in the

217 In this way, the pathology of amyloid plaques is envisioned as highly correlated with,

218 microglia in the brain, concentrated around amyloid plaques, is a prominent feature of Alzheimer's d

219 e that acetylcholinesterase, also present in amyloid plaques, is aberrant in peripheral tissues such

220 Mutant brains displayed fewer amyloid plaques, less amyloid-beta (Abeta), and diminish

221 Pathognomonic accumulation of cerebral beta-amyloid plaques likely results from imbalanced productio

222 Insoluble amyloid plaques likely sequester soluble HMW oligomers,

223 n effect was most pronounced for lowering of amyloid plaque load and plaque number, which suggests ef

224 er this accurate and noninvasive approach to amyloid plaque load detection will translate into a bene

225 n and glucose metabolism in association with amyloid plaque load in a transgenic AD mouse model.

226 PICALM contributes to amyloid plaque load in brain likely via its effect on Ab

227 lial fibrillary acid protein (GFAP) and beta-amyloid plaque load in the hippocampus and the adjacent

228 in the brain interstitial fluid and reduced amyloid plaque load in the hippocampus compared with con

229 eased soluble and insoluble Abeta levels and amyloid plaque load in the hippocampus.

230 no significant differences were observed on amyloid plaque load or soluble fibrillar Abeta by quanti

231 CR affects levels of GFAP expression but not amyloid plaque load provides some insight into the means

232 In aged mice, total Abeta levels and amyloid plaque load were selectively reduced in the TFEB

233 and the presenilin-1 mutant DeltaE9 reduces amyloid plaque load, as well as Abeta40 and Abeta42 leve

234 eases Tau hyperphosphorylation, lowers brain amyloid plaque load, improves learning and memory, and p

235 We found a significant decrease in amyloid plaque load, insoluble Abeta and soluble Abeta o

236 nimals as a gold standard assessment of beta-amyloid plaque load.

237 LM overexpression increased Abeta levels and amyloid plaque load.

238 The gene deletions increased amyloid plaque load: APP/PS1 Gfap(-/-)Vim(-/-) mice had

239 op AD-like disease including accumulation of amyloid plaques, loss of synaptic and neuronal proteins,

240 related to permeability and the presence of amyloid plaque may reduce the permeability of a vessel a

241 The formation of hIAPP amyloid plaques near islet cells has been linked to the

242 eatment aimed at engaging myeloid cells with amyloid plaques neither directed peripherally derived my

243 nd tau mutations, and progressively develops amyloid plaques, neurofibrillary tangles, and synaptic d

244 Alzheimer's disease (AD) is hallmarked by amyloid plaques, neurofibrillary tangles, and widespread

245 eated mice displayed decreased inflammation, amyloid plaques, NFTs, cell death, and an extended life

246 use of categorical measures for certain non-amyloid-plaque, non-neurofibrillary-tangle neuropatholog

247 rected peripherally derived myeloid cells to amyloid plaques nor altered Abeta burden.

248 m isoform may neither interact directly with amyloid plaques nor engage in cell-surface signaling.

249 Notably, BDNF did not affect amyloid plaque numbers, indicating that direct amyloid r

250 a(11-42) and Abeta(17-42)) are also found in amyloid plaques of AD and in the preamyloid lesions of D

251 hat zinc inhibits the formation of insoluble amyloid plaques of hIAPP; however, there remains signifi

252 Because MCs have been found close to amyloid plaques of patients with Alzheimer's disease (AD

253 A major component of ex vivo amyloid plaques of patients with dialysis-related amyloi

254 on (18)F-FDG PET, and detection of cerebral amyloid plaque on amyloid PET--are able to evaluate the

255 allow for the accurate in vivo detection of amyloid plaques, one hallmark of Alzheimer disease.

256 myloid angiopathy in the complete absence of amyloid plaques or neurofibrillary tangles.

257 in (Abeta), but before the appearance of the amyloid plaques or neuronal loss in the Tg2576 AD transg

258 the locus affects the deposition of neuritic amyloid plaque (p = 0.009).

259 o restore adequate Abeta removal and counter amyloid plaque pathogenesis in AD.

260 evated extracellular Abeta levels that drive amyloid plaque pathogenesis.

261 calizes after uptake, has been implicated in amyloid plaque pathogenesis.

262 0-4.4), and to have lower degrees of diffuse amyloid plaque pathology (mean [SD] Consortium to Establ

263 sosomes was revealed by the worsening of the amyloid plaque pathology arising from JIP3 haploinsuffic

264 positive association between age and average amyloid plaque pathology in these animals, but there was

265 in addition to alpha-synuclein pathology and amyloid plaque pathology, are the strongest pathological

266 wered plaque load in AD mice with aggressive amyloid plaque pathology.

267 s of brain Abeta and greater accumulation of amyloid plaque pathology.

268 P = .03) and inversely correlated with total amyloid plaques (Pearson r = -0.48; P < .01) and tangles

269 region-specific deposition of extracellular amyloid plaques principally composed of aggregated amylo

270 Furthermore, MABT-mediated amyloid plaque removal was demonstrated using in vivo li

271 mer disease is the presence of extracellular amyloid plaques resulting from the aggregation of amyloi

272 containing abundant NFTs but bound poorly to amyloid plaque-rich, NFT-poor AD brain homogenates.

273 spongiform change, and diffuse multicentric amyloid plaques, selectively immunoreactive for prion pr

274 mples from non-AD individuals, those without amyloid plaques show a lower level of lipid oxidation th

275 the overlap between regions that show early amyloid plaque signal on positron emission tomography an

276 hich overexpresses amyloid beta and develops amyloid plaques similar to those in the brains of patien

277 eactive astrocytes have been observed around amyloid plaques since the disease was first described, t

278 Neuron, DeMattos et al. demonstrate that an amyloid plaque-specific antibody removes existing Abeta

279 46% of participants and was associated with amyloid plaques, tangles, and hippocampal sclerosis but

280 After controlling for amyloid plaques, tangles, and hippocampal sclerosis, TDP

281 loid-beta peptide, the main component of the amyloid plaques that are associated with Alzheimer disea

282 ified MT1-MMP degraded parenchymal fibrillar amyloid plaques that form in the brains of Abeta precurs

283 Cortical beta-amyloid plaques, the first stage of AD pathology, can be

284 n's disease (PD) to form large proteinaceous amyloid plaques, the spread of which throughout the brai

285 been shown experimentally (in the absence of amyloid plaques) to impair hippocampal synaptic plastici

286 tedate the pathological effects of fibrillar amyloid plaque toxicity.

287 Clearance of amyloid plaques upon immunization with AN1792 effectivel

288 tion between regional glucose metabolism and amyloid plaques using linear models.

289 athologic burden of neurofibrillary tangles, amyloid plaques, vascular lesions, and Lewy bodies.

290 The periphery of parenchymal amyloid plaques was largely composed of CAA mutant Abeta

291 ificantly enhanced clearance of pre-existing amyloid plaques was observed when gantenerumab was coadm

292 In APP/PS1 mice, the formation of amyloid plaques was sufficient to induce the entry of ce

293 ic abnormalities observed in the vicinity of amyloid plaques were blocked.

294 Amyloid plaques were not affected, but the beneficial ef

295 an Abeta and develop early-onset parenchymal amyloid plaques, were bred to Tg-SwDI mice, which produc

296 reports indicating accelerated deposition of amyloid plaques, which are composed of amyloid-beta pept

297 (AD) is characterized by the accumulation of amyloid plaques, which are predominantly composed of amy

298 rain leads to the formation of extracellular amyloid plaques, which is one of the pathological hallma

299 amyloid-beta (Abeta) as toxic oligomers and amyloid plaques within the brain appears to be the patho

300 d beta-peptide (Abeta) that ultimately forms amyloid plaques within the human brain.