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 nces in binding site polarity of polymorphic amyloid plaque.

3 istributed relatively furthest from the core amyloid plaque.

4 llings that resemble the dystrophic axons at amyloid plaques.

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

6 ic gadolinium (Gd) imaging agent, for MRI of amyloid plaques.

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

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

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

10 on of the synaptic pathology associated with amyloid plaques.

11 CASP4, more microglia were clustered around amyloid plaques.

12 in axonal dystrophy and synaptic loss around amyloid plaques.

13 all dose levels for in vivo imaging of beta amyloid plaques.

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

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

16 stsynaptic structures within the vicinity of amyloid plaques.

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

18 nature and are not directly associated with amyloid plaques.

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

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

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

22 revention in presymptomatic subjects bearing amyloid plaques.

23 other species that prevent the formation of amyloid plaques.

24 onfirmed neurodegeneration in the absence of amyloid plaques.

25 eta-correlated proteins are colocalized with amyloid plaques.

26 ction of cerebral amyloid angiopathy but not amyloid plaques.

27 with loss of dendritic spines independent of amyloid plaques.

28 ages and metabolomic biomarkers representing amyloid plaques.

29 mouse model of AD, before deposition of beta amyloid plaques.

30 ents with NT1 suggests delayed appearance of amyloid plaques.

31 ain fluorescence microscopy images to locate amyloid plaques.

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

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

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

35 Alzheimer's disease pathological hallmarks: amyloid plaques (A), phosphorylated tau (T), and accompa

36 protein plays a key role in the formation of amyloid plaques, a hallmark of Alzheimer's disease (AD).

37 Amyloid plaques, a neuropathological hallmark of Alzheim

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

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

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

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

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

43 We reconstructed a whole human amyloid plaque and established that plaques are formed b

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

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

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

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

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

49 For AD-related pathologies of amyloid plaques and Braak stage, e2 had large and highly

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

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

52 ne that identifies specific neuropathologies-amyloid plaques and cerebral amyloid angiopathy-in immun

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

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

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

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

57 Although amyloid plaques and fibrillary tangles are hallmarks of

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

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

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

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 e condition characterized by accumulation of amyloid plaques and neurofibrillary tangles in the brain

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

69 t observation of pathological markers of AD (amyloid plaques and neurofibrillary tangles) in aged chi

70 ative dementia associated with deposition of amyloid plaques and neurofibrillary tangles, formed by a

71 The emergence of PET probes for amyloid plaques and neurofibrillary tangles, hallmarks o

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

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 ent using sensory stimuli, or GENUS) reduced amyloid plaques and phosphorylated tau in multiple mouse

76 estores slow wave power, halts deposition of amyloid plaques and prevents neuronal calcium dysregulat

77 Alzheimer's disease (AD) is characterized by amyloid plaques and progressive cerebral atrophy.

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

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

80 Amyloid plaques and tau tangles are common pathological

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

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

83 on, migration, clustering in the vicinity of amyloid plaques and the uptake and degradation of Abeta.

84 HFD significantly increased amyloid plaques and worsened cognitive performance compa

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

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

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

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

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

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

91 onkeys naturally develop cognitive deficits, amyloid plaques, and the same qualitative pattern and se

92 Amyloid plaques are a key pathological hallmark of Alzhe

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

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

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 m individuals with PD and is also present in amyloid plaques associated with Alzheimer's disease.

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

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

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

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

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

104 Furthermore, knockout of CD33 reduces amyloid plaque burden in mouse models of AD.

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

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

107 5XFAD mice improved spatial memory, reduced amyloid plaque burden, and neuroinflammation.

108 ting miR-195 ameliorates cognitive deficits, amyloid plaque burden, and tau hyper-phosphorylation in

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

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

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

112 The formation of amyloid plaques by aggregated amyloid beta (Abeta) pepti

113 -optimized protocol reduced the formation of amyloid plaques by more than 70%.

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

115 ry age-related tauopathy lacks the requisite amyloid plaques central to Alzheimer's disease.

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

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

118 tective effects against diffuse and neuritic amyloid plaques compared with e3/e3 and e4 carriers in t

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

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

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

122 mer's disease (AD) is cerebral deposition of amyloid plaques composed of amyloid beta (Abeta) peptide

123 opathologically by presence of extracellular amyloid plaques composed of fibrillar amyloid beta (Abet

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

125 Amyloid plaques comprised of insoluble, fibrillar amyloi

126 Amyloid plaques comprising misfolded proteins are the ha

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

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

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

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

131 ferential staining of transgenic mouse Abeta amyloid plaque cores compared to peripheral coronas usin

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

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

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

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

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

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

146 aducanumab only in cortical regions prone to amyloid plaque deposition, regardless of the reference r

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

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

149 d inflammatory dysregulation, and subsequent amyloid plaque deposition.

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

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

152 Amyloid plaque deposits in the brain are indicative of A

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

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

155 e of amyloid beta (Abeta) peptide-containing amyloid plaque development.

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

157 2 injected AD transgenic correlated with the amyloid plaque distribution histologically.

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

159 isol, have been recognized as key factors in amyloid plaque formation and aggravation of AD.

160 ich overproduction of Abeta peptide leads to amyloid plaque formation and associated neuritic dystrop

161 st known for its role in Alzheimer's disease amyloid plaque formation but also contributes to neurode

162 ng these pathways may therapeutically reduce amyloid plaque formation in cerebral vessels and the bra

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

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

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

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

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

168 model of the disease, either before or after amyloid plaque formation.

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

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

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

172 However, limited studies of metabolites in amyloid plaques have been performed due to the drawbacks

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

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

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

176 These Abeta species can generally form amyloid plaques implicated in the neurodegeneration of A

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

178 we reconstructed a high-accuracy 3D-model of amyloid plaques in a fully automated fashion, employing

179 amma-secretase activity and the formation of amyloid plaques in a transgenic mouse model (5xFAD) of e

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

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

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

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

184 -peptide (Abeta(42)), a major constituent of amyloid plaques in Alzheimer's disease, in vitro and in

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

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

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

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

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

190 without (Spearman rho = 0.15; P = .33), beta-amyloid plaques in cohort 1.

191 HSV-1 DNA has been detected in AD amyloid plaques in human brains, and treatment with the

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

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

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

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

196 d positron emission tomography (PET) detects amyloid plaques in the brain, a core neuropathological f

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

198 es, leading to the successful PET imaging of amyloid plaques in the brains of 5xFAD mice versus those

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

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

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

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

203 rotein beta(2)-microglobulin (beta(2)m) into amyloid plaques in the joints of long-term hemodialysis

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

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

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

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

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

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

210 culminating in an impaired response to beta-amyloid plaques in vivo.

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

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

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

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

215 ), a protein fragment whose aggregation into amyloid plaques is linked with Alzheimer's disease.

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

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

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

219 the comparative computational evaluation of amyloid plaque-like objects by MSI: a fast PLAQUE PICKER

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

221 Insoluble amyloid plaques likely sequester soluble HMW oligomers,

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

223 We found that sTREM2 reduces amyloid plaque load and rescues functional deficits of s

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

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

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

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

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

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

232 consistent outcome of Trem2 deficiency than amyloid plaque load, suggesting that the microglial pack

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

234 LM overexpression increased Abeta levels and amyloid plaque load.

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

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

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

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

239 tion of BACE1 transcripts and an increase in amyloid plaques, neurofibrillary tangles, and cognitive

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

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

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

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

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

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

246 ory-like alterations are observed around the amyloid plaques of Alzheimer's disease (AD), little is k

247 ain tissue non-fibrillar Abeta structures in amyloid plaques of cases with autosomal dominant and spo

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

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

250 reatment significantly reduced the extent of amyloid plaques, oligomers, phagocytic microglia, and in

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

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

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

254 in monkeys, but so far without detection of amyloid plaques or tau pathology.

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

256 evated extracellular Abeta levels that drive amyloid plaque pathogenesis.

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

258 0-4.4), and to have lower degrees of diffuse amyloid plaque pathology (mean [SD] Consortium to Establ

259 campus and reach an effective dose to reduce amyloid plaque pathology and promote neurogenesis.

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

261 u-217 and p-tau-181 were highly specific for amyloid plaque pathology in the discovery cohort (n = 36

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

263 Amyloid plaque pathology was significantly reduced in al

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

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

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

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

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

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

270 We demonstrate that amyloid plaque seeding is increased in the absence of fu

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

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

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

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

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

276 46% of participants and was associated with amyloid plaques, tangles, and hippocampal sclerosis but

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

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

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

280 roperties may influence the polymorphisms of amyloid plaques through the cross-seeding process.

281 sing SHIELD revealed widespread reduction of amyloid plaques throughout neocortex after multi-sensory

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

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

284 tissue domains in a 100-mum diameter around amyloid plaques using spatial transcriptomics.

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

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

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

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

289 nd how different DNs evolve to surround core amyloid plaques, we monitored the growth of DNs in AD mo

290 Amyloid plaques were accumulated more in the medial pref

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

292 Amyloid plaques were not affected, but the beneficial ef

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

294 loid-beta1-42 peptide, the main component of amyloid plaques, were restricted to the hippocampus.

295 A-positive DNs were often closer to the core amyloid plaque, whereas RTN3 immunoreactive DNs were mos

296 Amyloid beta (Abeta) is a major component of amyloid plaques, which are a key pathological hallmark f

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 AD)-related neuropathology, characterized by amyloid plaques with amyloid beta (Abeta) and neurofibri

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