ライフサイエンスコーパス: senile plaque

1 ontain extracellular Abeta amyloid deposits (senile plaques).

2 erebral vasculature and, less frequently, in senile plaques.

3 e recruited from the blood and accumulate in senile plaques.

4 mponent of Alzheimer disease (AD)-associated senile plaques.

5 ng the deposition of amyloid beta (Abeta) in senile plaques.

6 kill neurons and eventually form deposits of senile plaques.

7 oid fibrils that accumulate at the center of senile plaques.

8 ated to contribute to amyloid depositions in senile plaques.

9 are observed associated with the majority of senile plaques.

10 aggregates into the fibrils that deposit in senile plaques.

11 es (microglia) that accumulate in and around senile plaques.

12 ggregates in the extracellular space to form senile plaques.

13 ocalization with neurofibrillary tangles and senile plaques.

14 ed most strikingly as the amyloid fibrils of senile plaques.

15 zheimer disease: neurofibrillary tangles and senile plaques.

16 s was seen for total senile plaques or cored senile plaques.

17 and formation of neurofibrillary tangles and senile plaques.

18 gical hallmarks of Alzheimer's disease (AD): senile plaques.

19 nt properties of beta-amyloid present in the senile plaques.

20 and microglial cells surrounding individual senile plaques.

21 otion, deposition, and/or persistence of the senile plaques.

22 clusters of reactive microglia that surround senile plaques.

23 -immunoreactive neurites are also present in senile plaques.

24 f the scavenger receptor in association with senile plaques.

25 beta) peptides accumulate extracellularly in senile plaques.

26 ranscription factor that is activated around senile plaques.

27 y disrupted in the cortex, specifically near senile plaques.

28 nd have been found colocalized with Abeta in senile plaques.

29 e presynapses engulf amyloid-beta-containing senile plaques.

30 tease thrombin is neurotoxic and found in AD senile plaques.

31 o generate the beta-amyloid (Abeta) found in senile plaques.

32 oid-beta (Abeta), the principal component of senile plaques.

33 apy on morphological changes associated with senile plaques.

34 enchyma and its subsequent accumulation into senile plaques.

35 ed against the Abeta peptide, a component of senile plaques.

36 than the Abeta(1-42) peptide which forms AD senile plaques.

37 phological abnormalities precede and lead to senile plaques.

38 ptide (A beta) is the primary constituent of senile plaques, a defining feature of Alzheimer's diseas

39 eptide (Abeta) is the primary constituent of senile plaques, a defining feature of Alzheimer's diseas

40 a-amyloid peptide (Abeta) deposition to form senile plaques, a hallmark of AD.

41 Amyloid-beta peptide (Abeta) accumulation in senile plaques, a pathological hallmark of Alzheimer's d

42 te and provides new insight into how and why senile plaques accumulate copper in vivo.

43 Senile plaques accumulate over the course of decades in

44 gical effect were present, we also looked at senile plaque and neurofibrillary tangle densities in th

45 d beta-protein, the principal constituent of senile plaques and a cytotoxic fragment involved in the

46 position of amyloid-beta (Abeta) peptides in senile plaques and accumulation of hyperphosphorylated t

47 Abeta depositions in brain parenchyma as senile plaques and along cerebrovasculature as cerebral

48 sor protein, resulting in the development of senile plaques and Alzheimer's disease.

49 use models, caffeine significantly decreases senile plaques and amyloid beta (Abeta) levels while als

50 ression found in microglia accumulating near senile plaques and apposing CB(1) cannabinoid receptor-p

51 rodents, and because NHPs naturally develop senile plaques and CAA with age, NHPs appear to be impor

52 main constituent of amyloid fibrils found in senile plaques and cerebral vessels in Alzheimer's disea

53 ide (A beta), the major protein component in senile plaques and cerebrovascular amyloidosis in the br

54 sive accumulation of beta-amyloid (Abeta) in senile plaques and in the cerebral vasculature is the ha

55 sive accumulation of beta-amyloid (Abeta) in senile plaques and in the cerebral vasculature is the ha

56 of fibrillar amyloid-beta protein (Abeta) in senile plaques and in the walls of cerebral blood vessel

57 tracellular amyloid-beta (Abeta), evident as senile plaques and intracellular neurofibrillary tangles

58 a are found to be intimately associated with senile plaques and may play a central role in mediating

59 ere only senile plaques, but there were both senile plaques and neurofibrillary tangles in 9%.

60 aggregates that are associated with amyloid senile plaques and neurofibrillary tangles in AD brains.

61 acterized pathologically by the abundance of senile plaques and neurofibrillary tangles in the brain.

62 d larger brain infarcts were identified, and senile plaques and neurofibrillary tangles in the neocor

63 mbrane attachment, and (or) association with senile plaques and neurofibrillary tangles is a major fe

64 Neuritic senile plaques and neurofibrillary tangles were identifi

65 f neocortical Alzheimer disease lesions (ie, senile plaques and neurofibrillary tangles) as assessed

66 id and tau proteins, which aggregate to form senile plaques and neurofibrillary tangles, respectively

67 Senile plaques and neurofibrillary tangles, the two hall

68 peptides) and Tau are the main components of senile plaques and neurofibrillary tangles, the two hist

69 nd the lesions that characterize the disease-senile plaques and neurofibrillary tangles-ramify system

70 hat redox-active iron is associated with the senile plaques and neurofibrillary tangles-the pathologi

71 re amyloid angiopathy but only rare neuritic senile plaques and neurofibrillary tangles.

72 , including loss of neurons and formation of senile plaques and neurofibrillary tangles.

73 e disorder characterized by the formation of senile plaques and neurofibrillary tangles.

74 with the classic neuropathologic markers of senile plaques and neurofibrillary tangles.

75 isease is characterized by the deposition of senile plaques and progressive dementia.

76 Participants with abundant senile plaques and some neurofibrillary tangles in the n

77 Amyloid senile plaques and tau neurofibrillary tangles are neuro

78 Amyloid senile plaques and tau neurofibrillary tangles are neuro

79 cterized by the presence of amyloid-positive senile plaques and tau-positive neurofibrillary tangles.

80 11-40/42 is generated prior to deposition in senile plaques and that N-terminally truncated Abeta pep

81 abundant deposition of ss-amyloid (Ass) 1-42 senile plaques and the formation of neurofibrillary tang

82 ary tangles and neuronal loss, the number of senile plaques and the percentage of the superior tempor

83 BCHE has been found in senile plaques and this new association of genetic varia

84 e had developed profuse Abeta-immunoreactive senile plaques and vascular deposits, some of which were

85 imer's disease and other tauopathies include senile plaques and/or neurofibrillary tangles.

86 brain Abeta deposits, preferentially mature senile plaques, and amyloid angiopathy.

87 densities of neurofibrillary tangles, total senile plaques, and cored senile plaques in subjects wit

88 ease (AD), we counted the number of neurons, senile plaques, and neurofibrillary tangles in a high-or

89 s of Alzheimer's disease as amyloid protein, senile plaques, and neurofibrillary tangles.

90 ns of beta-amyloid, a major component of the senile plaques, and of the excitatory amino acid glutama

91 se exhibit either neurofibrillary tangles or senile plaques, and only a few display both.

92 Extracellular senile plaques are a central pathological feature of Alz

93 Senile plaques are a characteristic histopathological fe

94 These data show that senile plaques are a potential reservoir of oligomeric A

95 Senile plaques are a prominent pathological feature of A

96 The fibrils in senile plaques are composed of 40- and 42-residue amyloi

97 in, large dystrophic neurites in a subset of senile plaques are conspicuously labeled with APLP1 and

98 Senile plaques are extracellular deposits of fibrillar b

99 Senile plaques are foci of local inflammatory processes,

100 We find that senile plaques are surrounded by a halo of oligomeric Ab

101 ric forms of Abeta-42 rather than fibrils or senile plaques are the key pathological substrates.

102 on, growth, and maturation of brain amyloid "senile" plaques are essential pathological processes in

103 zheimer lesions--neurofibrillary tangles and senile plaques--are present in aged chimpanzees.

104 indicate that HGF/SF may be increased within senile plaques as a function of the gliosis and microgli

105 ity was present in the neuritic component of senile plaques as well as in neurofibrillary tangles.

106 show widespread neurofibrillary tangles and senile plaques as well as Lewy body formation and nigral

107 e (A beta), the primary protein component in senile plaques associated with Alzheimer's disease (AD),

108 protein (AbetaP) is the major constituent of senile plaques associated with Alzheimer's disease (AD).

109 (Abeta) is the primary protein component of senile plaques associated with Alzheimer's disease and h

110 Senile plaques associated with Alzheimer's disease conta

111 osis had a greater neurofibrillary tangle or senile plaque burden than subjects with Alzheimer diseas

112 isease, Abeta fibrils constitute the core of senile plaques, but Abeta protofibrils may represent the

113 ected symmetrically; in 72%, there were only senile plaques, but there were both senile plaques and n

114 ocannabinoid signalling, particularly around senile plaques, can exacerbate synaptic failure in Alzhe

115 ta-amyloid (Abeta), which accumulates in the senile plaques characteristic for Alzheimer's disease.

116 ides (Abeta) are the major components of the senile plaques characteristic of Alzheimer's disease.

117 The accumulation of senile plaques composed of amyloid beta (Abeta) fibrils

118 The presence of senile plaques composed of amyloid-beta (Abeta) polypept

119 Alzheimer's disease is characterized by senile plaques composed of polymeric fibrils of beta amy

120 Senile plaques composed of the peptide Abeta contribute

121 Extracellular senile plaques composed predominantly of fibrillar amylo

122 Alzheimer's patients contains extracellular senile plaques composed primarily of deposits of fibrill

123 gical hallmark of Alzheimer's disease is the senile plaque, composed of beta-amyloid fibrils, microgl

124 The latter include senile plaques, composed mainly of an amyloid (Abeta) co

125 Senile plaques comprised of Abeta peptides are a hallmar

126 tures of Alzheimer's disease (AD) brains are senile plaques, comprising beta-amyloid (Abeta) peptides

127 lzheimer's disease (AD) is the deposition of senile plaques consisting largely of a peptide known as

128 n-negative neurites that are associated with senile plaques containing amyloid beta peptides of the 1

129 glia are immune system cells associated with senile plaques containing beta-amyloid (Abeta) in Alzhei

130 gical hallmark of Alzheimer's disease is the senile plaque, containing beta-amyloid fibrils, microgli

131 to modified species of the peptide found in senile plaque cores.

132 Abeta42, a major component of senile plaques, decreases SIRT6 expression, and Abeta42-

133 ied Abeta-42 (AN-1792) has demonstrated that senile plaque disruption occurred in immunized humans as

134 Although senile plaques focally disrupt neuronal health, the func

135 ufficient neurofibrillary tangles (NFTs) and senile plaques for the neuropathological diagnosis of AD

136 duction are predicted to result in decreased senile plaque formation, a proposed contributor to neuro

137 of AEP from 5XFAD or APP/PS1 mice decreases senile plaque formation, ameliorates synapse loss, eleva

138 Abeta aggregation and toxicity, and inhibits senile plaque formation.

139 Senile plaques formed by beta-amyloid peptides (Abeta) a

140 oid (Abeta), which is the major component of senile plaques found in AD.

141 a), one of the primary protein components of senile plaques found in Alzheimer disease, is believed t

142 id-beta (Abeta) the primary component of the senile plaques found in Alzheimer's disease (AD) is gene

143 (A beta) is the primary protein component of senile plaques found in Alzheimer's disease.

144 Senile plaques found in the Alzheimer's disease brain ar

145 release amyloid beta, the main component in senile plaques found in the brains of patients with Alzh

146 t here a comprehensive proteomic analysis of senile plaques from postmortem AD brain tissues.

147 a), the major component of Alzheimer disease senile plaques, from a human neuronal cell line.

148 ly high Cu(2+) ion concentrations present in senile plaques has provoked a substantial interest in th

149 ncipal constituent of the amyloid fibrils in senile plaques, has been documented.

150 beta), which are the primary constituents of senile plaques, have been shown to activate tyrosine kin

151 Together, these data demonstrate that senile plaques impair neuritic calcium homeostasis in vi

152 at higher levels than the 42-mer (Abeta42), senile plaque in diseased brains is composed primarily o

153 apoptosis, and Abeta is the key component of senile plaques in AD brain.

154 roduct of APP proteolysis and a component of senile plaques in AD, were detected in RGCs by immunohis

155 provide insights into the pathophysiology of senile plaques in AD.

156 peptide (Abeta) is the amyloid component of senile plaques in Alzheimer disease (AD) brains.

157 o acid peptide that is the main component of senile plaques in Alzheimer Disease (AD).

158 eurons; it co-localizes with amyloid beta in senile plaques in Alzheimer disease brains.

159 d-beta peptide (Abeta), which accumulates in senile plaques in Alzheimer disease.

160 he three-dimensional structure of individual senile plaques in Alzheimer disease.

161 ave differential effects on the formation of senile plaques in Alzheimer's brains and that RTN3 has a

162 Senile plaques in Alzheimer's disease (AD) are composed

163 Accumulation of amyloid-beta (Abeta) into senile plaques in Alzheimer's disease (AD) is a hallmark

164 Abeta is the primary component of senile plaques in Alzheimer's disease (AD), and its mech

165 d that amyloid Abeta, the major component of senile plaques in Alzheimer's disease (AD), binds Cu wit

166 Amyloid-beta (Abeta), major constituent of senile plaques in Alzheimer's disease (AD), is generated

167 e generation of Abeta, the main component of senile plaques in Alzheimer's disease (AD), is precluded

168 HspB1, an sHsp commonly associated with senile plaques in Alzheimer's disease (AD), prevents the

169 eta peptide deposits, the major component of senile plaques in Alzheimer's disease (AD), was mapped i

170 eta fragments implicated in the formation of senile plaques in Alzheimer's disease (AD).

171 beta peptide (Abeta), the major component of senile plaques in Alzheimer's disease (AD).

172 (Abeta) is the primary protein component of senile plaques in Alzheimer's disease and is believed to

173 (A beta) is the primary protein component of senile plaques in Alzheimer's disease and is believed to

174 -protein (A beta) is the main constituent of senile plaques in Alzheimer's disease and is derived by

175 subjects and found that synapse loss around senile plaques in Alzheimer's disease correlates with th

176 The major constituent of senile plaques in Alzheimer's disease is a 42-aa peptide

177 Amyloid-beta, the major constituent of senile plaques in Alzheimer's disease, is derived from t

178 Amyloid-beta, the primary constituent of senile plaques in Alzheimer's disease, is hypothesized t

179 al membranes, but is abnormally localized to senile plaques in Alzheimer's disease.

180 beta-amyloid (Abeta), the major component of senile plaques in Alzheimer's disease.

181 loid peptide (Abeta), a major constituent of senile plaques in Alzheimer's disease.

182 ce of beta-amyloid, which forms the cores of senile plaques in Alzheimer's Disease.

183 oid-beta protein (Abeta) deposits similar to senile plaques in Alzheimer's disease.

184 eptides, the core components of the cerebral senile plaques in Alzheimer's disease.

185 1-42) peptide, which is a major component of senile plaques in Alzheimer's, can directly induce incre

186 of MMP2 expression in astrocytes surrounding senile plaques in APP/PS1 transgenic mice brains.

187 noreactivity in astroglial cells surrounding senile plaques in brain tissue sections from authentic A

188 gh levels by inflammatory cells infiltrating senile plaques in brain tissues from AD patients.

189 yloid (Abeta) peptides that are deposited in senile plaques in brains of aged individuals and patient

190 s (NFTs) were counted in four brain regions, senile plaques in five and LBs in four.

191 ss glutamate and occur in close proximity to senile plaques in human Alzheimer's disease (AD) brain.

192 42 is the major Abeta species in parenchymal senile plaques in most Alzheimer's diseased brains in sp

193 d monoacylglycerol lipase, begin to surround senile plaques in probable Alzheimer's disease (Braak st

194 ary tangles, total senile plaques, and cored senile plaques in subjects with psychosis vs subjects wi

195 disease, the formation of Abeta fibrils and senile plaques in the brain initiates a cascade of event

196 eposition of amyloid beta peptide (Abeta) as senile plaques in the brain is the pathological hallmark

197 tomography have provided measures of amyloid senile plaques in the brain of demented patients and pat

198 Amyloid beta protein (AbetaP) forms senile plaques in the brain of the patients with Alzheim

199 se (AD) is characterized by large numbers of senile plaques in the brain that consist of fibrillar ag

200 ition of the beta-amyloid (Abeta) peptide in senile plaques in the brain, leading to neuronal dysfunc

201 of fibrillar amyloid deposits in the form of senile plaques in the brain.

202 position of beta-amyloid (Abeta) peptides as senile plaques in the brain.

203 age-related increase in diffuse and compact senile plaques in the brain.

204 sition of amyloid beta (Abeta) peptides into senile plaques in the brain.

205 ase (AD) is the presence of large numbers of senile plaques in the brain.

206 mulation of beta-amyloid peptides (Abeta) in senile plaques in the brains of affected patients.

207 beta-Amyloid peptide accumulation in senile plaques in the brains of patients with Alzheimer'

208 ides (Abeta40 and 42) that aggregate to form senile plaques in the brains of patients with Alzheimer'

209 Senile plaques in the cerebral parenchyma are a pathogno

210 Amyloid beta protein (A beta P) forms senile plaques in the cerebrocortical blood vessels and

211 position of amyloid-beta (Abeta) peptides in senile plaques in the hippocampus and cerebral cortex.

212 ing agents for targeting Abeta aggregates in senile plaques in the living human brain.

213 005) cortices, and also with lower counts of senile plaques in the motor cortex (p=0.001).

214 Abeta and Abeta(x-42/43) but not Abeta(x-40) senile plaques in the superior temporal sulcus when comp

215 er scanning imaging of thioflavine S-stained senile plaques in the Tg2576 transgenic mouse model of A

216 a-amyloid before extracellular beta-amyloid (senile plaques) in Down syndrome.

217 ining in the amyloid deposits of dense-core (senile) plaques, in the amyloid angiopathy surrounding d

218 beta-amyloid (Abeta), the main component of senile plaques, induced a significant decrease in dynami

219 beta-amyloid (Abeta), the main component of senile plaques, induced a significant decrease in dynami

220 beta-amyloid (Abeta), the main component of senile plaques, induces abnormal posttranslational proce

221 er disease-affected brains mainly consist of senile plaques, inflammation stigmata, and oxidative str

222 Amyloid-beta peptide (Abeta) aggregate in senile plaque is a key characteristic of Alzheimer's dis

223 ion of inflammatory microglia in Alzheimer's senile plaques is a hallmark of the innate response to b

224 beta (Abeta) peptide deposition as fibrillar senile plaques is a key element in the pathology of Alzh

225 e main component of Alzheimer's disease (AD) senile plaques is amyloid-beta peptide (Abeta), a proteo

226 rogression from oligomers to fibrils forming senile plaques is currently considered a protective mech

227 which is implicated in AD by its presence in senile plaques, its transport of Abeta across the blood-

228 Senile plaques labeled with thioflavin-S were procured b

229 s for the burden of neurofibrillary tangles, senile plaques, Lewy bodies (LBs), and Lewy neurites (LN

230 beta-amyloid (Abeta) accumulation, including senile plaque-like structures in the hippocampus and tem

231 Senile plaque load was quantitated in the hippocampus an

232 At 15 and 19 months of age, senile plaque load was significantly greater in females

233 ized by two histopathological hallmarks: the senile plaques made of amyloid-beta (Abeta) peptide fibr

234 post mortem by the presence of extracellular senile plaques, made primarily of aggregation of amyloid

235 Most demented dogs displayed senile plaques, mainly in the frontal and temporal corte

236 upport the hypothesis that components of the senile plaques may inhibit neurite outgrowth.

237 lesions, including neurofibrillary tangles, senile plaque neurites and neuropil threads.

238 racterized by a build-up of Abeta peptide as senile plaques, neurodegeneration, and memory loss.

239 pathways may be the key to understanding how senile plaques, neurofibrillary tangles and apoptosis ar

240 oid-beta (Ass) peptide forming extracellular senile plaques, neurofibrillary tangles made of hyperpho

241 characterized by regional concentrations of senile plaques, neurofibrillary tangles, and extensive n

242 Besides senile plaques, neurofibrillary tangles, and neuronal lo

243 e neurodegenerative disease characterized by senile plaques, neurofibrillary tangles, dystrophic neur

244 he Abeta peptide, a major constituent of the senile plaques observed in Alzheimer's disease.

245 The major peptide component of senile plaques of AD, beta-amyloid (Abeta), stimulates t

246 als, two important biomarkers present in the senile plaques of Alzheimer's disease (AD) brain, has be

247 eta) peptides at a high concentration in the senile plaques of Alzheimer's disease (AD) patients and

248 have demonstrated the presence of CRP in the senile plaques of Alzheimer's disease (AD).

249 The senile plaques of Alzheimer's disease are foci of local

250 Cu(2+) ions are found concentrated within senile plaques of Alzheimer's disease patients directly

251 production of amyloid beta peptide found in senile plaques of Alzheimer's disease patients.

252 In fully developed senile plaques of Alzheimer's disease, however, it is th

253 ase (AD) is characterized by the presence of senile plaques of amyloid-beta (Abeta) peptides derived

254 ane attack complex (MAC) are co-localized in senile plaques of brains from Alzheimer's disease (AD) p

255 of Abeta as the principal component of brain senile plaques of individuals with AD.

256 ince Abeta is found as insoluble deposits in senile plaques of the AD brain, and the Abeta peptide ca

257 In the present study, the effect of senile plaques on neurite outgrowth was studied by cultu

258 However, the effect of senile plaques on neuronal morphology and function is di

259 (Abeta) peptides are the major components of senile plaques, one of the main pathological hallmarks o

260 erlapping 40%-50% reduction in the number of senile plaques, one of the pathological hallmarks of AD.

261 Amyloid (senile) plaques, one of the two pathologic hallmarks of

262 lationship with psychosis was seen for total senile plaques or cored senile plaques.

263 er AMY plaques are non-amyloid precursors to senile plaques or if they represent an independent type

264 one to the development of AD or to increased senile plaques or neurofibrillary tangle formation in th

265 The degree of senile plaques or neurofibrillary tangles was not differ

266 his is caused by fibrillar deposits known as senile plaques or soluble oligomeric forms of amyloid be

267 Given the elevated concentration of Cu in senile plaques, our results suggest that Cu interactions

268 The extracellular senile plaques prevalent in brain tissue in Alzheimer's

269 The core of the senile plaque primarily is composed of the 39-43 amino a

270 logical hallmark of Alzheimer disease is the senile plaque principally composed of tightly aggregated

271 umulation of beta-amyloid (Abeta) peptide as senile plaques, progressive neurodegeneration, and memor

272 at some have speculated may be precursors to senile plaques remains to be determined, as is the relat

273 n (A beta), the principal constituent of the senile plaques seen in Alzheimer's disease (AD), is deri

274 sing amyloid precursor protein (APP) develop senile plaques similar to those found in Alzheimer's dis

275 Remarkably, spectra obtained for senile plaque (SP) cores isolated from AD brain are esse

276 (AD) include therapies designed to decrease senile plaque (SP) formation and/or promote clearance of

277 oteinase inhibitor found in association with senile plaques (SP) in Alzheimer's disease (AD).

278 Abeta peptide is the major component of senile plaques (SP), which accumulate in the brain of a

279 Senile plaques (SPs) and neurofibrillary tangles (NFTs)

280 e (AD) is characterized by the deposition of senile plaques (SPs) and neurofibrillary tangles (NFTs)

281 estration of RNA in Alzheimer's disease (AD) senile plaques (SPs) and the production of intraneuronal

282 sition of neurofibrillary tangles (NFTs) and senile plaques (SPs) has been characterized extensively

283 A beta deposition in the form of senile plaques (SPs) has recently been described in pati

284 paratus, neurofibrillary tangles (NFTs), and senile plaques (SPs) in the hippocampus of six cases of

285 position of amyloid-beta peptides (Abeta) in senile plaques (SPs) is a central pathological feature o

286 he pathogenesis of Alzheimer's disease (AD), senile plaques (SPs), and neurofibrillary tangles (NFTs)

287 l lobar degeneration, including beta-amyloid senile plaques, tau neurofibrillary tangles, and fused i

288 (AD), and the deposition of Abeta within the senile plaques that are a hallmark of AD is thought to b

289 rks is the accumulation of the extracellular senile plaques that are mainly composed of amyloid beta

290 PECT imaging agents for the detection of the senile plaques, the development of bi-functional molecul

291 6) are associated with senile plaques, the fibrillar, beta-sheet assemblies of

292 beta) aggregates are the main constituent of senile plaques, the histological hallmark of Alzheimer's

293 Although microglia are an integral part of senile plaques, their role in the development of Alzheim

294 eposition of the same peptide in the form of senile plaques, there is considerable interest in the re

295 f fibrillar amyloid beta proteins (Abeta) in senile plaques throughout the cerebral cortex are consis

296 l hallmark of AD is the presence of numerous senile plaques throughout the hippocampus and cerebral c

297 Alzheimer disease (AD) is characterized by senile plaques, which are mainly composed of beta amyloi

298 rains shows the presence of large numbers of senile plaques, whose major component is the beta-amyloi

299 Treatment of the senile plaques with the chelator ethylenediaminetetraace

300 a protofibrils accumulate at the exterior of senile plaques, yet the protofibril-fibril interplay is