ライフサイエンスコーパス: senile

1 group I intron in the sea anemone Metridium senile.

2 ated from the venom of sea anemone Metridium senile.

3 The senile and neuritic plaque neuropathology of Alzheimer's

4 a peptide (Abeta) are the major component of senile and vascular plaques found in the brains of Alzhe

5 ith significantly decreased B lymphocytes in senile APPswe, PS1M146V and TauP301L transgenic mice.

6 l density reduction, pulmonary emphysema and senile atrophy of skin.

7 Advancement of the levator aponeurosis for senile blepharoptosis may be preformed via a minimally i

8 diagnosis often coincided with diagnoses of senile cataract and glaucoma and tested the associations

9 Sixty eyes of 52 patients with age-related senile cataract and regular corneal astigmatism ranging

10 a patient with uveitis is more complex than senile cataract extraction, because it involves multiple

11 dence linking cigarette smoking with risk of senile cataract is well-established, it is unclear wheth

12 rence in nocturnal urine aMTS6 level between senile cataract patients and controls was not statistica

13 4.43 ng aMTS6/mg creatinine (mean +/- SD) in senile cataract patients; this was 76% of the level meas

14 rcent confidence interval, 73.3 to 84.2) for senile cataract to 10.5 percent of recommended care (95

15 Standardized incidence ratios (SIRs) for senile cataract was significantly increased to 1.80 afte

16 ing (PPV group) and 15 consecutive eyes with senile cataract with a healthy macula (control group) we

17 go many modifications, some of which lead to senile cataract.

18 lation included 150 eyes of 86 patients with senile cataract.

19 4 +/- 7 years; 12 males and 10 females) with senile cataracts and 22 healthy controls (aged 61 +/- 8

20 Senile cataracts are associated with oxidation, fragment

21 Senile cataracts are associated with progressive oxidati

22 hanism for lens aging and the development of senile cataracts in humans.

23 scent of processes thought to occur in human senile cataracts in which normal proteins become altered

24 Fifty (2.4%) of 12,004 senile cataracts operated at Pravara Rural Hospital, Lon

25 irculatory melatonin level and the extent of senile cataracts.

26 not differ between subjects with and without senile cataracts.

27 s that lacked phagocytic macrophages such as senile change of the Alzheimer's type.

28 ain disease (AGD; n = 5), tangle-predominant senile dementia (TPSD; n = 5), Pick disease (n = 4), fam

29 imer's disease (AD), the most common type of senile dementia affecting the elderly.

30 d with an increased risk of subsequent AD or senile dementia development.

31 jects, 1589 (5.3%) were diagnosed with AD or senile dementia during a mean follow-up period of 4.4 ye

32 to calculate the hazard ratios (HR) of AD or senile dementia for the 2 cohorts after adjusting for pr

33 nt in cognitive performance in patients with senile dementia of Alzheimer type.

34 Alzheimer's disease/senile dementia of the Alzheimer type (AD/SDAT) is the m

35 ciated with familial and sporadic late-onset senile dementia of the Alzheimer's type.

36 l Adult Children Study and Healthy Aging and Senile Dementia Study at the Knight Alzheimer Disease Re

37 alysis showed that the adjusted HR for AD or senile dementia was 1.35 (95% CI, 0.89-2.06) for exudati

38 The incidence of AD or senile dementia was higher in patients with AMD than in

39 rden on society, and is the leading cause of senile dementia worldwide.

40 rative disorder that is the leading cause of senile dementia, afflicting millions of individuals worl

41 imer's disease (AD), the most common type of senile dementia, is associated to the build-up of misfol

42 Alzheimer disease (AD), the most common senile dementia, is characterized by amyloid plaques, va

43 the subsequent development of dementia (eg, senile dementia, vascular dementia, frontotemporal demen

44 Alzheimer's disease/senile dementia-free survival analysis was assessed usin

45 her reported neuritic plaques in 12 cases of senile dementia.

46 Alzheimer's disease, Parkinson's disease, or senile dementia.

47 Synaptic dysfunction occurs early in senile dementias, presumably as a result of decreased le

48 mer's Disease (AD) is the most common of the senile dementias, the prevalence of which is increasing

49 clinical indices and progression measures in senile dementias.

50 neration to be useful targets for therapy of senile dementias.-Goetzl, E.

51 Senile graying of human hair has been the subject of int

52 usive of the hair shaft, as a key element in senile hair graying, which does not exclusively affect f

53 Interestingly, recombinant M. senile MsrB bound iron, and further analyses suggested t

54 uid (CSF) levels of proteins associated with senile (neuritic) plaques and neurofibrillary tangles.

55 n regions reported to have high densities of senile (neuritic) plaques with activated microglia.

56 amyloid beta-peptide (Abeta) in the form of senile (or amyloid) plaques is one of the main character

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

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

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

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

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

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

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

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

65 Senile plaque load was quantitated in the hippocampus an

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

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

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

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

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

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

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

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

74 Senile plaques accumulate over the course of decades in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 Senile plaques and neurofibrillary tangles, the two hall

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

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

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

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

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

96 Amyloid senile plaques and tau neurofibrillary tangles are neuro

97 Amyloid senile plaques and tau neurofibrillary tangles are neuro

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

99 11-40/42 is generated prior to deposition in senile plaques and that N-terminally truncated Abeta pep

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

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

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

103 Extracellular senile plaques are a central pathological feature of Alz

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

105 Senile plaques are a prominent pathological feature of A

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

107 Senile plaques are extracellular deposits of fibrillar b

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

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

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

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

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

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

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

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

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

117 Extracellular senile plaques composed predominantly of fibrillar amylo

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

119 Senile plaques comprised of Abeta peptides are a hallmar

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

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

122 Although senile plaques focally disrupt neuronal health, the func

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 1-42) peptide, which is a major component of senile plaques in Alzheimer's, can directly induce incre

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

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

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

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

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

161 42 is the major Abeta species in parenchymal senile plaques in most Alzheimer's diseased brains in sp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 Senile plaques in the cerebral parenchyma are a pathogno

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

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

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

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

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

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

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

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

185 Senile plaques labeled with thioflavin-S were procured b

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

202 Treatment of the senile plaques with the chelator ethylenediaminetetraace

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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, induced a significant decrease in dynami

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

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

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

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

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

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

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

228 Besides senile plaques, neurofibrillary tangles, and neuronal lo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

243 apy on morphological changes associated with senile plaques.

244 enchyma and its subsequent accumulation into senile plaques.

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

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

247 phological abnormalities precede and lead to senile plaques.

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

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

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

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

252 kill neurons and eventually form deposits of senile plaques.

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

254 ated to contribute to amyloid depositions in senile plaques.

255 are observed associated with the majority of senile plaques.

256 aggregates into the fibrils that deposit in senile plaques.

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

258 ggregates in the extracellular space to form senile plaques.

259 ocalization with neurofibrillary tangles and senile plaques.

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

261 zheimer disease: neurofibrillary tangles and senile plaques.

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

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

264 ranscription factor that is activated around senile plaques.

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

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

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

268 IDUA possibly via the clearance pathway for senile platelets.

269 nd do not preclude their administration to a senile population, these drugs have potential for the tr

270 ne ameliorates pathological effects in these senile PS1/APP mice.

271 ic the symptoms of common disorders, such as senile purpura, and have subtle histologic findings.

272 Senile reticular pigmentary change was the predominant p

273 rpigmentary changes, reticular pseudodrusen, senile reticular pigmentary changes, cobblestone degener

274 ous retinal detachment, typical degenerative senile retinoschisis, peripheral laser coagulation scars

275 fold, retinal hole, and typical degenerative senile retinoschisis.

276 The terms giant fornix syndrome, senile sunken upper lids, and prostaglandin-associated p

277 ibute to neuronal dysfunctions that underlie senile symptoms and Alzheimer's disease.

278 Senile systemic amyloidosis (SSA) is one such pathology

279 Senile systemic amyloidosis (SSA), however, cannot be ex

280 ases of familial TTR-related amyloidosis and senile systemic amyloidosis (SSA), TTR is deposited as a

281 gical basis of heart dysfunction in sporadic senile systemic amyloidosis and familial amyloid cardiom

282 lyses have been described for transthyretin (senile systemic amyloidosis and familial amyloid polyneu

283 y into amyloid fibrils that putatively cause senile systemic amyloidosis and familial amyloid polyneu

284 nsthyretin causes the human amyloid diseases senile systemic amyloidosis or familial amyloid polyneur

285 have the potential to modulate the course of senile systemic amyloidosis or familial amyloid polyneur

286 type (wt) TTR amyloid deposits are linked to senile systemic amyloidosis, a common disease of aging,

287 type transthyretin (TTR) is responsible for senile systemic amyloidosis, and more than 100 mutations

288 ures associated with three amyloid diseases: senile systemic amyloidosis, familial amyloid polyneurop

289 normal quaternary structures associated with senile systemic amyloidosis, familial amyloid polyneurop

290 n and deposition of wild-type transthyretin (senile systemic amyloidosis, SSA) or monoclonal immunogl

291 s found in amyloid deposits of patients with senile systemic amyloidosis.

292 ild-type TTR, a condition that characterizes senile systemic amyloidosis.

293 TR in individuals older than age 65 y causes senile systemic amyloidosis.

294 les show cardiac deposition resembling human senile systemic amyloidosis.

295 obulin light chains, and the hereditary and "senile systemic" (ATTR) variants from mutant and wild-ty

296 ations of CLU were measured in familial TTR, senile systemic, and Ig light chain amyloidosis patient

297 in tissues from patients with familial TTR, senile systemic, and Ig light chain amyloidosis.

298 xide reductase (MsrB) homolog from Metridium senile that has four in-frame UGA codons and two nearly

299 ght chain amyloidosis without typical signs, senile transthyretin, or hereditary amyloidosis with a c

300 to have probably been cases of indeterminate senile tremor or dystonic tremor.