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

24 and intraocular lens (IOL) implantation for senile cataracts.

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 nson's disease (PD), vascular dementia (VD), senile dementia (SD), mild cognitive impairment (MCI), a

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

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

31 TD) is the second most prevalent form of pre-senile dementia after Alzheimer's disease.

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

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

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

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

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

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

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

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

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

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

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

43 FTD, the second most common form of pre-senile dementia, can also be caused by genetic mutations

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

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

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

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

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

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

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

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

52 clinical indices and progression measures in senile dementias.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 Senile plaque load was quantitated in the hippocampus an

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

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

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

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

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

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

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

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

76 Senile plaques accumulate over the course of decades in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 Senile plaques and neurofibrillary tangles, the two hall

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

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

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

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

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

98 Amyloid senile plaques and tau neurofibrillary tangles are neuro

99 Amyloid senile plaques and tau neurofibrillary tangles are neuro

100 11-40/42 is generated prior to deposition in senile plaques and that N-terminally truncated Abeta pep

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

118 Senile plaques comprised of Abeta peptides are a hallmar

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

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

121 Although senile plaques focally disrupt neuronal health, the func

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

159 42 is the major Abeta species in parenchymal senile plaques in most Alzheimer's diseased brains in sp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 Senile plaques in the cerebral parenchyma are a pathogno

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

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

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

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

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

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

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

182 Senile plaques labeled with thioflavin-S were procured b

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

199 Treatment of the senile plaques with the chelator ethylenediaminetetraace

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

224 Besides senile plaques, neurofibrillary tangles, and neuronal lo

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

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

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

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

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

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

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

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

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

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

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

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

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

238 beta) peptides accumulate extracellularly in senile plaques.

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

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

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

242 apy on morphological changes associated with senile plaques.

243 enchyma and its subsequent accumulation into senile plaques.

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

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

246 phological abnormalities precede and lead to senile plaques.

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

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

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

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

251 o generate the beta-amyloid (Abeta) found 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 gical hallmarks of Alzheimer's disease (AD): senile plaques.

261 ranscription factor that is activated around senile plaques.

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

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

264 IDUA possibly via the clearance pathway for senile platelets.

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

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

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

268 Senile reticular pigmentary change was the predominant p

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

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

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

272 ment (n = 60), myopic glaucoma (n = 38), and senile sclerotic (n = 50).

273 After adjusting for confounders, senile sclerotic discs had the lowest cpCD (37.1% [95% c

274 ealthy and glaucomatous eyes were highest in senile sclerotic eyes (0.928) and lowest in generalized

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

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

277 Senile systemic amyloidosis (SSA) is one such pathology

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

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

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

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

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

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

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

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

286 have another common age-related comorbidity, senile systemic amyloidosis, a nongenetic disease associ

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.