ライフサイエンスコーパス: CAA

1 CAA deposition leads to several clinical complications,

2 CAA is associated with a high prevalence of magnetic res

3 CAA pathology is very common in older community-dwelling

4 CAA patients were younger than HE and AD subjects (68 +/

5 CAA subjects demonstrated reduced response amplitude (pe

6 CAA was significantly associated with lobar ICH, both ov

7 CAA was very common (84.9%; 94 had no-to-minimal, 233 mi

8 ation in the cerebrospinal fluid (CSF) of 10 CAA-ri, 8 CAA, 14 multiple sclerosis, and 25 control sub

9 A total of 2340 CAA papers were published between 1954 and 2014.

10 human cDNA fragment of the TBP gene with 64 CAA/CAG repeats (TBPQ64).

11 he cerebrospinal fluid (CSF) of 10 CAA-ri, 8 CAA, 14 multiple sclerosis, and 25 control subjects.

12 were included, 44 had an LCRA, and 22 had a CAA.

13 of a specific gene subset enriched for AAA, CAA, and GAA codons is impaired in the absence of URM1-

14 bromoacetic acid (BAA) >> chloroacetic acid (CAA); this rank order was observed with other toxicologi

15 lved in homeostasis of cationic amino acids (CAAs).

16 s among CPH cellular antioxidant activities (CAA), except for the high CAA of the 120 min hydrolysate

17 imulus by the cellular antioxidant activity (CAA) assay and the hemolysis test.

18 asured by the cellular antioxidant activity (CAA) assay than bay leaf and reduced the hydrogen peroxi

19 ays, like the cellular antioxidant activity (CAA) assay, are gaining importance as they provide a bio

20 BTS, ORAC and cellular antioxidant activity (CAA) assays.

21 one assay for cellular antioxidant activity (CAA), allowed identifying five distinctive groups of hyd

22 ancer (CRC) and colorectal advanced adenoma (CAA)] frequently develop in individuals at ages when oth

23 isolated from cancer-associated adipocytes (CAAs) and fibroblasts (CAFs) than in those from ovarian

24 Although advanced CAA is present in approximately (1/4) of brains with Alz

25 e response to visual stimulation in advanced CAA.

26 recognized as cationic antibacterial agents (CAAs), inhibit bacterial growth by interacting with the

27 colorectal (LCRA) and coloanal anastomoses (CAA) are associated with high leakage rate.

28 ratio, 2.40; 95% CI, 1.06-5.45; P = .04) and CAA presentation with symptomatic intracerebral hemorrha

29 have a selective reduction in Abeta1-40 and CAA.

30 ifying therapies for the treatment of AD and CAA.

31 involved in the pathogenesis of both AD and CAA.

32 l and imaging features of ICH due to CAA and CAA neuropathological severity are taken into account.

33 Scavenger capacity in both DPPH and CAA assays, assessed the highest antioxidant effect for

34 amyloid deposits, vascular dysfunction, and CAA-related brain injury.

35 rmation, CAA-induced vessel dysfunction, and CAA-related microhemorrhage.

36 ficant association between APOE epsilon2 and CAA.

37 ng m(-2) and 37 +/- 21.7 ng m(-2) for HB and CAA, respectively, sustaining MMHg concentrations availa

38 s (ODNs) leads to cognitive improvements and CAA reduction, without associated toxicity.

39 Patients with both KD and CAA had longer fever duration and delayed intravenous im

40 Treatment of failed LCRA and CAA is not frequently proposed.

41 olecular mechanisms that regulate plaque and CAA deposition in the vast majority of sporadic AD patie

42 play between parenchymal amyloid plaques and CAA is unclear.

43 ated Abeta deposition as amyloid plaques and CAA without affecting Abeta production.

44 is associated with more neuritic plaques and CAA, but has no independent effect on Braak NFT stage.

45 spectively 483 consecutive LARs with TME and CAA carried out in a single center between 1996 and 2005

46 atients with chemotherapy-associated anemia (CAA).

47 Coronary artery aneurysm (CAA) formation is the major complication of KD and the l

48 Abeta) plaques, cerebral amyloid angiopathy (CAA) and neurofibrillary tangles.

49 ovasculature as cerebral amyloid angiopathy (CAA) are hallmarks of AD.

50 Although cerebral amyloid angiopathy (CAA) has important clinical implications, our understand

51 Cerebral amyloid angiopathy (CAA) has never been more relevant.

52 rhage (ICH) and cerebral amyloid angiopathy (CAA) in a systematic review of published neuropathologic

53 y induces acute cerebral amyloid angiopathy (CAA) in neonatally-injected transgenic CRND8 mice.

54 Sporadic cerebral amyloid angiopathy (CAA) is a common age related cerebral small vessel disea

55 troke, advanced cerebral amyloid angiopathy (CAA) is also associated with ischemic lesions and vascul

56 Cerebral amyloid angiopathy (CAA) is associated with lobar intracerebral haemorrhage

57 Cerebral amyloid angiopathy (CAA) is characteristically associated with magnetic reso

58 Cerebral amyloid angiopathy (CAA) is characterized by deposition of amyloid beta pept

59 Cerebral amyloid angiopathy (CAA) is characterized by the deposition of amyloid beta

60 Cerebral amyloid angiopathy (CAA) is common in the ageing brain and is associated wit

61 in the field of cerebral amyloid angiopathy (CAA) over six decades, from 1954 to 2014, using advanced

62 Cerebral amyloid angiopathy (CAA) results from deposition of beta-amyloid in the medi

63 irect effect on cerebral amyloid angiopathy (CAA) severity, whereas APOEepsilon4 is associated with m

64 rteriopathy and cerebral amyloid angiopathy (CAA)) is an important cause of spontaneous intracerebral

65 scular amyloid (cerebral amyloid angiopathy (CAA), and cardiovascular risk factors increase dementia

66 postulated that cerebral amyloid angiopathy (CAA), characterised by cortical vascular amyloid deposit

67 dition known as cerebral amyloid angiopathy (CAA), is a common pathological feature of patients with

68 eries, known as cerebral amyloid angiopathy (CAA), occurs both in the setting of Alzheimer's disease

69 oid plaques and cerebral amyloid angiopathy (CAA).

70 arly markers of cerebral amyloid angiopathy (CAA).

71 associated with cerebral amyloid angiopathy (CAA).

72 ion in sporadic cerebral amyloid angiopathy (CAA).

73 lood vessels as cerebral amyloid angiopathy (CAA).

74 core AD lesion, cerebral amyloid angiopathy (CAA).

75 y recognised in cerebral amyloid angiopathy (CAA).

76 stic markers of cerebral amyloid angiopathy (CAA).

77 oid deposition (cerebral amyloid angiopathy [CAA]) but not in patients with high parenchymal amyloid

78 oid deposition (cerebral amyloid angiopathy, CAA) is associated with cerebral microbleeds, but the pr

79 , and DMHg over Canadian Arctic Archipelago (CAA) waters.

80 the view that small vessel diseases such as CAA can cause cortical atrophy even in the absence of Al

81 nown as cellular antioxidant activity assay (CAA), was implemented in different cell lines: human col

82 ased on the consensus sequence of FsrA, T/AT/CAA/GGGAA/G, which is consistent with the binding charac

83 Third, anti-ROS therapy attenuates CAA-related microhemorrhage.

84 The profile with the highest average CAA (62.41 +/- 1.48%), shown by hydrolysates obtained by

85 ort between the cell types, the Caco-2-based CAA assay appears to be a more appropriate method for th

86 However, later in life, beta-CAA-reactive T-cells expanded to supernormal levels.

87 lymph node T-cell autoimmunity to other beta-CAAs.

88 eat reduction in Th1 responses to other beta-CAAs.

89 There was no association between CAA and ICH in any location (OR 1.21, 95% CI 0.87 to 1.6

90 There is an association between CAA and lobar ICH, although the association might be str

91 While the association between CAA and lobar intracerebral haemorrhage (with its high r

92 to analyze the spatial relationship between CAA and microbleeds.

93 bleeds, but the precise relationship between CAA burden and microbleeds is undefined.

94 full-length HTT genomic sequence with 97 CAG/CAA repeats and all regulatory elements.

95 d plaques can serve as a scaffold to capture CAA mutant Abeta peptides and prevent their accumulation

96 frequently paired with the synonymous codon CAA to code for polyglutamine repeats.

97 ces binding affinity to the glutamine codons CAA and CAG and increases the rate of GTP hydrolysis by

98 s genes by precisely converting four codons (CAA, CAG, CGA, and TGG) into STOP codons without DSB for

99 tRNA(Gln1)(UUG) responds to the less common CAA codon for Gln.

100 lymorphism and histopathologically confirmed CAA.

101 17 individuals with pathologically confirmed CAA-ri and 37 control group members with pathologically

102 hort of 60 patients, (10 each) control, CRC, CAA, breast cancer, pancreatic cancer, and lung cancer.

103 sidered to be a rare neurological curiosity, CAA is now recognised as an important cause of spontaneo

104 al, 105 patients with pathologically defined CAA were included: 52 with autopsies, 22 with brain biop

105 markers in clinical-radiologically diagnosed CAA.

106 tudy used Tg-SwDI mice, which have extensive CAA.

107 bred to Tg-SwDI mice, which produce familial CAA mutant human Abeta and develop cerebral microvascula

108 ological assessment of postmortem brains for CAA severity.

109 The Boston criteria for CAA, in use in one form or another for the last 20 years

110 Reliable noninvasive diagnostic criteria for CAA-ri would allow some patients to avoid the risk of br

111 well as a look towards future directions for CAA research and clinical practice.

112 eceptor is a putative therapeutic target for CAA and related conditions.

113 of microinfarcts (P = .006) and a trend for CAA and microinfarcts (P = .052).

114 electrogenic transport that is selective for CAAs and strongly activated at low extracytosolic pH.

115 ROS are a key contributor to CAA formation, CAA-induced vessel dysfunction, and CAA-related microhem

116 cerebrovascular inflammation resulting from CAA.

117 tudies reveal that miR21 is transferred from CAAs or CAFs to the cancer cells, where it suppresses ov

118 this GC 5'ss required a high density of GAA/CAA-containing splicing enhancers in the exonized segmen

119 e prevalent in patients with KD who also had CAA.

120 ely 200 participants) of APOE and hereditary CAA or familial Alzheimer's disease.

121 ed as a mediator of the effect of hereditary CAA on cortical atrophy, accounting for 63% of the total

122 xidant activities (CAA), except for the high CAA of the 120 min hydrolysate obtained from one day ger

123 ties for a sample to exhibit ACP with higher CAA increased with each unit of positively charged amino

124 However, CAA increased when peptides-PC interaction occurred.

125 etrics methods, we systematically identified CAA-related articles from PubMed, collected metadata and

126 sonance imaging (MRI) techniques to identify CAA-associated vascular dysfunction.

127 Using amyloid-beta immunostaining, CAA severity was graded in 5 regions (midfrontal, inferi

128 eing the primary species that accumulates in CAA.

129 reflect distinct pathophysiologic aspects in CAA, no studies to date have combined these structural i

130 Our results indicate that amyloid burden in CAA subjects (with primarily vascular amyloid) but not A

131 e total brain small vessel disease burden in CAA.

132 Changes in CAA research themes (2000-2014) were defined using a top

133 reduction in CAA formation and a decrease in CAA-induced vasomotor impairment.

134 ke (global or occipital/global) is higher in CAA than comparison groups, and a ratio <1 indicates the

135 singly, despite the several-fold increase in CAA levels, APP/PS1;Clu(-/-) mice had significantly less

136 renchyma but an equally striking increase in CAA within the cerebrovasculature of APP/PS1;Clu(-/-) mi

137 o reduce the cerebrovascular inflammation in CAA.

138 ng new insights into potential mechanisms in CAA.

139 unction is attributed both to a reduction in CAA formation and a decrease in CAA-induced vasomotor im

140 of a total MRI small vessel disease score in CAA.

141 ral amyloid angiopathy-related inflammation (CAA-ri) is an important diagnosis to reach in clinical p

142 ral amyloid angiopathy-related inflammation (CAA-ri) is characterized by vasogenic edema and multiple

143 Yet, despite remarkable recent interest, CAA remains under-recognised by neurologists and stroke

144 at mRNA (CAG100) and a non-toxic interrupted CAA/G mRNA repeat (CAA/G105) for microarray analysis.

145 hippocampal administration of biotin-labeled CAA mutant Abeta peptide accumulated on and adjacent to

146 ndent increase in the proportion of tRNA(Leu(CAA)) containing m(5)C at the wobble position, which cau

147 these transgenic mice have relatively little CAA.

148 Content analysis identified 16 major CAA research themes and their differential evolution in

149 ilon4+ vs epsilon4-: severe vs mild/moderate CAA, OR 2.5, 95% CI 1.4 to 4.5, p=0.002; severe vs moder

150 No associations of mild-to-moderate CAA with cognition were found.

151 to-very severe CAA, but not mild-to-moderate CAA, is associated with lower performance in specific co

152 % CI 1.4 to 4.5, p=0.002; severe vs moderate CAA, OR 1.7, 95% CI 0.9 to 3.1, p=0.11).

153 ulting in fewer parenchymal plaques but more CAA because of loss of CLU chaperone activity, complicat

154 udy examined a single-center neuropathologic CAA cohort of eligible patients from the Massachusetts G

155 SAH and cortical superficial siderosis-a new CAA haemorrhagic imaging signature and (b) whether acute

156 nd severe CAA and 232 persons with AD and no CAA.

157 present in many foods, bestowed virtually no CAA in HepG2 cells.

158 s (healthy participants or patients with non-CAA deep intracerebral haemorrhage) and patients with Al

159 Forty-two nondemented CAA patients, 50 HE subjects, and 43 AD/MCI patients had

160 individuals with CAA-ri and noninflammatory CAA.

161 ith pathologically confirmed noninflammatory CAA.

162 In the control group having noninflammatory CAA with lobar ICH, 1 of 21 (5%) met the criteria for po

163 In the control group having noninflammatory CAA with no ICH, 11 of 16 (69%) met the criteria for pos

164 by introducing multiple tandem CAG (but not CAA) codons into this ORF.

165 (0.13%; 95% CI 0.11% to 0.15%; p<0.0001) of CAA publications increased yearly.

166 ications related to ineffectual clearance of CAA.

167 ymal amyloid plaques was largely composed of CAA mutant Abeta.

168 ng (MRI) contrast for the early detection of CAA; and c) treating cerebrovascular inflammation result

169 DN, both before and after the development of CAA, negated short-term memory deficits, as assessed by

170 The inadvertent development of CAA-like pathology in patients treated with amyloid-beta

171 ion between diagnosis of AD and diagnosis of CAA and number of microinfarcts, between diagnosis of AD

172 ur data suggest that a reliable diagnosis of CAA-ri can be reached from basic clinical and magnetic r

173 valid alternative tool for the diagnosis of CAA-ri.

174 Patients with pathologic evidence of CAA (ie, any presence of CAA from routinely collected br

175 isms by which insoluble Abeta in the form of CAA causes cerebrovascular (CV) dysfunction are not clea

176 is-Dutch type (HCHWA-D) is a genetic form of CAA that can be diagnosed before the onset of clinical s

177 Familial forms of CAA exist in the absence of appreciable parenchymal amyl

178 d uptake (global and occipital-to-global) of CAA relative to comparison groups.

179 h Alzheimer disease (AD), fewer than half of CAA cases meet pathologic criteria for AD.

180 thophysiology and clinical manifestations of CAA continues to evolve rapidly, with the use of transge

181 Lobar microbleed count, another marker of CAA severity, also remained as an independent predictor

182 le utility of amyloid imaging as a marker of CAA severity.

183 PH oxidase-derived ROS are a key mediator of CAA-induced CV deficits.

184 the first functional 3-dimensioinal model of CAA in bioengineered human vessels.

185 It may also clarify the origin of CAA abnormalities in Batten disease.

186 port the hypothesis that the pathogenesis of CAA-ri may be mediated by a selective autoimmune reactio

187 s review will discuss the pathophysiology of CAA and focus on new imaging modalities and laboratory b

188 During the acute phase of CAA-ri, anti-Abeta autoantibodies were specifically incr

189 ibodies in the acute and remission phases of CAA-ri.

190 hemic attack-like episode were predictors of CAA in persons with AD.

191 hologic evidence of CAA (ie, any presence of CAA from routinely collected brain biopsy specimen, biop

192 Presence of CAA was assessed according to the Boston criteria.

193 POE) gene is associated with the presence of CAA, both APOE-epsilon4 and epsilon2 are associated with

194 al studies that quantified the prevalence of CAA in patients with ICH and in a control group without

195 re associated with significant reductions of CAA pathology lacking adverse effects.

196 Associations with severity of CAA-associated vasculopathic changes (fibrinoid necrosis

197 ble ordinal regression analysis, severity of CAA-associated vasculopathic changes (odds ratio, 2.40;

198 of the clinical and radiological spectrum of CAA has continued to evolve, and there are new insights

199 proteins are lysosomal/vacuolar exporters of CAAs and suggest that small-molecule transport is a cons

200 EPVS may be secondary to, and indicative of, CAA with value as a new neuroimaging marker.

201 ber of connected investigators publishing on CAA (coefficient 16.74; 95% CI 14 to 19.49; p<0.0001) as

202 After failed LCRA or CAA, redo anastomosis has a high success rate and accept

203 perficial siderosis prevalence (but no other CAA severity markers) was higher among patients with cSA

204 pe was partly complemented by overexpressing CAA-decoding tRNA(Gln)(UUG), an inefficient wobble-decod

205 o the subcortical white matter) and possible CAA-ri (not requiring the white matter hyperintensities

206 the criteria for both probable and possible CAA-ri.

207 11 of 16 (69%) met the criteria for possible CAA-ri, and 1 of 16 (6%) met the criteria for probable C

208 , 1 of 21 (5%) met the criteria for possible CAA-ri, and none met the criteria for probable CAA-ri.

209 Patients with probable or possible CAA (n=76) had a higher prevalence of severe (>40) centr

210 eeting modified Boston criteria for probable CAA were analysed for cortical superficial siderosis (fo

211 ficity of prespecified criteria for probable CAA-ri (requiring asymmetric white matter hyperintensiti

212 A-ri, and none met the criteria for probable CAA-ri.

213 d 1 of 16 (6%) met the criteria for probable CAA-ri.

214 al of 372 patients with possible or probable CAA who met the modified Boston criteria were recruited

215 This probable CAA cohort provides additional evidence for distinct dis

216 med on 25 nondemented subjects with probable CAA (mean +/- standard deviation age, 70.2 +/- 7.8 years

217 We included 33 patients with probable CAA presenting with acute cSAH and 97 without cSAH at pr

218 clinical symptoms in patients with probable CAA without lobar intracerebral haemorrhage.

219 ng 106 patients with CAA (>90% with probable CAA) and 138 controls (96 healthy elderly, 42 deep intra

220 re, we use transgenic mouse models producing CAA mutants (Tg-SwDI) or overproducing human wild-type A

221 ion levels of ApoE-a factor known to promote CAA formation.

222 Non-mutated Abeta fibril seeds promoted CAA mutant Abeta fibril formation in vitro.

223 ed with PrP cerebral amyloid angiopathy (PrP-CAA) and Gerstmann-Straussler-Scheinker (GSS) syndrome.

224 and C termini, similar to those found in PrP-CAA and GSS brain tissues.

225 hology and an unexpected benefit in reducing CAA and associated micro-hemorrhages, i.c.v.-targeted pa

226 l persons had some CAA, we averaged regional CAA scores and created class variable predictors for no-

227 d a non-toxic interrupted CAA/G mRNA repeat (CAA/G105) for microarray analysis.

228 ants included 193 persons with AD and severe CAA and 232 persons with AD and no CAA.

229 association between APOE-epsilon2 and severe CAA.

230 d by predominant preamyloid deposits, severe CAA, and abundant neurofibrillary tangles in the presenc

231 We found a possible association of severe CAA with APOE-epsilon4 but not APOE-epsilon2.

232 nical variables for the prediction of severe CAA.

233 ersons ultimately found to have no or severe CAA at autopsy using logistic regression.

234 APOE-epsilon2 promotes progression to severe CAA with associated vasculopathic changes that cause ves

235 psilon2+) genotypes on progression to severe CAA.

236 derate (0.5-2.5) and moderate-to-very severe CAA (>2.5).

237 ts, and Lewy bodies, moderate-to-very severe CAA was associated with lower perceptual speed (p = 0.01

238 Moderate-to-very severe CAA, but not mild-to-moderate CAA, is associated with lo

239 sociation of epsilon4+ genotypes with severe CAA (epsilon4+ vs epsilon4-: severe vs mild/moderate CAA

240 iers of the APOE epsilon4 allele with severe CAA compared with those without CAA had a higher prevale

241 Persons with severe CAA compared with those without CAA were more likely to

242 mal amyloid pathology in persons with severe CAA suggests a difference in beta-amyloid trafficking.

243 (s) > 0.63), and almost all persons had some CAA, we averaged regional CAA scores and created class v

244 polipoprotein E (APOE) genotype and sporadic CAA.

245 sociation between APOE epsilon4 and sporadic CAA.

246 ed in patients with the more common sporadic CAA.

247 on of vascular amyloid pathology in sporadic CAA, and a biomarker of efficacy in future intervention

248 on of vascular amyloid pathology in sporadic CAA, and a biomarker of efficacy in future intervention

249 ith HCHWA-D (rho=-0.58, p=0.003) or sporadic CAA (r=-0.4, p=0.015), but not in controls.

250 HWA-D group; patients with probable sporadic CAA without dementia; two independent cohorts of healthy

251 vere atrophy than the patients with sporadic CAA (2.1 mm [SD 0.14], difference 0.07 mm, 95% CI 0.11 t

252 hology, as well as in patients with sporadic CAA and healthy and Alzheimer's disease controls.

253 The 63 patients with sporadic CAA without dementia had thinner cortices (2.17 mm [SD 0

254 healthy controls; 63 patients with sporadic CAA without dementia; two healthy control cohorts with 6

255 e of microinfarcts was mainly AD rather than CAA related.

256 wild-type Abeta (Tg2576) to demonstrate that CAA-mutant vascular amyloid influences wild-type Abeta d

257 ew insights into the independent impact that CAA has on cognition in the context of ageing and intrac

258 Our findings also suggest that CAA-related cortical atrophy is at least partly mediated

259 g correlation (rho = 0.52, p < 0.001) in the CAA group but not in HE or AD.

260 the PLCB4/B1 genes might be involved in the CAA pathogenesis of KD.

261 The 17 patients in the CAA-ri group were a mean (SD) of 68 (8) years and 8 (47%

262 In the CAA-ri group, 14 of 17 (82%) met the criteria for both p

263 our (7.0%) patients developed leakage of the CAA and 3 patients had leakage of the small bowel anasto

264 bidity occurred in 34% and dehiscence of the CAA in 7.0%.

265 reveals the rapidly developing nature of the CAA research landscape, providing a novel quantitative a

266 According to the CAA assay, the stir-fried sample displayed the highest l

267 with Alzheimer's disease age-matched to the CAA group.

268 horts of healthy controls age-matched to the CAA group; and patients with Alzheimer's disease age-mat

269 When the CAA assay was employed to study phenolic antioxidants us

270 Within the CAA group, longer time to peak correlated with overall v

271 S are more common in lobar ICH attributed to CAA than other ICH.

272 tential mechanism by which ROS contribute to CAA pathogenesis is also identified because apocynin sub

273 a indicate that ROS are a key contributor to CAA formation, CAA-induced vessel dysfunction, and CAA-r

274 clinical and imaging features of ICH due to CAA and CAA neuropathological severity are taken into ac

275 ci that might predispose patients with KD to CAA formation, a genome-wide association screen was perf

276 The mechanisms leading to CAA have not been established, and no therapeutic target

277 d the importance of establishing how and why CAA develops; without this information, the use of these

278 available from 5 (497 participants, 353 with CAA).

279 he allele-specific associations of APOE with CAA and their mechanisms.

280 ositions 21-23 are primarily associated with CAA, although they manifest with strikingly different cl

281 preliminary evidence of an association with CAA of polymorphisms in the transforming growth factor b

282 matically reviewed genetic associations with CAA to better understand its pathogenesis.

283 investigate other genetic associations with CAA.

284 showed an association of APOE epsilon4 with CAA (epsilon4 present vs absent, pooled OR 2.7, 95% CI 2

285 nt-echo scans obtained from individuals with CAA-ri and noninflammatory CAA.

286 Seven studies, including 106 patients with CAA (>90% with probable CAA) and 138 controls (96 health

287 loid-PET uptake in symptomatic patients with CAA (per Boston criteria) versus control groups (healthy

288 omising therapeutic target for patients with CAA and AD.

289 obal amyloid-PET ratio between patients with CAA and controls was above 1, with an average effect siz

290 e ratio did not differ between patients with CAA versus patients with deep intracerebral haemorrhage

291 ET uptake ratio was above 1 in patients with CAA versus those with Alzheimer's disease, with an avera

292 s 34%; p<0.0001) compared with patients with CAA without cSAH.

293 In patients with CAA, addition of IV ferric gluconate to darbepoetin fail

294 PET burden and distribution in patients with CAA, useful for future larger studies.

295 iron improves ESA efficacy in patients with CAA.

296 is-positive, but cSAH-negative subjects with CAA (76% vs 30%; p<0.0001).

297 Those with CAA compared with those without CAA more commonly had in

298 with severe CAA compared with those without CAA had a higher prevalence of stroke (11.1% vs 3.9%, re

299 Those with CAA compared with those without CAA more commonly had intracerebral hemorrhage (9.3% vs

300 with severe CAA compared with those without CAA were more likely to carry an APOE epsilon4 allele (6