ライフサイエンスコーパス: CAA

1 CAA assay showed that extracts of P. trunciflora fruits

2 CAA deposition leads to several clinical complications,

3 CAA occurs with normal aging and to various degrees in A

4 CAA onset in mice was at 22 to 24 months, first in front

5 nned intact formalin-fixed hemispheres of 12 CAA cases with magnetic resonance imaging (MRI), followe

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

7 Additionally, machine learning identifies 31 CAAs that robustly alter response to 56 chemotherapeutic

8 72 CAAs and 88 synergistically co-occurring CAA pairs multi

9 These results suggest that each time a CAA was discovered and embedded during evolution, it pro

10 e uses a common set of 20 coded amino acids (CAAs) to construct proteins.

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

12 V(max), SUV(mean), cardiac amyloid activity (CAA; i.e., SUV(mean) x left ventricular [LV] volume), an

13 , including a cellular antioxidant activity (CAA) and protein glycation assays, to offer an improved

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

15 ng a modified cellular antioxidant activity (CAA) assay with comparisons to data from in vitro antiox

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

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

18 stibility and cellular antioxidant activity (CAA) of protein hydrolysates.

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

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

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

22 smooth muscle (alpha-SMA) and cardiac (alpha-CAA) to skeletal muscle alpha-actin (alpha-SKA) that, in

23 Here, we analyse CAA profiles of 23,427 tumours, identifying aspects of t

24 -RBF) was evaluated using ABTS, ORAC 6.0 and CAA assays and ME-RBF demonstrated 26-fold, 12-fold and

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

26 importance of hypertensive arteriopathy and CAA scores as predictors of [(11)C]PK11195.

27 ing of the molecular profiles of CADASIL and CAA appears to support potential for common mechanisms u

28 the overlapped proteins between CADASIL and CAA are expressed by fibroblasts.

29 CADASIL and CAA protein profiles from recently published proteomics-

30 p, the molecular overlap between CADASIL and CAA was explored.

31 teins that are regulated in both CADASIL and CAA.

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

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

34 cular mechanism underlying CAA formation and CAA-induced cerebrovascular pathology is unclear.

35 9 at AT-rich PAM sites such as GAT, GAA, and CAA.

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

37 fficient of variation for SUV(max), %ID, and CAA and 3.8% for SUV(mean) All 4 quantitative metrics ha

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

41 play between parenchymal amyloid plaques and CAA is unclear.

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

43 ding probable orders in which CAAs occur and CAAs predicting tissue-specific metastasis.

44 Chromosome arm aneuploidies (CAAs) are pervasive in cancers.

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

46 tions, especially coronary artery aneurysms (CAA).

47 who develop giant coronary artery aneurysms (CAA).

48 TgSwDI mouse, a cerebral amyloid angiopathy (CAA) and AD model.

49 ) deposition in cerebral amyloid angiopathy (CAA) and Alzheimer disease (AD) is arguably the clearest

50 In cerebral amyloid angiopathy (CAA) and Alzheimer's disease (AD), the amyloid beta (Abe

51 , haemorrhages, cerebral amyloid angiopathy (CAA) and arteriosclerosis, were examined.

52 Cerebral amyloid angiopathy (CAA) and beta-amyloid (Abeta) deposition in the brain pa

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

54 y (CADASIL) and cerebral amyloid angiopathy (CAA) are two distinct vascular angiopathies that share s

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

56 beta to prevent cerebral amyloid angiopathy (CAA) has not been rigorously followed, although the caus

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

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

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

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

61 Cerebral amyloid angiopathy (CAA) is characterized by the accumulation of amyloid bet

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

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

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

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 Cerebral amyloid angiopathy (CAA), where beta-amyloid (Abeta) deposits around cerebra

69 dition known as cerebral amyloid angiopathy (CAA), which impairs blood-brain barrier (BBB) function a

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

71 stic markers of cerebral amyloid angiopathy (CAA).

72 arly markers of cerebral amyloid angiopathy (CAA).

73 ion in sporadic cerebral amyloid angiopathy (CAA).

74 lood vessels as cerebral amyloid angiopathy (CAA).

75 y recognised in cerebral amyloid angiopathy (CAA).

76 oid plaques and cerebral amyloid angiopathy (CAA).

77 rteriopathy and cerebral amyloid angiopathy (CAA).

78 isease (AD) and cerebral amyloid angiopathy (CAA).

79 detected in the Canadian Arctic Archipelago (CAA) and in the Greenland Sea.

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

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

82 how a single neuropathologic process such as CAA may result in hemorrhagic or ischemic brain lesions

83 urin-NFAT signaling reduces APOE4-associated CAA pathology in vitro and in vivo.

84 te-like mural cells induces APOE4-associated CAA pathology.

85 BACE1 inhibitor treatment starting at CAA onset and continuing for 4 months revealed a 90% Abe

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

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

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

89 l adenocarcinoma (Caco-2) cells and bestowed CAA, determined by monitoring the fluorescence of 2',7'-

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

91 hogenic implications of interactions between CAA and AD.

92 py are another probable intersection between CAA and AD, representing overload of perivascular cleara

93 The intersections between CAA and AD point to a crucial role for improving vascula

94 The relationship between CAA severity and microbleeds and microinfarcts as well a

95 After stratification by CAA presence/absence, we found that in those cases in wh

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

97 a consensus binding specificity of 5'-TTG-CG-CAA-3', with a central CpG/CpG and two outer CpA/TpG din

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

99 17 individuals with pathologically confirmed CAA-ri and 37 control group members with pathologically

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

101 D-CAA M(+) showed greater age-dependent FLR PiB retention

102 egions (FLR) was measured by PiB-PET in 19 D-CAA mutation carriers (M(+) ; 13 without neurologic symp

103 Increased PiB retention in D-CAA and correlation with reduced CSF Abeta40 suggest thi

104 2, PiB retention was substantially less in D-CAA than ADAD (p < 0.001).

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

106 APPDutch mice develop CAA in the absence of parenchymal amyloid, mimicking her

107 markers in clinical-radiologically diagnosed CAA.

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

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

110 lowed, although the causal role of Abeta for CAA and related hemorrhages is undisputed.

111 ological assessment of postmortem brains for CAA severity.

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

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

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

115 ein (APOE4) is the strongest risk factor for CAA, yet the mechanisms underlying this genetic suscepti

116 E e4 allele significantly increased risk for CAA.

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

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

119 hways and the effects of removing Abeta from CAA-positive vessels.

120 cerebrovascular inflammation resulting from CAA.

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

122 higher efficacy than other colourful fruits (CAA(50) 935.25 mg FW/mL cell medium).

123 , reduced perivascular clearance and further CAA and AD progression.

124 and in adult KD patients who developed giant CAA in childhood.

125 persisted in 2 patients who developed giant CAA.

126 alprotectin in pediatric patients with giant CAA 1 year post-KD and in adult KD patients who develope

127 mics was performed on 9 KD adults with giant CAA and matched healthy controls.

128 ence of inflammation in KD adults with giant CAA by shotgun proteomics that revealed a signature of a

129 the acute phase of KD in patients with giant CAA.

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

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

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

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

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

135 cifically, we studied in silico hypothetical CAA sets of 3-19 amino acids comprised of 1913 structura

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

137 Although FXIIIa co-localizes with Abeta in CAA, the ability of FXIIIa to cross-link Abeta has not b

138 eing the primary species that accumulates in CAA.

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

140 e total brain small vessel disease burden in CAA.

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

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

143 ribute to the formation of Abeta deposits in CAA and Alzheimer's disease.

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

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

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

147 o reduce the cerebrovascular inflammation in CAA.

148 ng new insights into potential mechanisms in CAA.

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

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

151 in-NFAT signaling as a therapeutic target in CAA and Alzheimer's disease.

152 logy compared with e3 homozygotes, including CAA.

153 reated with 2 mg Na(2)SeO(3)/100 g increased CAA (51.47%), demonstrating the potential health benefit

154 ction between Abeta and fibrinogen increases CAA and plays an important role in cerebrovascular damag

155 Increasing CAA severity at the whole-brain or regional level was no

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

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

158 these transgenic mice have relatively little CAA.

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

160 SUV(max), SUV(mean), CAA, %ID, and visual grade were moderately positively co

161 uride SPECT/CT scanner, SUV(max), SUV(mean), CAA, and %ID measured by absolute quantitation of (99m)T

162 eals the role of pericytes in APOE4-mediated CAA and highlights calcineurin-NFAT signaling as a thera

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

164 % 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).

165 hat even hypothetical sets containing modern CAA members are especially adaptive; it is difficult to

166 l properties relative to those of the modern CAA set.

167 Many possible subsets of the modern CAAs or other presently uncoded amino acids could have c

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

169 rap the developing set to include still more CAAs.

170 reviously implicated in the RNAP3 TSS motif (CAA).

171 of the CAG repeat in HTT [reference: (CAG)n-CAA-CAG], since variants within this region have been pr

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

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

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

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

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

177 individuals with CAA-ri and noninflammatory CAA.

178 ith pathologically confirmed noninflammatory CAA.

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

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

181 72 CAAs and 88 synergistically co-occurring CAA pairs multivariately predict good or poor survival f

182 (0.13%; 95% CI 0.11% to 0.15%; p<0.0001) of CAA publications increased yearly.

183 ications related to ineffectual clearance of CAA.

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

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

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

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

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

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

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

191 angiopathy (HCAA) is a rare familial form of CAA in which mutations within the (Abeta) peptide cause

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

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

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

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

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

197 The pathogenic pathways of CAA and AD intersect at the levels of Abeta generation,

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

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

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

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

202 ubacute gross haemorrhage in the presence of CAA.

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

204 a-reducing treatments in patients at risk of CAA and in presymptomatic HCHWA-D.

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

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

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

208 might contribute to further understanding of CAA pathogenesis in KD.

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

210 d of patients with KD, IVIG-resistant KD, or CAA.

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

212 hypertensive arteriopathy score outperformed CAA in predicting [(11)C]PK11195 binding globally and in

213 ndividuals with the interrupting penultimate CAA codon.

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

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

216 11 of 16 (69%) met the criteria for possible CAA-ri, and 1 of 16 (6%) met the criteria for probable C

217 , 1 of 21 (5%) met the criteria for possible CAA-ri, and none met the criteria for probable CAA-ri.

218 Abeta reduction in CSF and largely prevented CAA progression and associated pathologies.

219 t early disease time points largely prevents CAA in the absence of parenchymal amyloid.

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

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

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

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

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

225 This probable CAA cohort provides additional evidence for distinct dis

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

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

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

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

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

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

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

233 Notably, in predicting drug response, CAAs substantially outperform mutations and focal deleti

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

235 association between APOE-epsilon2 and severe CAA.

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

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

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

239 psilon2+) genotypes on progression to severe CAA.

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

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

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

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

244 ed in patients with the more common sporadic CAA.

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

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

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

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

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

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

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

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

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

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

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

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

257 In the CAA assay, pecan phenolics were taken up by human colore

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

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

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

261 egrees C) compared to the cold waters of the CAA (0.7 degrees C) that were associated with the larges

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

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

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

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

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

267 ed another variant in this region, where the CAA-CAG sequence is duplicated, which was associated wit

268 We explore the hypothesis that the CAAs were selectively fixed due to their unique adaptive

269 Thus, CAAs predict cancer prognosis, shape tumour evolution, m

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

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

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

273 Similarly to CAA, our in vitro BBB displayed significantly more amylo

274 However, the molecular mechanism underlying CAA formation and CAA-induced cerebrovascular pathology

275 a decrease of both Abeta40 and Abeta42 upon CAA onset, supporting the idea that combined reduction o

276 amicroscopy and immunoassays for visualizing CAA and assessing Abeta in cerebrospinal fluid (CSF) and

277 Beyond this, the ex vivo CAA-RBC assay determined the cellular antioxidant activi

278 sence, we found that in those cases in which CAA was present, APOE e2 significantly increased risk fo

279 evolution including probable orders in which CAAs occur and CAAs predicting tissue-specific metastasi

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

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

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

283 y, XLOC_006277 abundance was associated with CAA, which might contribute to further understanding of

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

285 ascular reactivity was impaired in mice with CAA, which corresponded to slower clearance rates.

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 urally occurring vasomotion in patients with CAA or AD may be a promising early therapeutic option fo

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

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

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

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

295 nce increased significantly in patients with CAA.

296 tectin levels in the plasma of patients with CAA.

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

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

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

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

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