ライフサイエンスコーパス: CAA

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

2 stic markers of cerebral amyloid angiopathy (CAA).

3 arly markers of cerebral amyloid angiopathy (CAA).

4 ion in sporadic cerebral amyloid angiopathy (CAA).

5 lood vessels as cerebral amyloid angiopathy (CAA).

6 y recognised in cerebral amyloid angiopathy (CAA).

7 oid plaques and cerebral amyloid angiopathy (CAA).

8 rteriopathy and cerebral amyloid angiopathy (CAA).

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

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

11 tions, especially coronary artery aneurysms (CAA).

12 who develop giant coronary artery aneurysms (CAA).

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

14 persisted in 2 patients who developed giant CAA.

15 nce increased significantly in patients with CAA.

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

17 tectin levels in the plasma of patients with CAA.

18 eing the primary species that accumulates in CAA.

19 markers in clinical-radiologically diagnosed CAA.

20 ications related to ineffectual clearance of CAA.

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

22 ng new insights into potential mechanisms in CAA.

23 these transgenic mice have relatively little CAA.

24 e total brain small vessel disease burden in CAA.

25 individuals with CAA-ri and noninflammatory CAA.

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

27 ith pathologically confirmed noninflammatory CAA.

28 ed in patients with the more common sporadic CAA.

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

30 association between APOE-epsilon2 and severe CAA.

31 o reduce the cerebrovascular inflammation in CAA.

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

33 psilon2+) genotypes on progression to severe CAA.

34 ubacute gross haemorrhage in the presence of CAA.

35 E e4 allele significantly increased risk for CAA.

36 logy compared with e3 homozygotes, including CAA.

37 teins that are regulated in both CADASIL and CAA.

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

39 9 at AT-rich PAM sites such as GAT, GAA, and CAA.

40 harms of screening and treatment with CEA or CAAS.

41 rap the developing set to include still more CAAs.

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

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

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

45 logical nodal-loop (TNL) in SrAs(3), whereas CaAs(3) exhibits a topologically trivial state.

46 ence (absence) of surface states in SrAs(3) (CaAs(3)).

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

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

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

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

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

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

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

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

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

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

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

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

59 hogenic implications of interactions between CAA and AD.

60 omising therapeutic target for patients with CAA and AD.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

76 72 CAAs and 88 synergistically co-occurring CAA pairs multi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

96 CAA assay showed that extracts of P. trunciflora fruits

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

120 ndividuals with the interrupting penultimate CAA codon.

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

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

123 This probable CAA cohort provides additional evidence for distinct dis

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

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

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

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

128 CAA deposition leads to several clinical complications,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

170 play between parenchymal amyloid plaques and CAA is unclear.

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

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

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

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

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

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

177 th a beta-hGly residue instead of a (S)-beta-Caa(l) constituent.

178 investigations on peptides with an (S)-beta-Caa(l) monomer at the N-terminus revealed a right-handed

179 in the corresponding peptides with (R)-beta-Caa(l) residues, where right-handed 12/10-helices are pr

180 s from C-linked carbo-beta-amino acids [beta-Caa(l)] with a d-lyxo furanoside side chain and beta-hGl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

206 % 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).

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

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

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

210 72 CAAs and 88 synergistically co-occurring CAA pairs multivariately predict good or poor survival f

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

227 CADASIL and CAA protein profiles from recently published proteomics-

228 (0.13%; 95% CI 0.11% to 0.15%; p<0.0001) of CAA publications increased yearly.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

245 17 individuals with pathologically confirmed CAA-ri and 37 control group members with pathologically

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

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

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

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

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

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

252 11 of 16 (69%) met the criteria for possible CAA-ri, and 1 of 16 (6%) met the criteria for probable C

253 , 1 of 21 (5%) met the criteria for possible CAA-ri, and none met the criteria for probable CAA-ri.

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

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

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

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

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

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

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

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

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

263 ological assessment of postmortem brains for CAA severity.

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

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

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

267 2, PiB retention was substantially less in D-CAA than ADAD (p < 0.001).

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

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

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

271 y (CEA) or carotid angioplasty and stenting (CAAS), the benefits from medications added to current st

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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