ライフサイエンスコーパス: CAA

1 stic markers of cerebral amyloid angiopathy (CAA).

2 oid plaques and cerebral amyloid angiopathy (CAA).

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

4 arly markers of cerebral amyloid angiopathy (CAA).

5 ion in sporadic cerebral amyloid angiopathy (CAA).

6 lood vessels as cerebral amyloid angiopathy (CAA).

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

8 y recognised in cerebral amyloid angiopathy (CAA).

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

10 eing the primary species that accumulates in CAA.

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

12 association between APOE-epsilon2 and severe CAA.

13 o reduce the cerebrovascular inflammation in CAA.

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

15 psilon2+) genotypes on progression to severe CAA.

16 cerebrovascular inflammation resulting from CAA.

17 nical variables for the prediction of severe CAA.

18 ficant association between APOE epsilon2 and CAA.

19 ifying therapies for the treatment of AD and CAA.

20 polipoprotein E (APOE) genotype and sporadic CAA.

21 sociation between APOE epsilon4 and sporadic CAA.

22 lymorphism and histopathologically confirmed CAA.

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

24 investigate other genetic associations with CAA.

25 markers in clinical-radiologically diagnosed CAA.

26 ications related to ineffectual clearance of CAA.

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

28 involved in the pathogenesis of both AD and CAA.

29 e response to visual stimulation in advanced CAA.

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

31 ng new insights into potential mechanisms in CAA.

32 these transgenic mice have relatively little CAA.

33 e total brain small vessel disease burden in CAA.

34 individuals with CAA-ri and noninflammatory CAA.

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

36 ith pathologically confirmed noninflammatory CAA.

37 ed in patients with the more common sporadic CAA.

38 harms of screening and treatment with CEA or CAAS.

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

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

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

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

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

44 CaaD activity, it shows only a low level cis-CaaD activity and lacks the specificity of cis-CaaD: Cg1

45 -103, and Glu-114) that are critical for cis-CaaD activity, it shows only a low level cis-CaaD activi

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

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

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

49 omising therapeutic target for patients with CAA and AD.

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

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

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

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

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

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

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

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

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

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

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

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

62 tive difference in diameter between pre-TAVI CAAD and nominal diameter of the selected prosthesis, wa

63 Both cis-CaaD and the T34 mutant generate (2R)-[2-D]acetoacetate,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 assessment and average diameter calculation (CAAD) before and after TAVI.

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

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

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

94 e loop closes down on the active site of cis-CaaD, but not on that of Cg10062.

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

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

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

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

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

100 amine what this loop might contribute to cis-CaaD catalysis and specificity, the residues were change

101 ts may suggest that some fraction of the cis-CaaD-catalyzed dehalogenation of cis-3-haloacrylates als

102 urse of a stereochemical analysis of the cis-CaaD-catalyzed reaction using this allene, the enzyme wa

103 cis-3-Chloroacrylic acid dehalogenase (cis-CaaD) catalyzes the hydrolytic dehalogenation of cis-3-h

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

105 aD activity and lacks the specificity of cis-CaaD: Cg10062 processes both isomers of 3-chloroacrylate

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

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

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

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

110 This probable CAA cohort provides additional evidence for distinct dis

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

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

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

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

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

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

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

118 ing because the accumulated evidence for cis-CaaD dehalogenation favored a mechanism involving direct

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

120 CAA deposition leads to several clinical complications,

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

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

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

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

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

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

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

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

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

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

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

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

133 carbon in C-linked-carbo-beta(3)-amino acid (Caa) from R to S.

134 cis-3-Chloroacrylic acid dehalogenase (cis-CaaD) from Pseudomonas pavonaceae 170 and a homologue fr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

165 play between parenchymal amyloid plaques and CAA is unclear.

166 In the presence of NaBH4 and the allene, cis-CaaD is completely inactivated after one turnover becaus

167 nalysis suggests that the T34A mutant of cis-CaaD is more Cg10062-like.

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

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

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

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

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

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

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

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

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

177 ha/beta-peptides were prepared from (S)-beta-Caa(l) (C-linked carbo-beta-amino acid with D-lyxo furan

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

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

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

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

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

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

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

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

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

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 ymal amyloid plaques was largely composed of CAA mutant Abeta.

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

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

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

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

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

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

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

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

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

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

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

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

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

203 % 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).

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

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

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

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

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

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

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

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

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

213 Median relative change in CAAD pre- and post-TAVI was -0.5% (interquartile range,

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

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

216 (0.13%; 95% CI 0.11% to 0.15%; p<0.0001) of CAA publications increased yearly.

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

218 thesized from alternating L-Ala and (R)-beta-Caa((r)), have shown the presence of 14/15-helix by NMR

219 new C-linked carbo-beta-amino acid, (R)-beta-Caa((r)), having a carbohydrate side chain with D-ribo c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

238 17 individuals with pathologically confirmed CAA-ri and 37 control group members with pathologically

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

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

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

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

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

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

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

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

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

248 11 of 16 (69%) met the criteria for possible CAA-ri, and 1 of 16 (6%) met the criteria for probable C

249 , 1 of 21 (5%) met the criteria for possible CAA-ri, and none met the criteria for probable CAA-ri.

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

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

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

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

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

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

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

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

258 ological assessment of postmortem brains for CAA severity.

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

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

261 A six-residue active site loop in cis-CaaD shows a conformation strikingly different from that

262 stent with a role for the loop region in cis-CaaD specificity and catalysis, but the precise role rem

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

264 CAA subjects demonstrated reduced response amplitude (pe

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

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

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

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

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

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

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

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

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

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

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

276 ysis of the enamine or imine tautomer in cis-CaaD versus direct hydration of the allene to yield acet

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

278 CAA was significantly associated with lobar ICH, both ov

279 Pre-TAVI CAAD was 23.1+/-1.8 mm; post-TAVI CAAD was 22.9+/-1.3 mm.

280 Pre-TAVI CAAD was 23.1+/-1.8 mm; post-TAVI CAAD was 22.9+/-1.3 mm

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

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

286 urst rate (compared to that of wild-type cis-CaaD), whereas Cg10062 shows no burst rate.

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

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

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

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

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

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

293 ng is the reaction of the T34A mutant of cis-CaaD with the alternate substrate, 2,3-butadienoate.

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

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

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

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

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

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

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