ライフサイエンスコーパス: cerebral amyloid angiopathy

1 he effects of these gene variants on risk of cerebral amyloid angiopathy.

2 lihood of developing Alzheimer's disease and cerebral amyloid angiopathy.

3 mice in parallel to significantly increased cerebral amyloid angiopathy.

4 partly by attenuating neuroinflammation and cerebral amyloid angiopathy.

5 plicated in other amyloid diseases including cerebral amyloid angiopathy.

6 mutations associated with familial forms of cerebral amyloid angiopathy.

7 tide (Abeta) in Alzheimer's disease (AD) and cerebral amyloid angiopathy.

8 th a hereditary amyloid disease known as PrP cerebral amyloid angiopathy.

9 that forms amyloid deposits associated with cerebral amyloid angiopathy.

10 d Asp-23 that cause familial forms of AD and cerebral amyloid angiopathy.

11 nd the walls of meningoencephalic vessels as cerebral amyloid angiopathy.

12 tions at Glu-22 with Alzheimer's disease and cerebral amyloid angiopathy.

13 neuronal and vascular degeneration in AD and cerebral amyloid angiopathy.

14 and Abeta peptides causing familial forms of cerebral amyloid angiopathy.

15 , which are pathological hallmarks of AD and cerebral amyloid angiopathy.

16 intracerebral hemorrhage is the hallmark of cerebral amyloid angiopathy.

17 e and that this contributes significantly to cerebral amyloid angiopathy.

18 aged cerebral blood vessels of patients with cerebral amyloid angiopathy.

19 sporadic AD and two pathways associated with cerebral amyloid angiopathy.

20 t risk of iatrogenic Alzheimer's disease and cerebral amyloid angiopathy.

21 ound B values, but not Braak tangle stage or cerebral amyloid angiopathy.

22 ial siderosis, with a particular emphasis on cerebral amyloid angiopathy.

23 farcts, Circle of Willis atherosclerosis, or cerebral amyloid angiopathy.

24 ts, displayed a prominent Abeta38-containing cerebral amyloid angiopathy.

25 fect of HJ6.3 on total plasma cholesterol or cerebral amyloid angiopathy.

26 with the immune system and the importance of cerebral amyloid angiopathy.

27 ial activation and enhancing astrocytosis or cerebral amyloid angiopathy.

28 ients with multiple lobar CMBs suggestive of cerebral amyloid angiopathy.

29 ng in 38 non-demented patients with probable cerebral amyloid angiopathy (69 +/- 10 years) and 29 sim

30 e causes, it is emerging as a key feature of cerebral amyloid angiopathy, a common and important age-

31 early manifestations of Iowa-type hereditary cerebral amyloid angiopathy, a form of the disorder with

32 redominantly of hyperphosphorylated tau; and cerebral amyloid angiopathy, a microangiopathy affecting

33 a patient with dementia can be secondary to cerebral amyloid angiopathy alone.

34 rly-phase trials of candidate treatments for cerebral amyloid angiopathy, an untreatable cause of hae

35 in the brains of wild-type mice, and formed cerebral amyloid angiopathy and Abeta plaques after a 12

36 -beta and phospho-tau pathology, severity of cerebral amyloid angiopathy and cortical microhaemorrhag

37 the blood vessel walls was characteristic of cerebral amyloid angiopathy and did not co-localize with

38 a with Lewy bodies, multiple system atrophy, cerebral amyloid angiopathy and elderly controls free of

39 CA1 also considerably increased the level of cerebral amyloid angiopathy and exacerbated cerebral amy

40 ctors may play a role in the pathogenesis of cerebral amyloid angiopathy and in the accumulation of A

41 The severity of cerebral amyloid angiopathy and microhaemorrhages did no

42 an age 85 +/- 6 years) with pathology-proven cerebral amyloid angiopathy and multiple microbleeds on

43 Cerebral amyloid angiopathy and neurofibrillary tangles

44 ht mediate the relationship between advanced cerebral amyloid angiopathy and neurologic dysfunction a

45 rfamily are involved in an inherited form of cerebral amyloid angiopathy and readily form amyloid fib

46 ce of the grey matter and in artery walls as cerebral amyloid angiopathy and tau protein accumulates

47 ral haemorrhage (39 with clinically probable cerebral amyloid angiopathy) and 47 age-matched controls

48 arteriolosclerotic small vessel disease and cerebral amyloid angiopathy, and determined the Braak ta

49 e form of frequent cortical amyloid plaques, cerebral amyloid angiopathy, and tauopathy.

50 maging are specific for microhaemorrhages in cerebral amyloid angiopathy, and that increasing the res

51 ing-defined microbleeds and microinfarcts in cerebral amyloid angiopathy, and to explore the patholog

52 genotype to risk of Alzheimer's disease and cerebral amyloid angiopathy, APOE has been studied in ot

53 clear that, at the pathophysiological level, cerebral amyloid angiopathy appears to be in part a prot

54 Neuroimaging markers of severe cerebral amyloid angiopathy are cortical microbleeds and

55 tomography can noninvasively detect isolated cerebral amyloid angiopathy before overt signs of tissue

56 mentia (FBD), previously designated familial cerebral amyloid angiopathy-British type, is an autosoma

57 a significant reduction of Abeta plaques and cerebral amyloid angiopathy burden and a reduction of th

58 ab, even in vessels where there was a severe cerebral amyloid angiopathy burden.

59 olipoprotein E4 genotype was associated with cerebral amyloid angiopathy, but not HS or arteriosclero

60 of parenchymal amyloid-beta (Abeta) plaques, cerebral amyloid angiopathy (CAA) and neurofibrillary ta

61 s and subgroups of 190 AD subjects exhibited cerebral amyloid angiopathy (CAA) and other frequently a

62 nile plaques and along cerebrovasculature as cerebral amyloid angiopathy (CAA) are hallmarks of AD.

63 c or primary angiitis of the CNS (PACNS) and cerebral amyloid angiopathy (CAA) are unusual vasculopat

64 utive patients with pathologically diagnosed cerebral amyloid angiopathy (CAA) for evidence of an inf

65 Although cerebral amyloid angiopathy (CAA) has important clinical

66 Cerebral amyloid angiopathy (CAA) has never been more re

67 between intracerebral haemorrhage (ICH) and cerebral amyloid angiopathy (CAA) in a systematic review

68 oligomeric strain selectively induces acute cerebral amyloid angiopathy (CAA) in neonatally-injected

69 Sporadic cerebral amyloid angiopathy (CAA) is a common age relate

70 Cerebral amyloid angiopathy (CAA) is a common cause of b

71 Cerebral amyloid angiopathy (CAA) is a common cause of s

72 he brain in the form of neuritic plaques and cerebral amyloid angiopathy (CAA) is a key feature of Al

73 to its role in hemorrhagic stroke, advanced cerebral amyloid angiopathy (CAA) is also associated wit

74 Cerebral amyloid angiopathy (CAA) is an age-associated c

75 Cerebral amyloid angiopathy (CAA) is associated with lob

76 Cerebral amyloid angiopathy (CAA) is characteristically

77 Cerebral amyloid angiopathy (CAA) is characterized by de

78 Cerebral amyloid angiopathy (CAA) is characterized by th

79 Cerebral amyloid angiopathy (CAA) is common in Alzheimer

80 Cerebral amyloid angiopathy (CAA) is common in the agein

81 Cerebral amyloid angiopathy (CAA) is the accumulation of

82 Cerebral amyloid angiopathy (CAA) may play a key role in

83 arch output and major trends in the field of cerebral amyloid angiopathy (CAA) over six decades, from

84 Cerebral amyloid angiopathy (CAA) results from depositio

85 euritic plaques, but has no direct effect on cerebral amyloid angiopathy (CAA) severity, whereas APOE

86 d densities of tangles, neuropil threads and cerebral amyloid angiopathy (CAA) similar to unimmunized

87 isease (mainly hypertensive arteriopathy and cerebral amyloid angiopathy (CAA)) is an important cause

88 st AD patients have cerebrovascular amyloid (cerebral amyloid angiopathy (CAA), and cardiovascular ri

89 We postulated that cerebral amyloid angiopathy (CAA), characterised by cort

90 d beta-protein (Abeta), a condition known as cerebral amyloid angiopathy (CAA), is a common pathologi

91 cerebral blood vessels, a condition known as cerebral amyloid angiopathy (CAA), is a key pathological

92 d beta-protein (Abeta), a condition known as cerebral amyloid angiopathy (CAA), is a key pathological

93 eptides in the walls of brain blood vessels, cerebral amyloid angiopathy (CAA), is common in patients

94 otein E (apoE) genotype in hemorrhage due to cerebral amyloid angiopathy (CAA), it is unclear whether

95 -beta (Abeta) in cerebral arteries, known as cerebral amyloid angiopathy (CAA), occurs both in the se

96 18-month-old APPsw (Tg2576) mice, a model of cerebral amyloid angiopathy (CAA), suggesting a pivotal

97 Cerebral amyloid angiopathy (CAA), the deposition of cer

98 There is increasing evidence that cerebral amyloid angiopathy (CAA), which itself can caus

99 proteinase-9 (MMP-9), in the pathogenesis of cerebral amyloid angiopathy (CAA)-induced spontaneous he

100 ta) has recently been reported to exacerbate cerebral amyloid angiopathy (CAA)-related microhemorrhag

101 mited by poor clearance of a core AD lesion, cerebral amyloid angiopathy (CAA).

102 disease (AD), are primarily associated with cerebral amyloid angiopathy (CAA).

103 ferential occipital distribution in sporadic cerebral amyloid angiopathy (CAA).

104 n the cerebral cortex and in blood vessel as cerebral amyloid angiopathy (CAA).

105 s the development of Alzheimer's disease and cerebral amyloid angiopathy (CAA).

106 ving elevated levels of soluble Abeta but no cerebral amyloid angiopathy (CAA).

107 lated disorders, including familial forms of cerebral amyloid angiopathy (CAA).

108 as plaques and in cerebral blood vessels as cerebral amyloid angiopathy (CAA).

109 ngophilic amyloid in blood vessels is called cerebral amyloid angiopathy (CAA).

110 ques and in the walls of cerebral vessels as cerebral amyloid angiopathy (CAA).

111 implicate similar inflammatory processes in cerebral amyloid angiopathy (CAA).

112 orrhage (cSAH) is increasingly recognised in cerebral amyloid angiopathy (CAA).

113 osis (CSS) are the characteristic markers of cerebral amyloid angiopathy (CAA).

114 the form of parenchymal amyloid plaques and cerebral amyloid angiopathy (CAA).

115 flow or reactivity might be early markers of cerebral amyloid angiopathy (CAA).

116 of amyloid in the cerebrovasculature [i.e., cerebral amyloid angiopathy (CAA)] and a heightened risk

117 erized by Abeta in the cerebral vasculature [cerebral amyloid angiopathy (CAA)] in the majority of pa

118 ients with high vascular amyloid deposition (cerebral amyloid angiopathy [CAA]) but not in patients w

119 Cerebrovascular deposition of beta-amyloid (cerebral amyloid angiopathy [CAA]) is a major cause of h

120 ced cerebrovascular beta-amyloid deposition (cerebral amyloid angiopathy, CAA) is associated with cer

121 A range of potential outcome markers for cerebral amyloid angiopathy can be measured against the

122 eta peptide in the wall of cerebral vessels (cerebral amyloid angiopathy), can lead to weakness and r

123 In cerebral amyloid angiopathy cohorts, cortical superficia

124 al hemorrhage, apolipoprotein E subtypes and cerebral amyloid angiopathy; deep intracerebral hemorrha

125 b administration has on reducing the rate of cerebral amyloid angiopathy deposition and restoring cer

126 mpairment in Alzheimer's disease and related cerebral amyloid angiopathy disorders.

127 in Alzheimer's disease and related familial cerebral amyloid angiopathy disorders.

128 Additionally, several familial forms of cerebral amyloid angiopathy exist including the Dutch (E

129 A PrP cerebral amyloid angiopathy has not been reported in dis

130 ucoencephalopathy (CADASIL)and some forms of cerebral amyloid angiopathy have a genetic basis.

131 individuals with CMBs related to symptomatic cerebral amyloid angiopathy have abnormal vascular react

132 hological findings include severe widespread cerebral amyloid angiopathy, hippocampal plaques, and ne

133 Restriction of analysis to definite/probable cerebral amyloid angiopathy ICH uncovered a stronger eff

134 Cerebral amyloid angiopathy in Alzheimer's disease is ch

135 f the brain and contributes significantly to cerebral amyloid angiopathy in Alzheimer's disease.

136 sited early in diffuse and focal plaques and cerebral amyloid angiopathy in humans and nonhuman prima

137 Autopsy revealed cerebral amyloid angiopathy in the complete absence of a

138 on in TgCRND8 mice and ADan (Danish Amyloid) cerebral amyloid angiopathy in the mouse model of FDD.

139 vessel disease (hypertensive arteriopathy or cerebral amyloid angiopathy) in a multicentre, cross-sec

140 arly onset, familial Alzheimer's disease and cerebral amyloid angiopathy, in which patients develop n

141 Cerebral amyloid angiopathy is a common form of small-ve

142 Cerebral amyloid angiopathy is a common neuropathologica

143 Sporadic cerebral amyloid angiopathy is a common, well-defined sm

144 orrhage; our results suggest that underlying cerebral amyloid angiopathy is a contributing factor to

145 As cerebral amyloid angiopathy is an almost invariable path

146 also have serious consequences; for example, cerebral amyloid angiopathy is an important cause of hae

147 Cerebral amyloid angiopathy is characterized by accumula

148 The Tg2576 transgenic mouse model of human cerebral amyloid angiopathy is characterized by age-depe

149 From a clinical standpoint, cerebral amyloid angiopathy is characterized by individu

150 Cerebral amyloid angiopathy is common among elderly pati

151 Cerebral amyloid angiopathy is commonly associated with

152 Prominent cerebral amyloid angiopathy is often observed in the bra

153 Determining the presence and burden of cerebral amyloid angiopathy is particularly important wh

154 in mice; however, its involvement in AD and cerebral amyloid angiopathy is poorly understood.

155 Imaging of cerebrovascular beta-amyloid (cerebral amyloid angiopathy) is complicated by the nearl

156 ta-protein (Abeta) deposition, also known as cerebral amyloid angiopathy, is a common pathological fe

157 e cerebral vasculature, a condition known as cerebral amyloid angiopathy, is increasingly recognized

158 nt of leptomeningeal, cortical and capillary cerebral amyloid angiopathy, large infarcts, lacunar inf

159 Seven pathologies-leptomeningeal cerebral amyloid angiopathy, large infarcts, lacunar inf

160 , atherosclerosis, arteriolar sclerosis, and cerebral amyloid angiopathy), Lewy bodies, transactive r

161 ic underlying microvascular abnormalities of cerebral amyloid angiopathy (lobar structures) and hyper

162 with microbleeds in locations suggestive of cerebral amyloid angiopathy (lobar with or without cereb

163 Although severe small vessel disease or cerebral amyloid angiopathy may contribute in some cases

164 t of treatment), without adversely affecting cerebral amyloid angiopathy, microhemorrhages, myelinati

165 ded moderate/severe occipital leptomeningeal cerebral amyloid angiopathy, moderate/severe arteriolosc

166 We hypothesized that in patients with cerebral amyloid angiopathy, multiple small spatially di

167 patients with severe small vessel disease or cerebral amyloid angiopathy, neither VEGF nor MAG:PLP1 c

168 ctures may damage the brain and give rise to cerebral amyloid angiopathy, neuronal dysfunction, and c

169 Cerebral amyloid angiopathy, non-neuritic and perivascul

170 The term 'cerebral amyloid angiopathy' now encompasses not only a

171 noreactivity (IR) is abundant in plaques and cerebral amyloid angiopathy of AD and Down syndrome pati

172 N) familial forms of Alzheimer's disease and cerebral amyloid angiopathy on the structure of the 21-3

173 al vascular pathology (small vessel disease, cerebral amyloid angiopathy or VWF).

174 Moreover, depletion of fibrinogen lessened cerebral amyloid angiopathy pathology and reduced cognit

175 By contrast, atherosclerosis and cerebral amyloid angiopathy pathology were associated wi

176 amyloid phase, but not Braak tangle stage or cerebral amyloid angiopathy predicted (11)C-Pittsburgh c

177 in the PrP gene (PRNP), associated with PrP cerebral amyloid angiopathy (PrP-CAA) and Gerstmann-Stra

178 thies; we propose to name this phenotype PrP cerebral amyloid angiopathy (PrP-CAA).

179 cal filaments tau neurofibrillary tangle and cerebral amyloid angiopathy ratings in the whole sample

180 examined the relationship between markers of cerebral amyloid angiopathy-related brain injury, networ

181 DNA from 94 unrelated patients with sporadic cerebral amyloid angiopathy-related hemorrhage found no

182 However, their contribution to cerebral amyloid angiopathy-related hemorrhage remains u

183 Cerebral amyloid angiopathy-related inflammation (CAA-ri

184 Cerebral amyloid angiopathy-related inflammation (CAA-ri

185 d imaging lesions was 9/39 (23%) in probable cerebral amyloid angiopathy-related intracerebral haemor

186 morrhage, and are three times more common in cerebral amyloid angiopathy-related intracerebral haemor

187 cerebral amyloid angiopathy and exacerbated cerebral amyloid angiopathy-related microhemorrhage in A

188 .5 [1.5-3.7]), and they had a higher risk of cerebral amyloid angiopathy (RR 6.6, 1.5-29.6).

189 p = 0.037; OR, 2.48; 95% CI, 1.06-5.82), and cerebral amyloid angiopathy severity (p = 0.032; OR, 4.1

190 d more cortical amyloid-beta plaque load and cerebral amyloid angiopathy than early disease onset and

191 o at risk of intracerebral hemorrhage due to cerebral amyloid angiopathy, the result of beta-amyloid

192 he structural brain network in patients with cerebral amyloid angiopathy to healthy control subjects

193 We used transgenic mice with prominent cerebral amyloid angiopathy to investigate the ability o

194 Many of the candidate outcomes for cerebral amyloid angiopathy trials are probably applicab

195 osited in blood vessels from subjects having cerebral amyloid angiopathy was 90 degrees out of phase

196 e brains of APP/PS1 and APP/PS1/AI mice, but cerebral amyloid angiopathy was reduced in APP/PS1/AI mi

197 ntly higher levels of hippocampal Abeta, and cerebral amyloid angiopathy was significantly more commo

198 To examine the effect of Apoa-I deletion on cerebral amyloid angiopathy, we measured insoluble Abeta

199 latter could be, at least partly, related to cerebral amyloid angiopathy, which belongs to the contin

200 centrum semi-ovale have been associated with cerebral amyloid angiopathy, while those in the basal ga

201 statin C amyloids cause a hereditary form of cerebral amyloid angiopathy whilst cystatin B aggregates

202 l examination of the proband revealed severe cerebral amyloid angiopathy, widespread neurofibrillary

203 (Abeta) sequence develop severe early-onset cerebral amyloid angiopathy with some of the related var