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1 of 'familial cerebellar ataxia with amyloid angiopathy'.
2 d enhancing astrocytosis or cerebral amyloid angiopathy.
3 le lobar CMBs suggestive of cerebral amyloid angiopathy.
4 rly for lobar hemorrhages related to amyloid angiopathy.
5 se gene variants on risk of cerebral amyloid angiopathy.
6 ing Alzheimer's disease and cerebral amyloid angiopathy.
7 to significantly increased cerebral amyloid angiopathy.
8 ating neuroinflammation and cerebral amyloid angiopathy.
9 ial dissection, vasculitis, or postvaricella angiopathy.
10 amyloid diseases including cerebral amyloid angiopathy.
11 ated with familial forms of cerebral amyloid angiopathy.
12 lzheimer's disease (AD) and cerebral amyloid angiopathy.
13 myloid disease known as PrP cerebral amyloid angiopathy.
14 en, and 5) led to the development of amyloid angiopathy.
15 id deposits associated with cerebral amyloid angiopathy.
16 se familial forms of AD and cerebral amyloid angiopathy.
17 eningoencephalic vessels as cerebral amyloid angiopathy.
18 wo pathways associated with cerebral amyloid angiopathy.
19 rentially mature senile plaques, and amyloid angiopathy.
20 ith Alzheimer's disease and cerebral amyloid angiopathy.
21 cored plaques, and mild or moderate amyloid angiopathy.
22 lay onset and retard progression of diabetic angiopathy.
23 yloid disease, hereditary cystatin C amyloid angiopathy.
24 d blood vessels severely affected by amyloid angiopathy.
25 ular degeneration in AD and cerebral amyloid angiopathy.
26 s causing familial forms of cerebral amyloid angiopathy.
27 logical hallmarks of AD and cerebral amyloid angiopathy.
28 morrhage is the hallmark of cerebral amyloid angiopathy.
29 o be associated with the severity of amyloid angiopathy.
30 d Alzheimer's disease despite severe amyloid angiopathy.
31 ontributes significantly to cerebral amyloid angiopathy.
32 od vessels of patients with cerebral amyloid angiopathy.
33 nic Alzheimer's disease and cerebral amyloid angiopathy.
34 t not Braak tangle stage or cerebral amyloid angiopathy.
35 th a particular emphasis on cerebral amyloid angiopathy.
36 gy of Alzheimer's disease and cerebral Abeta angiopathy.
37 Willis atherosclerosis, or cerebral amyloid angiopathy.
38 rominent Abeta38-containing cerebral amyloid angiopathy.
39 total plasma cholesterol or cerebral amyloid angiopathy.
40 Alzheimer disease but can also cause amyloid angiopathy.
41 ystem and the importance of cerebral amyloid angiopathy.
42 ry was significantly associated with amyloid angiopathy.
44 nted patients with probable cerebral amyloid angiopathy (69 +/- 10 years) and 29 similar aged control
45 merging as a key feature of cerebral amyloid angiopathy, a common and important age-related cerebral
47 ons of Iowa-type hereditary cerebral amyloid angiopathy, a form of the disorder with little or no pla
48 yperphosphorylated tau; and cerebral amyloid angiopathy, a microangiopathy affecting both cerebral co
49 th muscle cells (SMCs) isolated from amyloid-angiopathy affected brain vessels accumulate intracellul
51 of candidate treatments for cerebral amyloid angiopathy, an untreatable cause of haemorrhagic stroke
52 ding a clue to the known association between angiopathies and diabetes and implying new gene candidat
53 wild-type mice, and formed cerebral amyloid angiopathy and Abeta plaques after a 12-month period of
54 ation, wound healing, scarring, angiogenesis/angiopathy and basement membrane physiology, as well as
55 0 and Abeta42 levels and accelerates amyloid angiopathy and cerebral beta-amyloidosis by diminishing
57 walls was characteristic of cerebral amyloid angiopathy and did not co-localize with prion protein de
59 ably increased the level of cerebral amyloid angiopathy and exacerbated cerebral amyloid angiopathy-r
61 role in the pathogenesis of cerebral amyloid angiopathy and in the accumulation of Abeta in the brain
63 ears) with pathology-proven cerebral amyloid angiopathy and multiple microbleeds on in vivo clinical
66 lationship between advanced cerebral amyloid angiopathy and neurologic dysfunction and that such larg
67 ved in an inherited form of cerebral amyloid angiopathy and readily form amyloid fibrils in vitro.
68 etween complement dysregulation and systemic angiopathy and suggest that complement activation may co
69 tter and in artery walls as cerebral amyloid angiopathy and tau protein accumulates as neurofibrillar
70 to be in part a protein elimination failure angiopathy and that this dysfunction is a feed-forward p
71 here a striking correlation between amyloid angiopathy and the location of mutation in PS-1 linked A
73 not Abeta42) levels, cerebrovascular amyloid angiopathy, and ApoE4 allele frequency were all highly c
75 been linked to HF through perfusion defects, angiopathy, and inflammation, whether patients with AD p
77 ic for microhaemorrhages in cerebral amyloid angiopathy, and that increasing the resolution of magnet
78 bleeds and microinfarcts in cerebral amyloid angiopathy, and to explore the pathological burden that
79 of Alzheimer's disease and cerebral amyloid angiopathy, APOE has been studied in other neurological
80 filament formation, cerebrovascular amyloid angiopathy, apolipoprotein E (ApoE) allotype, and synapt
81 e pathophysiological level, cerebral amyloid angiopathy appears to be in part a protein elimination f
82 roimaging markers of severe cerebral amyloid angiopathy are cortical microbleeds and microinfarcts.
83 ninvasively detect isolated cerebral amyloid angiopathy before overt signs of tissue damage such as h
84 viously designated familial cerebral amyloid angiopathy-British type, is an autosomal dominant disord
85 uction of Abeta plaques and cerebral amyloid angiopathy burden and a reduction of the total brain lev
87 ge, and pathologically showed severe amyloid angiopathy but only rare neuritic senile plaques and neu
90 f 190 AD subjects exhibited cerebral amyloid angiopathy (CAA) and other frequently associated lesions
92 itis of the CNS (PACNS) and cerebral amyloid angiopathy (CAA) are unusual vasculopathies generally re
93 th pathologically diagnosed cerebral amyloid angiopathy (CAA) for evidence of an inflammatory respons
96 ebral haemorrhage (ICH) and cerebral amyloid angiopathy (CAA) in a systematic review of published neu
97 n selectively induces acute cerebral amyloid angiopathy (CAA) in neonatally-injected transgenic CRND8
101 orm of neuritic plaques and cerebral amyloid angiopathy (CAA) is a key feature of Alzheimer's disease
103 emorrhagic stroke, advanced cerebral amyloid angiopathy (CAA) is also associated with ischemic lesion
113 ajor trends in the field of cerebral amyloid angiopathy (CAA) over six decades, from 1954 to 2014, us
115 but has no direct effect on cerebral amyloid angiopathy (CAA) severity, whereas APOEepsilon4 is assoc
116 ngles, neuropil threads and cerebral amyloid angiopathy (CAA) similar to unimmunized AD, but lacked p
117 pertensive arteriopathy and cerebral amyloid angiopathy (CAA)) is an important cause of spontaneous i
118 ve cerebrovascular amyloid (cerebral amyloid angiopathy (CAA), and cardiovascular risk factors increa
121 beta), a condition known as cerebral amyloid angiopathy (CAA), is a common pathological feature of pa
122 ssels, a condition known as cerebral amyloid angiopathy (CAA), is a key pathological feature of Alzhe
123 beta), a condition known as cerebral amyloid angiopathy (CAA), is a key pathological feature of Alzhe
124 lls of brain blood vessels, cerebral amyloid angiopathy (CAA), is common in patients with Alzheimer's
125 notype in hemorrhage due to cerebral amyloid angiopathy (CAA), it is unclear whether apoE genotype in
126 cerebral arteries, known as cerebral amyloid angiopathy (CAA), occurs both in the setting of Alzheime
127 w (Tg2576) mice, a model of cerebral amyloid angiopathy (CAA), suggesting a pivotal role for Bim in A
129 is increasing evidence that cerebral amyloid angiopathy (CAA), which itself can cause haemorrhage (CA
131 been reported to exacerbate cerebral amyloid angiopathy (CAA)-related microhemorrhage in a transgenic
148 e cerebrovasculature [i.e., cerebral amyloid angiopathy (CAA)] and a heightened risk of micro-hemorrh
150 ascular amyloid deposition (cerebral amyloid angiopathy [CAA]) but not in patients with high parenchy
151 deposition of beta-amyloid (cerebral amyloid angiopathy [CAA]) is a major cause of hemorrhagic stroke
152 ar beta-amyloid deposition (cerebral amyloid angiopathy, CAA) is associated with cerebral microbleeds
153 tential outcome markers for cerebral amyloid angiopathy can be measured against the ideal criteria of
154 e wall of cerebral vessels (cerebral amyloid angiopathy), can lead to weakness and rupture of the ves
157 olipoprotein E subtypes and cerebral amyloid angiopathy; deep intracerebral hemorrhage and the potent
158 has on reducing the rate of cerebral amyloid angiopathy deposition and restoring cerebral vascular he
159 ates atherosclerotic progression, peripheral angiopathy development, and arterial hypertension, all o
162 , several familial forms of cerebral amyloid angiopathy exist including the Dutch (E22Q) and Iowa (D2
166 CMBs related to symptomatic cerebral amyloid angiopathy have abnormal vascular reactivity and cerebra
168 P23-144, associated with a heritable amyloid angiopathy, have previously been shown to contain a comp
169 s include severe widespread cerebral amyloid angiopathy, hippocampal plaques, and neurofibrillary tan
173 sence of severe or moderately severe amyloid angiopathy in five family members with clinical dementia
174 ffuse and focal plaques and cerebral amyloid angiopathy in humans and nonhuman primates, whereas it i
176 ase in the number of new plaques and amyloid angiopathy in the area immediately surrounding the infar
179 xtent of leptomeningeal and cortical amyloid angiopathy in the normal aged subjects and in the AD pat
180 rphologic features and the role of choroidal angiopathy in various disease states that, in the future
181 ypertensive arteriopathy or cerebral amyloid angiopathy) in a multicentre, cross-sectional study.
182 ial Alzheimer's disease and cerebral amyloid angiopathy, in which patients develop neuritic plaques a
183 r Abeta plaques versus cerebral beta-amyloid angiopathy, indicating that different amyloid types and
187 lts suggest that underlying cerebral amyloid angiopathy is a contributing factor to the occurrence of
190 consequences; for example, cerebral amyloid angiopathy is an important cause of haemorrhagic stroke.
192 sgenic mouse model of human cerebral amyloid angiopathy is characterized by age-dependent cerebrovasc
193 From a clinical standpoint, cerebral amyloid angiopathy is characterized by individual focal lesions
197 the presence and burden of cerebral amyloid angiopathy is particularly important when planning to st
199 rebrovascular beta-amyloid (cerebral amyloid angiopathy) is complicated by the nearly universal overl
200 ) deposition, also known as cerebral amyloid angiopathy, is a common pathological feature of Alzheime
201 ature, a condition known as cerebral amyloid angiopathy, is increasingly recognized as an important c
202 eal, cortical and capillary cerebral amyloid angiopathy, large infarcts, lacunar infarcts, microhaemo
203 pathologies-leptomeningeal cerebral amyloid angiopathy, large infarcts, lacunar infarcts, microinfar
204 , arteriolar sclerosis, and cerebral amyloid angiopathy), Lewy bodies, transactive response DNA-bindi
205 ques, gross infarcts, microinfarcts, amyloid angiopathy, Lewy bodies, APOE epsilon4 presence, and cli
206 rovascular abnormalities of cerebral amyloid angiopathy (lobar structures) and hypertensive vasculopa
207 in locations suggestive of cerebral amyloid angiopathy (lobar with or without cerebellar microbleeds
209 ere small vessel disease or cerebral amyloid angiopathy may contribute in some cases, abnormal vascul
210 without adversely affecting cerebral amyloid angiopathy, microhemorrhages, myelination, or neuromuscu
211 re occipital leptomeningeal cerebral amyloid angiopathy, moderate/severe arteriolosclerosis in occipi
212 in in an age-dependent manner, forms amyloid angiopathy morphologically similar to that seen in the h
213 sized that in patients with cerebral amyloid angiopathy, multiple small spatially distributed lesions
214 ere small vessel disease or cerebral amyloid angiopathy, neither VEGF nor MAG:PLP1 correlated signifi
215 ephaly, small vessel disease, and hereditary angiopathy, nephropathy, aneurysms, and cramps (HANAC) s
216 the brain and give rise to cerebral amyloid angiopathy, neuronal dysfunction, and cellular toxicity.
218 ic lesions neither halted progression of the angiopathy nor provided appreciable benefit at the 24-mo
220 is abundant in plaques and cerebral amyloid angiopathy of AD and Down syndrome patients, colocalizin
222 nd in the vasculature (cerebral beta-amyloid angiopathy) of beta-amyloid precursor protein transgenic
223 of Alzheimer's disease and cerebral amyloid angiopathy on the structure of the 21-30 fragment of the
225 ial Alzheimer's disease, congophilic amyloid angiopathy, or hereditary cerebral hemorrhage with amylo
226 teriovenous shunts, biopsy-proven microrenal angiopathy, or thrombocytopenia and thus were diagnosed
227 n, generally, but also to facilitate amyloid angiopathy particularly in cases in which the mutation l
228 tion of fibrinogen lessened cerebral amyloid angiopathy pathology and reduced cognitive impairment in
229 ntrast, atherosclerosis and cerebral amyloid angiopathy pathology were associated with a lower level
230 protein deposits in human cystatin C amyloid angiopathy patients have also been found in tissues outs
231 t not Braak tangle stage or cerebral amyloid angiopathy predicted (11)C-Pittsburgh compound B standar
232 (PRNP), associated with PrP cerebral amyloid angiopathy (PrP-CAA) and Gerstmann-Straussler-Scheinker
234 neurofibrillary tangle and cerebral amyloid angiopathy ratings in the whole sample and within indivi
235 tionship between markers of cerebral amyloid angiopathy-related brain injury, network efficiency, and
236 ated patients with sporadic cerebral amyloid angiopathy-related hemorrhage found no other instances o
240 three times more common in cerebral amyloid angiopathy-related intracerebral haemorrhage than in oth
241 was 9/39 (23%) in probable cerebral amyloid angiopathy-related intracerebral haemorrhage versus 6/75
242 angiopathy and exacerbated cerebral amyloid angiopathy-related microhemorrhage in APP23/ABCA1-/- mic
243 e who were previously enrolled in the Bypass Angiopathy Revascularization Investigation to compare in
245 48; 95% CI, 1.06-5.82), and cerebral amyloid angiopathy severity (p = 0.032; OR, 4.16; 95% CI, 1.13-1
246 dense-core (senile) plaques, in the amyloid angiopathy surrounding diseased blood vessels, and in th
247 myloid-beta plaque load and cerebral amyloid angiopathy than early disease onset and tremor dominant
248 s may facilitate development of beta-amyloid angiopathy that is more frequent in varepsilon 4/ vareps
250 d from brain blood vessels with amyloid-beta angiopathy - the cells that were shown previously to acc
251 acerebral hemorrhage due to cerebral amyloid angiopathy, the result of beta-amyloid deposition in cer
252 uding microinfarcts, microhemorrhages, bland angiopathy, thrombotic angiopathy with platelet and fibr
254 in network in patients with cerebral amyloid angiopathy to healthy control subjects and examined the
255 nsgenic mice with prominent cerebral amyloid angiopathy to investigate the ability of ponezumab, an a
256 the candidate outcomes for cerebral amyloid angiopathy trials are probably applicable also to other
257 essels from subjects having cerebral amyloid angiopathy was 90 degrees out of phase from that in the
260 s of hippocampal Abeta, and cerebral amyloid angiopathy was significantly more common compared with P
261 ffect of Apoa-I deletion on cerebral amyloid angiopathy, we measured insoluble Abeta isolated from ce
263 at least partly, related to cerebral amyloid angiopathy, which belongs to the continuum of cerebral s
264 e have been associated with cerebral amyloid angiopathy, while those in the basal ganglia have been a
265 cause a hereditary form of cerebral amyloid angiopathy whilst cystatin B aggregates are found in cas
266 the proband revealed severe cerebral amyloid angiopathy, widespread neurofibrillary tangles, and unus
267 n with loss of cholinergic neurons, gliosis, angiopathy with mononuclear cell cuffing, progressive ca
268 isease, familial porencephaly and hereditary angiopathy with nephropathy aneurysm and cramps (HANAC)
269 crohemorrhages, bland angiopathy, thrombotic angiopathy with platelet and fibrin thrombi, neuronal ne
270 develop severe early-onset cerebral amyloid angiopathy with some of the related variants manifesting
271 e expected increase in prevalence of amyloid angiopathy with the ageing population, suggest that, in
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