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1 ird, anti-ROS therapy attenuates CAA-related microhemorrhage.
2 -induced vessel dysfunction, and CAA-related microhemorrhage.
3 rance of pre-existing plaque without causing microhemorrhage.
4 onse leading to vasogenic edema and cerebral microhemorrhage.
5 oid but increase VAbeta and the incidence of microhemorrhage.
6 luding brain T cell infiltration or cerebral microhemorrhage.
7 taining, and occasionally presented signs of microhemorrhage.
8 ith certain anti-Abeta antibodies can induce microhemorrhage.
9  age, and there was little to no evidence of microhemorrhage.
10 onal risk for individuals APOE-e4(+) or with microhemorrhage.
11 sociated with reductions in microgliosis and microhemorrhages.
12 ion of the blood-brain barrier, and cerebral microhemorrhages.
13 sease model without inducing microgliosis or microhemorrhages.
14  as CNS T cell or macrophage infiltration or microhemorrhages.
15 gliosis, and the vaccination did not lead to microhemorrhages.
16 hemorrhage, or intraparenchymal white matter microhemorrhages.
17  a marked increase in the number of cerebral microhemorrhages.
18 enous thrombosis (1.4%), eight with multiple microhemorrhages (11.3%), 22 with perfusion abnormalitie
19 ility maps (mean +/- standard deviation, 9.8 microhemorrhages +/- 12.8 vs 13.7 microhemorrhages +/- 1
20 ation, 9.8 microhemorrhages +/- 12.8 vs 13.7 microhemorrhages +/- 16.6; P = .019).
21 ity mapping-derived quantitative measures of microhemorrhages all decreased over time, suggesting tha
22 ir higher mortality is likely not due to the microhemorrhages alone.
23 ity mapping-derived quantitative measures of microhemorrhages also decreased over time: -0.85 mm(3) p
24                                         ARIA-microhemorrhage and ARIA-superficial siderosis occurred
25 association between the presence of vascular microhemorrhage and branched dilated microvessels in the
26 imaging abnormalities with edema or cerebral microhemorrhage and no evidence of central nervous syste
27 A during the study period, 44 had at least 1 microhemorrhage and/or superficial siderosis before init
28 E (edema and/or sulcal effusion) and ARIA-H (microhemorrhage and/or superficial siderosis) independen
29 es of ARIA-edema/effusions (ARIA-E) and ARIA-microhemorrhages and hemosiderin deposition (ARIA-H) wer
30 al and symmetric cerebral lesions, including microhemorrhages and hyperintensities on fluid-attenuate
31         In contrast, HAE-4 did not stimulate microhemorrhages and instead rescued CAA-induced cerebro
32  hemosiderin deposits, including parenchymal microhemorrhages and leptomeningeal superficial siderosi
33                                The number of microhemorrhages and quantitative susceptibility mapping
34 cular phenotype in the lung including edema, microhemorrhage, and vascular congestion, increased F-ac
35 nd 4) the presence of lactate with necrosis, microhemorrhages, and edema (r = 0.996, P < 0.0001 in th
36 tensity volume (WMH), silent brain infarcts, microhemorrhages, and hippocampus volume across groups b
37 ve rat brains detected cerebral hemorrhages, microhemorrhages, and ischemia with middle cerebral arte
38  hemorrhagic infarctions, neuronal ischemia, microhemorrhages, and microvascular alterations suggests
39 microangiopathies, including microaneurysms, microhemorrhages, and nerve layer infarcts known as cott
40 sis for the association of ischemic lesions, microhemorrhages, and strokes in humans.
41 ormalities, acute ischemic lesions, multiple microhemorrhages, and white matter-enhancing lesions.
42 r hyperintensities, lacunar infarctions, and microhemorrhages), APOE4 genotype (apolipoprotein E gene
43 sive cell mediated inflammation and cerebral microhemorrhages are two forms of toxicity which can occ
44  30.4]; p = 0.055), as were individuals with microhemorrhage at baseline (OR = 13.7, CI[1.2, 163.2];
45 brain were present, including microinfarcts, microhemorrhages, bland angiopathy, thrombotic angiopath
46             Here, we show neuroinflammation, microhemorrhages, brain hypoxia, and neuropathology that
47 the leakage of blood-brain barrier (BBB) and microhemorrhage caused by IME insertions contribute to i
48 ationship between gut dysbiosis and cerebral microhemorrhages (CMH) in young and aged CKD mice (3 vs.
49                                     Cerebral microhemorrhages (CMHs) are associated with cerebrovascu
50 rosis count: HR, 1.9; 95% CI, 1.3-2.6; total microhemorrhage count: HR, 1.3; 95% CI, 1.0-1.5) may be
51           T2-weighted hyperintense areas and microhemorrhages did not collocate by visual inspection.
52  mice developed multifocal brain parenchymal microhemorrhages during infection.
53 cerebellar edema formation without affecting microhemorrhage formation or blood-brain barrier permeab
54                      An identical pattern of microhemorrhages has previously been described in mounta
55 te cerebral amyloid angiopathy (CAA)-related microhemorrhage in a transgenic animal model.
56 was observed in CAA-vessels with evidence of microhemorrhage in aged APPsw transgenic mice, but not d
57 l amyloid but increased vascular amyloid and microhemorrhage in amyloid precursor protein (APP) trans
58 cerbated cerebral amyloid angiopathy-related microhemorrhage in APP23/ABCA1-/- mice.
59 , FUS-BBBD did not increase the incidence of microhemorrhage in mice with or without 07/2a mAb treatm
60   In the healthy GC there was no evidence of microhemorrhage in participants that had only simple cap
61  chronic, passive immunization on VAbeta and microhemorrhage in PDAPP mice by comparing antibodies wi
62 itary abnormalities, with a low incidence of microhemorrhage in the chronic phase.
63 xic and vasogenic cerebral edema followed by microhemorrhages in 2 adult UK cases, comparing them wit
64 vation in female Tg mice, modestly increased microhemorrhages in 50 cGy irradiated male WT mice, and
65                                        Brain microhemorrhages in CM suggest a clotting disorder, but
66 10 of 11 patients) and (b) multiple punctate microhemorrhages in juxtacortical and callosal white mat
67 5%), and extensive and isolated white matter microhemorrhages in nine of 37 patients (24%; 95% CI: 10
68                   Vasculitis associated with microhemorrhages in the brain dominates the pathological
69          Post-mortem MRI confirmed extensive microhemorrhages in the temporal, parietal and occipital
70 e effects, including meningoencephalitis and microhemorrhage, in WT mice and a transgenic mouse model
71                 GzmB deficiency also reduced microhemorrhage, inflammation, and fibroblast accumulati
72                              Occult cerebral microhemorrhage is common in patients with moderate to s
73 existing plaque but manifested a significant microhemorrhage liability.
74                          Conclusion Cerebral microhemorrhage load is associated spatially with tau ac
75 ce indicates an association between cerebral microhemorrhages (MHs) and amyloid beta accumulation in
76 rsely affecting cerebral amyloid angiopathy, microhemorrhages, myelination, or neuromuscular function
77 revealed brain infarctions (n = 12/23, 52%), microhemorrhages (n = 10/23, 44%), and inflammatory proc
78 d cerebral cortical hemorrhagic infarctions, microhemorrhages, neuronal ischemia, and microvascular i
79                               Comparisons of microhemorrhage number, size, and magnetic susceptibilit
80 he increased vascular amyloid deposition and microhemorrhage observed with unmodified IgG.
81                     Safety (lack of edema or microhemorrhage) of FUS was also improved during alert c
82    Seventy-seven percent (451 of 585) of the microhemorrhages on susceptibility-weighted images had a
83                                    ARIA with microhemorrhage or hemosiderosis occurred in 29.2% of th
84 e patients, MRI of the brain showed multiple microhemorrhages predominantly in the splenium of the co
85 OE epsilon4 allele number, greater number of microhemorrhages, presence of cortical superficial sider
86 pecificity and exposure levels on VAbeta and microhemorrhage rates have not been well established, no
87 s were analyzed to determine the presence of microhemorrhage related to branched dilated microvessels
88 urthermore, the anti-AB antibody exacerbated microhemorrhage severity, which highly correlated with r
89 face were often abnormal morphologically and microhemorrhages sometimes occurred.
90  further highlights a role of microinfarcts, microhemorrhages, strategic white matter tracts, loss of
91                              The presence of microhemorrhages, tortuous capillaries, dilated capillar
92 ce for the detection and characterization of microhemorrhages, venous structures and other sources of
93 infarct, subcortical gray matter injury, and microhemorrhage was associated with neurocognitive outco
94                             The incidence of microhemorrhage was increased in the high-dose 3D6 group
95                                              Microhemorrhage was observed in all vaccinated APPSw/NOS
96 tion of the sonobiopsy parameters, no excess microhemorrhage was observed in the treated cerebral hem
97                                              Microhemorrhage was present in the majority of participa
98                The longitudinal evolution of microhemorrhages was monitored in a subset of patients b
99 r 266 or 3D6 would exacerbate CAA-associated microhemorrhage, we treated aged PDAPP mice with either
100                                   VAbeta and microhemorrhage were assessed using concomitant Abeta im
101 on, neurodegeneration, neuroinflammation and microhemorrhage were found in the brains of the parabiot
102 phalopathy and juxtacortical and/or callosal microhemorrhages were brain imaging features in critical
103                                              Microhemorrhages were found in the nail bed of 65.1% of
104       In these patients, a smaller number of microhemorrhages were identified at follow-up imaging co
105                                              Microhemorrhages were identified by two radiologists ind
106             Among the 603 patients, cerebral microhemorrhages were identified in 43 patients, with si
107                                     Further, microhemorrhages were increased by 3D6 in the APP/PS1/co
108                  These studies revealed that microhemorrhages were more numerous in mice lacking Cx43
109                                     Cerebral microhemorrhages were observed in a small percentage of
110 ficantly fewer vascular amyloid deposits and microhemorrhages were observed in mice administered the
111 the incidence and severity of CAA-associated microhemorrhage when PDAPP transgenic mice were treated
112        We found that CSD for 14 days induced microhemorrhages where plasma fibrinogen leaked into per
113  can significantly mitigate the incidence of microhemorrhage while still preventing or reducing VAbet
114 rhage, active and prior stroke, mass effect, microhemorrhages, white matter changes, microvascular di
115                          HIP rats have brain microhemorrhages, white matter injury, and neurologic de
116                             This resulted in microhemorrhages with release of neurotoxic hemoglobin-d
117 age-dependent increase in CAA and associated microhemorrhage, with the APPsw model having an earlier

 
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