ライフサイエンスコーパス: BBB

1 BBB-associated neuropathogenesis in HIV-infected patient

2 st of the metabotropic glutamate receptor-1 (BBB-mGluR1), a widely abundant CNS target, or an IgG tha

3 The 3D BBB models were constructed with human brain endothelial

4 crossing antibody fragment FC5 was used as a BBB carrier.

5 as a potential substitute for pericytes in a BBB model.

6 aracterized bispecific antibodies in which a BBB-crossing antibody fragment FC5 was used as a BBB car

7 is system work synergistically to accentuate BBB-specific attributes-permitting the analysis of compl

8 neurological diseases in which there is also BBB malfunction, and highlighting current disease-modify

9 vous system (CNS) through regions of altered BBB permeability - for example, into circumventricular o

10 gs suggest that chronic social stress alters BBB integrity through loss of tight junction protein Cld

11 ole of human BCRP in limiting absorption and BBB penetration of substrate compounds and to investigat

12 ients at emergency department admission, and BBB permeability was assessed at 24 hour follow up via p

13 quired for normal forebrain angiogenesis and BBB function in mouse embryos, but the role of this rece

14 Massive neuronal death and BBB leakage indicate brain damage, which is further supp

15 ays a role in TBI-triggered inflammation and BBB breakdown.

16 ere protected from the neuroinflammatory and BBB permeability effects of MWCNTs.

17 y required for endothelial Wnt signaling and BBB integrity under pathological conditions in adult mic

18 ed in an ex vivo model, free of vascular and BBB components.

19 ma TNF-alpha and IL-1beta levels, as well as BBB permeability, were significantly increased in nAChRa

20 istology, and for EBD fluorescence to assess BBB permeability.

21 post-thrombolysis ICH, but rapidly assessing BBB damage before tPA administration is highly challengi

22 Restoration of the blood-brain barrier (BBB) after antiangiogenic therapy of gliomas with bevaci

23 tic in order to fortify blood brain barrier (BBB) and dampen leukocyte extravasation into CNS during

24 these Abs to cross the blood-brain barrier (BBB) and induce neuropathology remain unresolved.

25 ause of the presence of blood-brain barrier (BBB) and the blood-tumor barrier (BTB).

26 The blood-brain barrier (BBB) and the glia limitans serve to prevent the migratio

27 across the endothelial blood-brain barrier (BBB) and then across the astrocytic glia limitans (GL).

28 b poorly penetrates the blood-brain barrier (BBB) because of efflux transport by P-glycoprotein (ABCB

29 Blood-brain barrier (BBB) breakdown and the associated microvascular hyperper

30 Although blood-brain barrier (BBB) compromise is central to the etiology of diverse ce

31 The blood-brain barrier (BBB) consists of endothelial cells, astrocytes, and peri

32 However, the blood-brain barrier (BBB) controls TH entry into the brain, and reduced TH av

33 Early blood brain barrier (BBB) damage is the major risk factor for fatal post-thro

34 m consequences of early blood-brain barrier (BBB) disruption after cerebral ischaemic/reperfusion (I/

35 Blood-brain barrier (BBB) disruption alters the composition of the brain micr

36 Blood brain barrier (BBB) disruption due to SBI can exacerbate brain edema in

37 Blood-brain barrier (BBB) disruption has long been recognised as an important

38 s (MB) causes localized blood-brain barrier (BBB) disruption that is currently being advocated for in

39 dictive for post-stroke blood brain barrier (BBB) disruption.

40 recruitment across the blood brain barrier (BBB) during neuroinflammation has been the least explore

41 ndothelial cells of the blood-brain barrier (BBB) during neurotropic viral infection.

42 ts a potential role for blood-brain barrier (BBB) dysfunction in the development of post-injury epile

43 ransport studies across blood-brain barrier (BBB) endothelial cells, at circulating concentrations, p

44 rug delivery across the blood-brain barrier (BBB) for treating many neurological disorders.

45 pathway is crucial for blood-brain barrier (BBB) formation in brain endothelial cells.

46 mechanism that governs blood-brain barrier (BBB) function in the rat cerebral cortex, and, by using

47 ics and consequences on blood-brain barrier (BBB) function remain poorly characterized.

48 ural ligands across the blood-brain barrier (BBB) has been identified as a means for antibody deliver

49 species (ROS) propagate blood-brain barrier (BBB) hyperpermeability and inflammation following TBI.

50 ficiently penetrant the blood-brain barrier (BBB) in different animal species and highly efficacious

51 Breakdown of the blood-brain barrier (BBB) in response to traumatic brain injury (TBI) allows

52 )-3 readily crosses the blood-brain barrier (BBB) in rodents and selectively binds to TrkB/C receptor

53 Disruption of the blood-brain barrier (BBB) is a defining and early feature of multiple scleros

54 The blood-brain barrier (BBB) is one of the most essential protection mechanisms

55 The blood-brain barrier (BBB) keeps neurotoxic plasma-derived components, cells,

56 ion and function at the blood-brain barrier (BBB) level remain unknown.

57 loss of Norrin, impairs blood-brain barrier (BBB) maintenance.

58 es in an in vitro human blood-brain barrier (BBB) model.

59 Culture-based blood-brain barrier (BBB) models are crucial tools to enable rapid screening

60 s in the context of the blood-brain barrier (BBB) pathology.

61 stance and insufficient blood-brain barrier (BBB) penetration of chemotherapeutics.

62 model of depression, on blood-brain barrier (BBB) permeability and infiltration of peripheral immune

63 tablishment of abnormal blood-brain barrier (BBB) permeability and its relationship to neuropathogene

64 etermined that areas of blood-brain barrier (BBB) permeability colocalized with a reduction of the ce

65 The blood-brain barrier (BBB) protects the brain from inflammation but the mechan

66 The blood-brain barrier (BBB) provides a constant homeostatic brain environment t

67 s with the cells of the blood-brain barrier (BBB) remain poorly understood.

68 The blood-brain barrier (BBB) restricts the uptake of many neuro-therapeutic mole

69 sport system across the blood-brain barrier (BBB) to the brain where it acts on the hypothalamus rece

70 em (CNS) compromise the blood-brain barrier (BBB) via increased vascular permeability, with the magni

71 broad disruption of the blood-brain barrier (BBB) was observed across the capillary bed with the smal

72 nd the integrity of the blood-brain barrier (BBB) were monitored.

73 al trial on opening the blood-brain barrier (BBB) with magnetic resonance (MR) imaging-guided focused

74 s, the impedance of the blood brain barrier (BBB), and the lack of therapeutic agents that can select

75 eater disruption of the blood-brain barrier (BBB), higher brain viral loads, and higher brain inflamm

76 The Blood-Brain Barrier (BBB), known as the major hindrance, greatly limits thera

77 anoparticles across the blood-brain barrier (BBB), we observed that nanoparticles are able to enter t

78 d with disorders of the blood-brain barrier (BBB), which mainly consists of brain microvascular endot

79 lls forming part of the blood-brain barrier (BBB).

80 cates disruption of the blood-brain barrier (BBB).

81 ain is regulated by the blood-brain barrier (BBB).

82 icroenvironments at the blood-brain barrier (BBB).

83 tive barrier termed the blood-brain barrier (BBB).

84 temporarily opening the blood-brain barrier (BBB).

85 protected by the intact blood-brain barrier (BBB).

86 se transport across the blood-brain barrier (BBB).

87 ect delivery inside the blood brain barrier (BBB).

88 tes permeability of the blood-brain barrier (BBB).

89 successfully bypass the blood-brain barrier (BBB).

90 beta and can cross the blood-brain barrier (BBB).

91 ood and penetrating the blood-brain barrier (BBB).

92 to maintain the normal blood-brain barrier (BBB).

93 sculature is a physical blood-brain barrier (BBB).

94 the brain, bypasses the blood-brain-barrier (BBB) and eliminates systemic side effects.

95 Blood brain-barrier (BBB) in vitro models have been widely reported in studie

96 Blood-Brain-Barrier (BBB) is a rigorous permeability barrier for maintaining

97 c acid (AIB), to assess blood-brain-barrier (BBB) permeability, following separate injections of levo

98 BBB involvement, we generated an iPSC-based BBB model of MCT8 deficiency, and we found that MCT8 was

99 lar level, the underlying mechanisms between BBB breakdown and neurodegeneration as a basis for devel

100 get for human CNS disorders characterized by BBB disruption.

101 from inflammation but the mechanisms causing BBB damage in CNS TB are uncharacterized.

102 nd on blood-brain barrier endothelial cells (BBB-ECs) that was previously shown to be involved in leu

103 Chronic BBB leakiness was associated with cognitive impairment,

104 The complex BBB microenvironment is reproduced in this system via ph

105 , endothelial receptor proteins that control BBB function are poorly defined.

106 skull porcine model, this study demonstrated BBB opening with a 230-kHz system in preparation for a c

107 they suggest that circumventing the diseased BBB to deliver active TH to the brain could be a viable

108 Blood-brain barrier disruption (BBB) and release of toxic blood molecules into the brain

109 opose the novel hypothesis that AngII-driven BBB breakdown constitutes a complementary mechanism by w

110 g computational methods usually predict drug BBB permeability from chemical structure and they genera

111 An early BBB breakdown and/or dysfunction have been shown in Alzh

112 al cells to suppress transcytosis and ensure BBB integrity.

113 Here, we examine BBB breakdown in animal models frequently used to study

114 extensive clinical usage, we aim to explore BBB permeability prediction from a new angle and introdu

115 nant brain tumors and effectively facilitate BBB closure in neurological disorders.

116 Slit2 may be beneficial for BBB protection during elective neurosurgeries.

117 as a basis for developing new therapies for BBB repair to control neurodegeneration.

118 during EAE/MS partially restores functional BBB integrity and limits immune cell infiltration into t

119 involved in creating rapid and heterogeneous BBB disruption in the capillary bed.

120 Among this series, 1b showed the highest BBB permeability (Pe = 16.4 x 10(-5) cm/s), probably as

121 lia of adult mice did not affect homeostatic BBB integrity, but resulted in BBB disruption and microv

122 However, BBB protective effects of Slit2 following SBI has not be

123 in nonhuman primates as a model of the human BBB.

124 zed the BBB spheroids to screen and identify BBB-penetrant cell-penetrating peptides (CPPs).

125 ted in a significant decrease (P = 0.004) in BBB permeability, as assessed by EBD fluorescence.

126 as associated with a comparative decrease in BBB leakage, inflammatory infiltration, and higher expre

127 Occludin in BBB pericytes decreased by 10% during the first 48 h aft

128 We review the changes that occur in BBB function and cerebral perfusion in patients with MS

129 on in neurodegenerative process, pitfalls in BBB measurements, and how targeting the BBB can influenc

130 t homeostatic BBB integrity, but resulted in BBB disruption and microvascular hemorrhage in mouse mod

131 catenin signaling plays an essential role in BBB formation and maintenance in healthy CNS, its role i

132 and maintenance in healthy CNS, its role in BBB repair in neurologic diseases such as MS remains unc

133 l flow-metabolism dissociation and increased BBB permeability are simultaneously induced by levodopa

134 armacological inhibition of Cyp1b1 increased BBB permeability for small molecular tracers, and Cyp1b1

135 it2 administered 1 h before injury increased BBB junction proteins, reduced BBB permeability, and dec

136 BB integrity parameters suggesting increased BBB permeability in aging rats.

137 erred extended neuroprotection via increased BBB integrity (elevated levels of tight-junction protein

138 Inhibition of Cyp1b1 in vivo increased BBB permeability being in line with its downregulation i

139 cludin and Claudin5, collectively indicating BBB dysfunction.

140 vide evidence that hyperfibrinolysis-induced BBB leakage is dependent on plasmin-mediated generation

141 ammatory marker transcription, MWCNT-induced BBB disruption and neuroinflammation were abrogated by p

142 t that recombinant Slit2 reduced SBI-induced BBB permeability, possibly by stabilizing BBB tight junc

143 arget of beta-catenin indirectly influencing BBB properties via its metabolic activity, and as a pote

144 We propose that CD8 T cells initiate BBB breakdown through perforin-mediated disruption of ti

145 Conversely, the intact BBB restricts efficient penetration of CNS-targeted drug

146 Importantly, BPN delivery across the intact BBB, just beyond the tumor edge, was also markedly incre

147 Interestingly, BBB disruption always goes hand-in-hand with hydrocephal

148 or glass implants, as well as increase local BBB permeability, increase macrophage activation, and de

149 can be ultimately responsible for localized BBB breakdown, and thus substantial changes in lesion to

150 in-5 in the mouse brain results in localized BBB disruption and behavioural changes.

151 tenin signaling is essential for maintaining BBB integrity and central nervous system homeostasis in

152 y important function of ALCAM in maintaining BBB integrity.

153 usly, the clinical potential of manipulating BBB permeability for neuroprotection and drug delivery i

154 ischemic cerebral microvessels and a massive BBB leakage at 4.5-hour post-ischemia.

155 content, high cellular uptake, and moderate BBB permeability renders these compounds promising boron

156 rol modality, real-time control of modulated BBB disruption with undetectable vascular damage remains

157 we report that self-assembling multicellular BBB spheroids display reproducible BBB features and func

158 te drug did not appreciably cross the mutant BBB.

159 rovascular unit and are essential for normal BBB function.

160 nses that are dependent on the disruption of BBB integrity.

161 xposure to TiO2 NPs and the dysregulation of BBB physiology associated with neuroinflammation and dec

162 ue was used to evaluate the effectiveness of BBB disruption, which was successful in all sessions.

163 CAM KO mice revealed a reduced expression of BBB junctional proteins.

164 din levels correlate well with the extent of BBB damage and thus may serve as a clinically relevant b

165 d occludin levels correlate to the extent of BBB damage using a rat model of ischemic stroke.

166 blastomas seems to be largely independent of BBB permeability and reflects the viability of tumor tis

167 t regulate BBB functions in HIV infection of BBB pericytes.

168 Levels of BBB opening, hemorrhage, and cavitation signal were meas

169 system displays comparatively low levels of BBB regulatory proteins, and is unable to discriminate b

170 n BMEC) (HBMEC) and in vivo (mice) models of BBB were used to dissect the role of alpha7 nAChR in up-

171 We showed an age-dependent modulation of BBB integrity parameters suggesting increased BBB permea

172 d thus be considered as potent regulators of BBB permeability and inflammation that influence leukocy

173 We discuss the role of BBB breakdown and dysfunction in neurodegenerative proce

174 However, the role of BBB breakdown in neurodegenerative disorders is still no

175 b in combination with six weekly sessions of BBB disruption using focused ultrasound.

176 Moreover, observations in terms of BBB permeability and brain inflammation underline age su

177 ve EAE was linked to the absence of ALCAM on BBB-ECs.

178 to investigate the effects of bevacizumab on BBB permeability and (18)F-FET uptake in a human xenogra

179 the BBB in the normal brain, their impact on BBB integrity during ischemia remains unclear.

180 ssessment, we need to evaluate the impact on BBB under realistic environmental conditions and take in

181 embly, attenuates both early- and late-onset BBB impairment, and improves long-term histological and

182 did not have increased brain viral loads or BBB disruption.

183 of nNOS inhibitors as measured by both PAMPA-BBB and Caco-2 assays.

184 rug 1r showed good permeability in the PAMPA-BBB model and high in vitro antioxidant activity, its co

185 443 muM) with high permeability in the PAMPA-BBB model.

186 n of tight junction proteins or paracellular BBB leakage.

187 y generally apply to small compounds passing BBB through passive diffusion.

188 R database having the potential to penetrate BBB, which could serve as start point for CNS drug repos

189 ll compounds and macro-molecules penetrating BBB through various mechanisms besides passive diffusion

190 To test potential BBB involvement, we generated an iPSC-based BBB model of

191 le and introduce a novel approach to predict BBB permeability from drug clinical phenotypes (drug sid

192 tive in the development of highly predictive BBB passage oriented models, and therefore, it can be of

193 duces markers of oxidative stress, preserves BBB permeability, and attenuates neuropathological indic

194 However, pronounced BBB permeation was noted, with frank albumin leakage aro

195 Reduced BBB integrity in NAc of stress-susceptible or mice injec

196 ury increased BBB junction proteins, reduced BBB permeability, and decreased neurodeficits 24 h post-

197 sfunction, and inactivation of EphA2 reduces BBB damage in ischemic stroke.

198 protein, Paxillin were involved in reducing BBB permeability in SBI rat model.

199 of the tight junction proteins that regulate BBB functions in HIV infection of BBB pericytes.

200 pe I IFNAR signaling in astrocytes regulates BBB permeability and protects the cerebellum from infect

201 ng that IFNAR signaling critically regulates BBB permeability in this brain region.

202 icellular BBB spheroids display reproducible BBB features and functions.

203 eed for new therapies to protect and restore BBB function, either by strengthening endothelial tight

204 Results BBB openings of approximately 1 cm(3) in volume were vis

205 s associated with greater clinical severity, BBB permeability, and neuroimaging damage during encepha

206 c S1pr1 knockout mice (S1pr1(iECKO) ) showed BBB breach for small-molecular-mass fluorescence tracers

207 ed BBB permeability, possibly by stabilizing BBB tight junction via Robo4 mediated Rac1 activation.

208 creased TJP expression in the Mtb-stimulated BBB co-cultures.

209 ty as a prognostic biomarker for post-stroke BBB complications, and are likely elevated early in pati

210 ly in patients who later develop post-stroke BBB disruption due to the presence of an invasive lympho

211 Here we discover that I/R induces subtle BBB leakage within 30-60 min, likely independent of gela

212 or an IgG that does not bind the CNS target (BBB-NiP).

213 Our findings show that BBB permeability was localized within the brainstem, olf

214 Together, these data suggest that BBB disruption may be a modifying factor in the developm

215 The BBB separates blood components from the brain microenvir

216 an not only increase DOX delivery across the BBB and BTB, but that it is retained in the tissue at si

217 promoting peripheral IL-6 passage across the BBB and depression.

218 ment of formulations for delivery across the BBB and relevant disease biology studies are required fo

219 ing DC binding and transmigration across the BBB in response to CCL2 chemotaxis.

220 rstanding of tumor cell migration across the BBB is limited.

221 the advances in the drug delivery across the BBB using various NPs in the last decade.

222 hat influence leukocyte transport across the BBB.

223 exploited to transport antibodies across the BBB.

224 d influx of the active form of TH across the BBB.

225 Also, the BBB penetration mechanisms are concluded in general, emp

226 dition, the drug delivery efficiency and the BBB opening volume have never been shown to be predictab

227 en biochemical cues and physical cues at the BBB affects the mechanisms of brain metastasis.

228 lly regulate P-glycoprotein transport at the BBB and offers potential clinical targets to modulate ne

229 ABCB1/ABCG2-mediated efflux transport at the BBB have been successfully developed in rodents, but it

230 able to export Abeta and desmosterol at the BBB level and these processes could be inhibited by prob

231 ast cancer resistance protein (Bcrp)) at the BBB limits many small molecules from freely reaching the

232 with tight junction molecule assembly at the BBB, explaining the increased permeability of CNS blood

233 may function in vivo to export Abeta at the BBB, in a process that can be antagonized by its putativ

234 g drugs that undergo efflux transport at the BBB.

235 nces in ABCG2/ABCB1 expression ratios at the BBB.

236 l growth factor (VEGF) in macrophages at the BBB.

237 egulator in iron mobilization pathway at the BBB.

238 phate (C1P), to modulate efflux pumps at the BBB.

239 the nose-to-brain (INB) route to bypass the BBB.

240 othelial cells (hBMVECs) that constitute the BBB receive brain iron status information via paracrine

241 t-beta-catenin signaling fully corrected the BBB disruption and hemorrhage defects of Gpr124-CKO mice

242 ve been applied to assist drugs to cross the BBB including osmotic disruption of the BBB and chemical

243 dPGS is able to cross the BBB, bind to P/L-selectins and accumulate selectively in

244 ved from dietary (poly)phenols may cross the BBB, reach brain cells, modulate microglia-mediated infl

245 channel-targeted peptide rapidly crosses the BBB after systemic delivery to modulate auditory process

246 ignificance, this review clearly depicts the BBB structure and comprehensively describes various NPs-

247 ix metalloproteinases (MMPs) can disrupt the BBB through their proteolytic activity on basement membr

248 B in brain tumors, as well as disrupting the BBB in the surrounding tissue.

249 Endothelial NOX4 breaks down the BBB, while neuronal NOX4 leads to neuronal autotoxicity.

250 ed pericyte coverage are responsible for the BBB disruption.

251 into the molecular mechanism involved in the BBB uptake of therapeutics.

252 est that brain endothelial S1P1 maintain the BBB by regulating the proper localization of tight junct

253 d ultrasound, are being used to modulate the BBB in a more precise and non-invasive manner.

254 pericytes and disrupted the BTB, but not the BBB, thereby increasing drug effusion into established t

255 the BBB including osmotic disruption of the BBB and chemical modification of prodrugs.

256 eases are characterized by disruption of the BBB and increased leukocyte infiltration into the CNS.

257 and localized proteolytic degradation of the BBB during cerebral ischemia.

258 astrocytes in innate immune responses of the BBB during viral infection of the CNS remains to be full

259 pericytes are builders and custodians of the BBB in the normal brain, their impact on BBB integrity d

260 Disruption of the BBB may contribute to various CNS diseases.

261 have been widely reported in studies of the BBB phenotype.

262 Using an in vitro model of the BBB, we identify NHE9, an endosomal cation/proton exchan

263 on the normal physiological functions of the BBB.

264 itis, and the virus causes disruption of the BBB.

265 that maintain the restrictive quality of the BBB.

266 ccompanied by MMP-mediated disruption of the BBB.

267 TJP) expression in a co-culture model of the BBB.

268 hyperfibrinolysis on the homeostasis of the BBB.

269 d gene therapy improved the integrity of the BBB.

270 uate short-term and long-term effects on the BBB, respectively, and in control animals without bevaci

271 herapies that may also have an effect on the BBB.

272 ors secreted by reactive astrocytes open the BBB by disrupting endothelial tight junctions (TJs), but

273 l acoustic cavitation effects of opening the BBB by low-intensity pFUS+MB, as evidenced by contrast-e

274 graphical approach was used to quantify the BBB leakage rate and local blood plasma volume.

275 ECs to promote angiogenesis and regulate the BBB.

276 Here, we report the BBB-regulatory role of endothelial sphingosine 1-phospha

277 Results The BBB leakage rate was significantly higher in patients co

278 In summary, the BBB is disrupted by downregulation of the Shh pathway an

279 s in BBB measurements, and how targeting the BBB can influence the course of neurological disorder.

280 hrenia and that drugs directly targeting the BBB may offer new therapeutic opportunities for treating

281 These findings suggest that the BBB does not function independently, but as a module wit

282 INTERPRETATION: The data show that the BBB is a target of antiepileptic treatment and, more spe

283 Finally, we have utilized the BBB spheroids to screen and identify BBB-penetrant cell-

284 rtance of systemic Abeta elimination via the BBB.

285 armaceutical industries as a high-throughput BBB penetration oriented screening method.

286 e mechanism by which pericytes contribute to BBB damage warrants further investigation, as it may yie

287 d microglia, which in turn may contribute to BBB disruption and encephalitis in susceptible mice.IMPO

288 Determination of compound's permeability to BBB is prerequisite in CNS drug discovery.

289 vacizumab therapy resulted in a trend toward BBB restoration (P = 0.055) and long-term therapy result

290 1 inhibition may be a strategy for transient BBB opening and delivery of small molecules into the CNS

291 addresses an unmet need to induce transient BBB opening for drug delivery in patients with malignant

292 inhibition of S1P1 function led to transient BBB breach.

293 20596 significantly attenuated TBI-triggered BBB compromise.

294 ic inflammation contributes to TBI-triggered BBB permeability.

295 rve that pneumococci colocalize with the two BBB endothelial receptors: polymeric immunoglobulin rece

296 n how albumin extravasation that occurs upon BBB dysfunction in various brain injuries can predispose

297 This robust in vitro BBB model could serve as a valuable next-generation plat

298 We also demonstrated in vivo BBB passage and tumor accumulation in a GBM orthotopic m

299 was downregulated in glioma vessels in which BBB function is lost.

300 molecule, were significantly associated with BBB disruption 24 hours post-hospital admission.

301 ); the IL-10 level correlated inversely with BBB permeability (P= .005).