ライフサイエンスコーパス: blood-brain barrier

1 testinal absorption and transport across the blood-brain barrier.

2 ndent signalling of endothelial cells of the blood-brain barrier.

3 associated with compromised integrity of the blood-brain barrier.

4 in microvasculature without compromising the blood-brain barrier.

5 pronounced than previously reported for the blood-brain barrier.

6 es that might affect the permeability of the blood-brain barrier.

7 very across a cellular spheroid model of the blood-brain barrier.

8 portion of recombinant enzymes can cross the blood-brain barrier.

9 n brain angiogenesis and in ensuring a tight blood-brain barrier.

10 unction channels in endothelial cells of the blood-brain barrier.

11 y and oral bioavailability and can cross the blood-brain barrier.

12 in both neurons and endothelial cells of the blood-brain barrier.

13 ture brain vascular traits, most notably the blood-brain barrier.

14 ts with supportive cells termed glia and the blood-brain barrier.

15 bly related to increased permeability of the blood-brain barrier.

16 roinflammation, and hyperpermeability of the blood-brain barrier.

17 brain regions and greater disruption of the blood-brain barrier.

18 contents that complete the disruption of the blood-brain barrier.

19 t dihydroergotamine is not able to cross the blood-brain barrier.

20 cassette (ABC) transporters expressed at the blood-brain barrier.

21 ble to be detached from the cell surface and blood-brain barrier.

22 infecting a host cell that then crosses the blood-brain barrier.

23 r brain tissue compartment across the intact blood-brain barrier.

24 improve the ability of peptides to cross the blood-brain barrier.

25 unction coupling in endothelial cells of the blood-brain barrier.

26 ibitor with high capability to penetrate the blood-brain barrier.

27 are missing machinery for diapedesis through blood-brain barrier.

28 at trimethylamine-N-oxide (TMAO) crosses the blood-brain barrier.

29 ects as well as the ability to penetrate the blood-brain barrier.

30 asons such as inability to readily penetrate blood brain barriers.

31 r PKCepsilon over other kinases, crossed the blood-brain barrier, achieved effective concentrations i

32 Blood-brain barrier activation and/or dysfunction are a

33 ch should address the longitudinal course of blood-brain barrier alterations in psychosis, to determi

34 lls leading to pathological inflammation and blood-brain barrier alterations.

35 forms of A-SAA completely crossed the intact blood-brain barrier, although the rate of SAA2.1 influx

36 Glucose transport across the blood brain barrier and into neural cells is critical fo

37 eatment and determined that SS31 crosses the blood brain barrier and reaches mitochondrial sites of f

38 brain is challenging, principally due to the blood brain barrier and the low metabolic stability of p

39 on of astrocytes results in breakdown of the blood-brain barrier and a large influx of CD8(+) effecto

40 II (IGF-II), a polypeptide that crosses the blood-brain barrier and acts as a cognitive enhancer.

41 ic cytokine interleukin 2 (IL2) disrupts the blood-brain barrier and alters brain microcirculation, u

42 tly, brain-derived exosomes, which cross the blood-brain barrier and circulate following injury, have

43 that asprosin in the circulation crosses the blood-brain barrier and directly activates orexigenic Ag

44 CED) provides a powerful means to bypass the blood-brain barrier and drive widespread distribution of

45 The increased VEGF in IPMK KO disrupts blood-brain barrier and enhances brain blood vessel perm

46 the mechanism by which prolactin crosses the blood-brain barrier and enters the brain is not complete

47 Mechanisms by which the blood-brain barrier and its associated solute transporte

48 f peripheral monocytes, stabilization of the blood-brain barrier and less neurodegeneration.

49 F-alpha antibody that does not penetrate the blood-brain barrier and prevents arthritis.

50 icarbazonato) copper(II)), which crosses the blood-brain barrier and releases (64)Cu bioreductively i

51 role that ABCG2 appears to play at the human blood-brain barrier and the lower potency of elacridar t

52 The sensory neurons lie outside of the blood-brain barrier and therefore, compared to central n

53 volves Th1, CD8, and B cell entry across the blood-brain barrier and virus clearance in the absence o

54 y showed that (11)C-JNJ-54173717 crossed the blood-brain barrier and was cleared from plasma mainly v

55 protein is important for passage through the blood-brain barrier and/or for neuroinvasiveness.

56 y parasite sequestration, a breakdown of the blood-brain barrier, and a strong inflammation in the br

57 helial cells in the brain, disruption of the blood-brain barrier, and cerebral microhemorrhages.

58 Compound 1 is orally available, crosses the blood-brain barrier, and displayed favorable pharmacokin

59 appears to effectively penetrate through the blood-brain barrier, and impedes the progression of neur

60 Finally, compound 3 crosses the blood-brain barrier, and it improves memory, cognitive f

61 -OH was more effective in crossing the fetal blood-brain barrier, and targeting activated microglia.

62 ase of brain inflammation, protection of the blood-brain-barrier, and improvement of neurological fun

63 n which deficits in microglial, endothelial (blood-brain barrier), ATPase activity and astrocytic cel

64 c Hedgehog (Shh) mimetic in order to fortify blood brain barrier (BBB) and dampen leukocyte extravasa

65 Early blood brain barrier (BBB) damage is the major risk facto

66 Blood brain barrier (BBB) disruption due to SBI can exac

67 hese 16 genes are predictive for post-stroke blood brain barrier (BBB) disruption.

68 dendritic cells (DCs) recruitment across the blood brain barrier (BBB) during neuroinflammation has b

69 The blood brain barrier (BBB) poses the greatest challenge t

70 of cytotoxic compounds, the impedance of the blood brain barrier (BBB), and the lack of therapeutic a

71 rain disorders by direct delivery inside the blood brain barrier (BBB).

72 Blood brain-barrier (BBB) in vitro models have been wide

73 Restoration of the blood-brain barrier (BBB) after antiangiogenic therapy o

74 mechanisms that allow these Abs to cross the blood-brain barrier (BBB) and induce neuropathology rema

75 mia demands a carrier that can penetrate the blood-brain barrier (BBB) and subsequently target the is

76 rs is challenging because of the presence of blood-brain barrier (BBB) and the blood-tumor barrier (B

77 The blood-brain barrier (BBB) and the glia limitans serve to

78 he vasculature, first across the endothelial blood-brain barrier (BBB) and then across the astrocytic

79 se inhibitor erlotinib poorly penetrates the blood-brain barrier (BBB) because of efflux transport by

80 Blood-brain barrier (BBB) breakdown and the associated m

81 We show here that following blood-brain barrier (BBB) breakdown, P2RY12 (purinergic

82 Although blood-brain barrier (BBB) compromise is central to the e

83 The blood-brain barrier (BBB) consists of endothelial cells,

84 protein-1 (LRP1) in brain capillaries of the blood-brain barrier (BBB) contributes to neurotoxic amyl

85 However, the blood-brain barrier (BBB) controls TH entry into the bra

86 Wnt/beta-catenin signaling is crucial for blood-brain barrier (BBB) development and maintenance; h

87 echanism and long-term consequences of early blood-brain barrier (BBB) disruption after cerebral isch

88 Blood-brain barrier (BBB) disruption alters the composit

89 Blood-brain barrier (BBB) disruption has long been recog

90 ast agent microbubbles (MB) causes localized blood-brain barrier (BBB) disruption that is currently b

91 e their protective or regenerative effect on blood-brain barrier (BBB) disruption, cerebral apoptosis

92 es the responses of endothelial cells of the blood-brain barrier (BBB) during neurotropic viral infec

93 ing evidence highlights a potential role for blood-brain barrier (BBB) dysfunction in the development

94 agnetic resonance imaging was used to assess blood-brain barrier (BBB) dysfunction.

95 ctions and in vitro transport studies across blood-brain barrier (BBB) endothelial cells, at circulat

96 ly deliver pharmacological agents across the blood-brain barrier (BBB) for treating brain diseases.

97 promising method of drug delivery across the blood-brain barrier (BBB) for treating many neurological

98 eta-catenin signaling pathway is crucial for blood-brain barrier (BBB) formation in brain endothelial

99 tudy, we reveal a new mechanism that governs blood-brain barrier (BBB) function in the rat cerebral c

100 NPs), the toxicokinetics and consequences on blood-brain barrier (BBB) function remain poorly charact

101 and transport of natural ligands across the blood-brain barrier (BBB) has been identified as a means

102 that reactive oxygen species (ROS) propagate blood-brain barrier (BBB) hyperpermeability and inflamma

103 endent cell lines, efficiently penetrant the blood-brain barrier (BBB) in different animal species an

104 Breakdown of the blood-brain barrier (BBB) in response to traumatic brain

105 rated that [(11)C]-(R)-3 readily crosses the blood-brain barrier (BBB) in rodents and selectively bin

106 ctivated encephalitogenic T cells across the blood-brain barrier (BBB) is a crucial step in the disea

107 Disruption of the blood-brain barrier (BBB) is a defining and early featur

108 The breakdown of the blood-brain barrier (BBB) is an important pathological c

109 The blood-brain barrier (BBB) is one of the most essential p

110 The blood-brain barrier (BBB) keeps neurotoxic plasma-derive

111 in, but its localization and function at the blood-brain barrier (BBB) level remain unknown.

112 Reck, combined with loss of Norrin, impairs blood-brain barrier (BBB) maintenance.

113 ls as well as monocytes in an in vitro human blood-brain barrier (BBB) model.

114 Culture-based blood-brain barrier (BBB) models are crucial tools to en

115 pocampal dentate gyrus in the context of the blood-brain barrier (BBB) pathology.

116 o acquirement of resistance and insufficient blood-brain barrier (BBB) penetration of chemotherapeuti

117 feat stress, a mouse model of depression, on blood-brain barrier (BBB) permeability and infiltration

118 We explored the establishment of abnormal blood-brain barrier (BBB) permeability and its relations

119 We determined that areas of blood-brain barrier (BBB) permeability colocalized with

120 The blood-brain barrier (BBB) poses a major challenge for de

121 The blood-brain barrier (BBB) protects the brain from inflam

122 The blood-brain barrier (BBB) provides a constant homeostati

123 ever, its interactions with the cells of the blood-brain barrier (BBB) remain poorly understood.

124 The blood-brain barrier (BBB) restricts the uptake of many n

125 d via a specific transport system across the blood-brain barrier (BBB) to the brain where it acts on

126 s glucose transporter (GLUT)-1 expression in blood-brain barrier (BBB) vascular endothelial cells (BE

127 central nervous system (CNS) compromise the blood-brain barrier (BBB) via increased vascular permeab

128 fter MWCNT exposure, broad disruption of the blood-brain barrier (BBB) was observed across the capill

129 epileptic seizures and the integrity of the blood-brain barrier (BBB) were monitored.

130 paration for a clinical trial on opening the blood-brain barrier (BBB) with magnetic resonance (MR) i

131 and molecular characteristics it becomes the blood-brain barrier (BBB), a selectively permeable and p

132 reduced survival, greater disruption of the blood-brain barrier (BBB), higher brain viral loads, and

133 The Blood-Brain Barrier (BBB), known as the major hindrance,

134 ctions, circulating AngII does not cross the blood-brain barrier (BBB), signalling to the brain via t

135 nce for movement of nanoparticles across the blood-brain barrier (BBB), we observed that nanoparticle

136 re commonly associated with disorders of the blood-brain barrier (BBB), which mainly consists of brai

137 molecules, which indicates disruption of the blood-brain barrier (BBB).

138 ron entry into the brain is regulated by the blood-brain barrier (BBB).

139 physically complex microenvironments at the blood-brain barrier (BBB).

140 m (CNS) forms a selective barrier termed the blood-brain barrier (BBB).

141 ls into the brain by temporarily opening the blood-brain barrier (BBB).

142 ive cancer cells are protected by the intact blood-brain barrier (BBB).

143 cates a role in glucose transport across the blood-brain barrier (BBB).

144 t apoE holoprotein is too large to cross the blood-brain barrier (BBB).

145 n the developing brain, resulting in a leaky blood-brain barrier (BBB).

146 study its effects on the homeostasis of the blood-brain barrier (BBB).

147 sorption potential, and ability to cross the blood-brain barrier (BBB).

148 n efflux pump, regulates permeability of the blood-brain barrier (BBB).

149 herapeutic drugs can successfully bypass the blood-brain barrier (BBB).

150 rowth factor receptor beta and can cross the blood-brain barrier (BBB).

151 is by invading the blood and penetrating the blood-brain barrier (BBB).

152 mplicated by the need to maintain the normal blood-brain barrier (BBB).

153 ng feature of this vasculature is a physical blood-brain barrier (BBB).

154 sed in endothelial cells forming part of the blood-brain barrier (BBB).

155 ive drug delivery to the brain, bypasses the blood-brain-barrier (BBB) and eliminates systemic side e

156 Blood-Brain-Barrier (BBB) is a rigorous permeability bar

157 (11)C]-isoaminobutyric acid (AIB), to assess blood-brain-barrier (BBB) permeability, following separa

158 o neural disease/injury is restricted by the blood-brain-barrier (BBB).

159 delivery of drug-tagged-nanocarriers across blood-brain-barriers (BBB) will allow site-specific and

160 r and how P2X7 receptor suppression protects blood-brain barrier(BBB) after intracerebral hemorrhage(

161 LCN2 crosses the blood-brain barrier, binds to the melanocortin 4 recepto

162 eveloped spherical nucleic acids (SNAs) as a blood-brain barrier-/blood-tumor barrier-penetrating nan

163 e plasminogen activator (tPA) may exacerbate blood-brain barrier breakdown after ischaemic stroke and

164 ithin a susceptible mouse model and suggests blood-brain barrier breakdown and T-cell-mediated neurop

165 Fibrinogen deposition at sites of blood-brain barrier breakdown is a prominent feature of

166 microglial activation, iron deposition, and blood-brain barrier breakdown.

167 rats revealed that both tracers crossed the blood-brain barrier but brain retention was not PDE5-spe

168 h factor (VEGF) originating from outside the blood-brain barrier, but no cellular source has been ide

169 The good penetration of the blood-brain barrier by AZD3759, and its promising clinic

170 Recently, transient disruption of the blood-brain barrier by microbubble-enhanced ultrasound h

171 A new three-dimensional model of the blood-brain barrier can be used to study processes that

172 o adhere to endothelial cells and breach the blood brain barrier, causing cause fatal meningitis.

173 with a higher migratory capacity across the blood-brain barrier, CD56(bright) NK cells represent the

174 f genes involved in the establishment of the blood-brain barrier (claudin 5a, zona occludens 1a and b

175 the physical and biochemical blockage of the blood-brain barrier, could be a precious tool to tackle

176 terostilbene, a compound that penetrates the blood-brain barrier, could suppress brain metastasis by

177 human Pavlovian fear conditioning under the blood-brain barrier crossing MMP inhibitor doxycyline in

178 GBMs more effectively, polymalic acid-based blood-brain barrier crossing nanobioconjugates were synt

179 n, target engagement, and disposition of the blood-brain barrier-crossing bispecific antibody antagon

180 ress excessive immune responses, ameliorated blood-brain barrier damage after cerebral ischaemia.

181 Blood-brain barrier disruption (BBB) and release of toxi

182 he evolution of grey/white matter injury and blood-brain barrier disruption after ICH can be assessed

183 The ensuing strong blood-brain barrier disruption and immune cell recruitme

184 Blood-brain barrier disruption and tight junction damage

185 ly accounted for by age- or disease-specific blood-brain barrier disruption is unclear, and this is a

186 m brain; and 3) hypertonic saline attenuates blood-brain barrier disruption via perivascular aquapori

187 um osmolality, regional brain water content, blood-brain barrier disruption, and aquaporin-4 protein

188 up showed significantly reduced brain edema, blood-brain barrier disruption, lesion volume, and brain

189 exhibited enhanced survival and a diminished blood-brain barrier disruption.

190 effects of inflammation, such as gliosis and blood-brain barrier disruption.

191 e intact apoE holoprotein does not cross the blood-brain barrier due to its size.

192 ceptor by its natural ligand EphrinA1 causes blood brain barrier dysfunction, and inactivation of Eph

193 Microvascular pathology and related blood-brain barrier dysfunction and neuroinflammation we

194 post-mortem immunohistochemistry to confirm blood-brain barrier dysfunction and neuroinflammation.

195 We consider how blood-brain barrier dysfunction could relate to glutamat

196 We conclude that the complex nature of blood-brain barrier dysfunction in psychosis might be re

197 terations in psychosis, to determine whether blood-brain barrier dysfunction is a cause or consequenc

198 verity, evidenced by increased infarct area, blood-brain barrier dysfunction, increased neurological

199 d and cerebrospinal fluid may be a result of blood brain barrier dysregulation and disruption of the

200 e been limited in their ability to cross the blood-brain barrier effectively and recognize and select

201 eases the gap junction coupling in the human blood-brain barrier endothelial cell line hCMEC/D3.

202 (ALCAM) is a cell adhesion molecule found on blood-brain barrier endothelial cells (BBB-ECs) that was

203 is due to an organ-specific role of NOX4 in blood-brain-barrier endothelial cells and neurons.

204 efficient, non-invasive means to bypass the blood-brain barrier for ischemic stroke treatment.

205 Angiogenesis and blood-brain barrier formation are required for normal ce

206 ha, and sAPPbeta), tangle pathology (P-tau), blood-brain-barrier function (albumin ratio), and glial

207 ARTICLE: For many decades a breakdown of the blood-brain barrier has been postulated to occur in migr

208 e (MB), a phenothiazine dye that crosses the blood-brain barrier, has been shown to hit multiple mole

209 Small molecule chaperones that cross the blood brain barrier help mutant GCase refold and traffic

210 e central nervous system (CNS) by regulating blood-brain barrier homeostasis and blood flow at the ca

211 Concomitant with blood-brain barrier impairment, supplemented cholesterol

212 Rosiglitazone, a blood-brain barrier-impermeant PPARgamma-selective agoni

213 , lupus-associated inflammation disrupts the blood-brain barrier in a discriminating way biased in fa

214 iable quantification of P-gp function at the blood-brain barrier in a pharmacologic situation.

215 st that this process involves opening of the blood-brain barrier in capillaries at the lesion edge, s

216 ation and contribute to the breakdown of the blood-brain barrier in CNS autoimmune diseases.

217 abortus contributes to the activation of the blood-brain barrier in neurobrucellosis and IL-1beta med

218 role for endothelial cells that comprise the blood-brain barrier in propagating peripheral-to-central

219 but much less is known about the role of the blood-brain barrier in psychiatric disorders.

220 it alters the integrity and cohesion of the blood-brain barrier in several pathophysiological states

221 We studied the permeability of the blood-brain barrier in six migraineurs and six control s

222 s 13, 15, and 16 were predicted to cross the blood-brain barrier in vitro and were significantly less

223 ibitor than crizotinib in vitro, crosses the blood-brain barrier in vivo, and shows clinical response

224 D3 cerebral endothelial cells, mimicking the blood-brain barrier inside our microfluidic organ-on-chi

225 r to inflammation, tissue damage and loss of blood brain barrier integrity associated with fatal expe

226 endothelial expression of CCL2 and preserved blood-brain barrier integrity after an ischaemic challen

227 Etifoxine improved blood-brain barrier integrity and diminished cell death.

228 nisms underlying ischemia-induced changes in blood-brain barrier integrity and function, including al

229 CNS angiogenesis and blood-brain barrier integrity are controlled by the cano

230 st agent (GBCA) exposure might be related to blood-brain barrier integrity by studying adult patients

231 ease when the host inflammatory response and blood-brain barrier integrity dictate clinical outcomes.

232 +) and CD8(+) T cells in the brain, improved blood-brain barrier integrity, and improved coma scores,

233 The neurotoxin quinolinic acid may impair blood-brain barrier integrity.

234 to indicate quinolinic acid-induced impaired blood-brain barrier integrity.

235 ly indicate quinolinic acid-induced impaired blood-brain barrier integrity.

236 1)C-dihydroergotamine is unable to cross the blood-brain barrier interictally or ictally demonstratin

237 ntal angiogenesis and the maintenance of the blood-brain barrier involve endothelial cell adhesion, w

238 triacylglycerol, whereas the transporter at blood brain barrier is specific for phospholipid form of

239 lung cancer patients, as penetration of the blood-brain barrier is important for optimal therapeutic

240 he brain of mice at specific sites where the blood-brain barrier is naturally absent.

241 In addition, as damage to the blood-brain barrier is one of the major consequences of

242 itical protein for clearing Abeta across the blood-brain barrier is the efflux transporter P-glycopro

243 An important function of the blood-brain barrier is to exclude pathogens from the cen

244 yte adhesion to brain endothelial cells, the blood-brain barrier main component, is a critical step i

245 The blood-brain barrier, mainly composed of brain microvascu

246 uno-histochemical (oxidative/nitrosative and blood-brain barrier markers) as well as blood borne biom

247 ce in an all-human, in vitro, 3-dimensional, blood-brain barrier model exemplifies tight-junction int

248 B model with a higher efficiency than in the blood-brain barrier model.

249 plasma markers of endothelial activation and blood-brain barrier/neurological injury are associated w

250 plasma markers of endothelial activation and blood-brain barrier/neurological injury during critical

251 elationships between endothelial activation, blood-brain barrier/neurological injury, and acute brain

252 that these associations were not mediated by blood-brain barrier/neurological injury.

253 colleagues also show that disruption of the blood-brain barrier occurs in hypertension, allowing cir

254 death, which leads to microglial activation, blood-brain barrier opening, and later, myelin damage.

255 lls to the site of damage through a breached blood-brain barrier or via brain lymphatics.

256 receptor binding and function and determined blood-brain barrier passage of drugs and demonstrate tar

257 We prevent blood-brain barrier passage of DT through PEGylation, wh

258 ere subsequently used for the development of blood-brain barrier passage-predictive statistical model

259 We suggest quantitative assessment of blood-brain barrier pathology as a clinically relevant p

260 c resonance imaging to quantitatively follow blood-brain barrier pathology in rats following status e

261 Our results show that early blood-brain barrier pathology in the piriform network is

262 Blood-brain barrier pathology is recognised as a central

263 The function of NB-360, a novel blood-brain barrier penetrant and orally available BACE1

264 determine for the first time the effect of a blood-brain barrier-penetrant IMPase inhibitor on human

265 est and thus increased the chance for better blood brain barrier penetration.

266 antagonist, has high receptor affinity, high blood-brain barrier penetration, and the ability to be r

267 o the intravenous (IV) route, which requires blood-brain barrier penetration.

268 raminidase (sialidase) activity and promotes blood-brain barrier penetration.

269 oxic to neuronal cells and shows significant blood brain barrier permeability.

270 sed capillary flow heterogeneity followed by blood-brain barrier permeability changes in the perilesi

271 ty of stimulation that efficiently increased blood-brain barrier permeability in 10 of 15 patients wi

272 lth and disease, including regulation of the blood-brain barrier permeability, angiogenesis, clearanc

273 c resonance imaging to quantitatively assess blood-brain barrier permeability.

274 functional capillary density, and increased blood-brain barrier permeability.

275 constriction that was comparable to the less blood-brain barrier-permeable 5-HT1BR agonist sumatripta

276 However, many Hsp90 inhibitors are not blood-brain barrier-permeable, and several present assoc

277 se morphine in injured tissue and to prevent blood-brain barrier permeation.

278 n endothelial cells completely abolished the blood-brain barrier protective effect of regulatory T ce

279 asement membrane, plays an important role in blood brain barrier regulation.

280 terictally or ictally demonstrating that the blood-brain barrier remains tight for dihydroergotamine

281 The blood brain barrier separates the circulating blood from

282 l drugs with optimal penetration through the blood-brain barrier should be considered even for patien

283 and neuroimaging studies that have examined blood-brain barrier structure and function in schizophre

284 ysfunction and increased permeability of the blood-brain barrier suggest that white matter microvascu

285 imilarity of the blood-ocular barrier to the blood-brain barrier suggests that BMs have great potenti

286 idylcholine (LPC) symporter expressed at the blood-brain barrier that transports LPCs containing DHA

287 cess to biological compartments, such as the blood-brain barrier, that have previously been difficult

288 Having crossed the blood-brain barrier, the T cells scan the leptomeningeal

289 ide potential therapeutic avenues within the blood-brain barrier to limit P-gp degradation in Alzheim

290 h plasma stability and was able to cross the blood-brain barrier to reverse morphine-induced, central

291 -mediated transport systems available at the blood-brain barrier, to access brain via tail vein injec

292 ith a P-glycoprotein inhibitor, which blocks blood-brain barrier transport of Abeta, resulted in sign

293 en shown to alter aggregation, toxicity, and blood-brain barrier transport of Abeta, suggesting it mi

294 e therapeutic targets that reside across the blood-brain barrier, underscoring the urgent need to dev

295 in vitro endothelial cell-based model of the blood-brain barrier, we confirmed that regulatory T cell

296 rain, are bone marrow derived, and cross the blood-brain barrier, we used a mouse MLIV model to test

297 nce such antibodies do not readily cross the blood-brain barrier, we used an AAV vector to deliver an

298 ity in Alzheimer's disease and implicate the blood-brain barrier, which controls central drug access.

299 However, diphtheria toxin (DT) crosses the blood-brain barrier, which limits its utility for ablati

300 be delivered across both the blood-tumor and blood-brain barriers with MR image-guided focused ultras