ライフサイエンスコーパス: CNS

1 CNS angiogenesis and blood-brain barrier integrity are c

2 CNS disease in humanized mice was characterized by glios

3 CNS lesions reflect events documented in vitro following

4 CNS responses were examined during spore attachment, fun

5 T+CC: ocular lesion, Pc = 0.0099, OR = 1.56; CNS lesion, Pc = 0.0052, OR = 3.42).

6 eneration or axonal regeneration after acute CNS injury.SIGNIFICANCE STATEMENT The roles of microglia

7 based on available evidence in administering CNS-directed prophylaxis.

8 ational machinery is thus a feature of adult CNS neurons.

9 ar signature of astrocyte types in the adult CNS, providing insights into their origin and functional

10 were thus used to determine how CD19 affects CNS recruitment of B cell subsets.

11 he healthy meninges that are activated after CNS injury.

12 offer significant therapeutic benefit after CNS injury; however, this process may take time and dema

13 al development and axonal regeneration after CNS injury.

14 herapeutic potential of Shh mimetics against CNS complications associated with HIV infection.

15 peutic interventions and develop alternative CNS-directed treatment strategies.

16 The excess risk of cerebral infarction among CNS tumor survivors increases with attained age.

17 identified the first orally bioavailable and CNS penetrant glucagon-like peptide-1 receptor (GLP-1R)

18 le safety profile in patients with NSCLC and CNS metastases who had either never received a tyrosine

19 in M83(+/-) mice also induced paralysis and CNS alphaS pathology, although less efficiently.

20 chanisms underlying CNS immune privilege and CNS drainage.

21 that triazole ureas can act as selective and CNS-active inhibitors for diacylglycerol lipases (DAGLs)

22 We review the method of assessing CNS relapse risk, factors that increase the likelihood o

23 Death of axotomized CNS neurons in vivo is prevented when the formation of A

24 with microglia transcriptome data, connects CNS lupus with other CNS diseases and provides an explan

25 ing may serve as a novel strategy to control CNS leukemia in patients, replacing conventional CNS-tox

26 veals a NRROS-mediated pathway that controls CNS-resident macrophage development and affects neurolog

27 leukemia in patients, replacing conventional CNS-toxic treatment.

28 heir role in drainage of the brain ISF, CSF, CNS-derived molecules, and immune cells from the CNS and

29 a progressive decline in the ability of cut CNS axons to form a new growth cone and then elongate.

30 omyelitis phenotype accompanied by decreased CNS inflammation and reduced frequency of IL-17- and GM-

31 factors that increase the risk of developing CNS cancers in affected individuals, coupled with a grea

32 The molecular mechanisms that dictate CNS function are multifaceted and it is unclear how irra

33 mature microglia in the healthy and diseased CNS.

34 on about pharmacologically driven downstream CNS drug effects; the brain hemodynamic response shows c

35 e-dependent oligodendrocyte apoptosis during CNS remyelination.

36 n promoting oligodendrocyte viability during CNS remyelination.SIGNIFICANCE STATEMENT We report that

37 rent disease courses, supporting the dynamic CNS damage hypothesis to explain MS heterogeneity.

38 lytic rates in T cells isolated from the EAE CNS correlate with upregulated expression of glycolytic

39 uction in immune cells isolated from the EAE CNS.

40 of which are associated with florid episodic CNS clinical syndromes in addition to peripheral neuropa

41 ted flavivirus that is associated with fetal CNS-damaging malformations during pregnancy in humans.

42 sor with early high general and late focused CNS expression.

43 Microglia are essential for CNS homeostasis and innate neuroimmune function, and pla

44 drug development and precision medicine for CNS disorders.

45 ons for the development of new therapies for CNS injury and diseases.

46 mpleted the trial), the rate of freedom from CNS infarction at 7 days was 32.0% with suction-based ex

47 The classifier that differentiates MS from CNS diseases that mimic MS clinically, pathophysiologica

48 ients deferred from testing truly had an HSV CNS infection.

49 into account differences in rodent and human CNS anatomy.

50 hite-matter projections throughout the human CNS.

51 se and later-phase trials is recommended, if CNS activity is anticipated and when relevant to the spe

52 enesis and a therapeutic role for miR-219 in CNS myelin repair.

53 D4 endocytosis in NDP/FZD4 signalling and in CNS vascular biology and disease.

54 The current study suggests that changes in CNS myelination occur as a downstream mechanism followin

55 ion but the mechanisms causing BBB damage in CNS TB are uncharacterized.

56 KEY POINTS: Dysfunctions in CNS regulation of arterial blood pressure lead to an inc

57 To drive type 1 immunity in CNS tissues, we infected GL261 tumor-bearing mice with a

58 arance of RABV-specific immune mechanisms in CNS tissues.

59 egulation of the Wnt/beta-catenin pathway in CNS inflammation and suggest novel therapeutic strategie

60 s M83 transgenic (M83(+/-)) mice resulted in CNS alphaS pathology associated with paralysis.

61 nd choroid plexus and discuss their roles in CNS homeostasis.

62 signaling has brain region-specific roles in CNS immune responses.

63 t PDGFRalpha+ cells perform diverse roles in CNS repair, as multipotential progenitors that generate

64 eactivation of Wnt/beta-catenin signaling in CNS vessels during EAE/MS partially restores functional

65 ies for disease modeling and cell therapy in CNS disorders.

66 l novel targets for host directed therapy in CNS TB.

67 ed that increased (64)Cu-rituximab uptake in CNS tissues corresponded with elevated B cells.

68 Key exclusion criteria included: CNS involvement, a stroke or intracranial haemorrhage le

69 eal injection of alphaS fibrils also induced CNS alphaS pathology in another alphaS transgenic mouse

70 ing humoral immune responses in the infected CNS is poorly defined.

71 mobilization and recruitment to the infected CNS, while delayed accumulation of virus-specific, isoty

72 iate the regenerative outcome in the injured CNS.

73 rsed by engrafting cells back into an intact CNS environment.

74 The only known CNS-permeant PKC inhibitor is the selective estrogen rec

75 w role for 2-arachidonoylglycerol, the major CNS endocannabinoid, in the modulation of chondroitin su

76 for 2-arachidonoylglycerol (2-AG), the major CNS endocannabinoid, in the modulation of CSPGs depositi

77 t7a- and Wnt7b-specific signals in mammalian CNS ECs to promote angiogenesis and regulate the BBB.

78 ion of neurotransmitter release in mammalian CNS synapses.

79 requency and speed observed in the mammalian CNS.

80 sing inhibitory connections in the mammalian CNS: the medial nucleus of the trapezoid body to lateral

81 ver, the role of local translation in mature CNS axons is unknown.

82 To model CNS infiltration by B cells, experimental autoimmune enc

83 DcpS inhibitors along with the in vivo mouse CNS PK profile of PF-DcpSi (compound 24), one of the ana

84 e activation and was protective for multiple CNS cell types, indicating its potential use as a therap

85 concentration predicts poor prognosis of non-CNS cancer patients.

86 Despite nondetectable CNS leukemia in many cases, prophylactic CNS-directed co

87 e set of ligands for mostly "nontraditional" CNS targets and classified as either "brain penetrant" o

88 but hold great promise for treating numerous CNS disorders.

89 Beyond 60 years of age, every year, 0.4% of CNS tumor survivors were hospitalized for a cerebral inf

90 ith the anti-inflammatory (M2) activation of CNS macrophages (microglia) in WNV-infected SCSC while i

91 will enable neuropharmacological analysis of CNS active compounds whilst simultaneously determining t

92 data suggest that additional augmentation of CNS-directed therapy is warranted for CNS2 disease.

93 s grade I or II by the WHO classification of CNS tumors.

94 , the contribution of CD19 in the context of CNS infections has not been evaluated.

95 ependent NKp46(+) ILCs in the development of CNS autoimmune disease.

96 and that are routinely used for infection of CNS neurons (SAD-G and N2C-G).

97 were detected in all mice, and infection of CNS visual system nuclei in the brain was common.

98 Injury of CNS nerve tracts remodels circuitry through dendritic sp

99 e is true for B cells using a mouse model of CNS autoimmunity that incorporates both T and B cell rec

100 ntaneous immunopathology in a mouse model of CNS inflammation.

101 and neuroprotective properties in models of CNS injury.

102 aments (DAPF) support excellent outgrowth of CNS neurons in vitro by cell attachment to the high dens

103 offer new insights into the pathogenesis of CNS disease in MPS patients, and support the use of sper

104 ntact BBB restricts efficient penetration of CNS-targeted drugs.

105 egy to promote the regenerative potential of CNS progenitors in diseases with remyelination failure.

106 RETATION: Older age is a strong predictor of CNS involvement in patients seropositive for CASPR2-IgG

107 stimuli on mechanisms governing programs of CNS myelination under normal and pathological conditions

108 sbiosis affects the onset and progression of CNS autoimmunity.

109 atory factor analysis of pooled questions of CNS-LS and PHQ-9 identified three underlying factors (la

110 urther demonstrated by specific reduction of CNS leukemia on in vivo VEGF capture by the anti-VEGF an

111 Regeneration of CNS myelin involves differentiation of oligodendrocytes

112 t may be further optimized for the repair of CNS damage.

113 NS-directed therapies may reduce the risk of CNS involvement; however, no consensus exists about dose

114 In this review, we discuss the role of CNS-resident and peripheral immune pathways in microbiot

115 of this review is to discuss the spectrum of CNS tumors arising in individuals with NF type 1 (NF1) a

116 -60 years, and had a first CIS suggestive of CNS demyelination and typical of relapsing-remitting mul

117 directly responsible for the suppression of CNS-damaging autoreactive T cells.

118 at age 50 years was highest in survivors of CNS malignancies (24.2 [95% CI 20.9-27.5]) and lowest in

119 molecule could be a target for treatment of CNS inflammation.

120 The molecular trigger of CNS myelination is unknown.

121 % vs 37.8%; p < 0.001) and varied by type of CNS injury; mortality was 79.6% in patients with intracr

122 ess the heterogeneity of cell types from one CNS region to another and are complicated by alterations

123 secretase activity before exposing to MAG or CNS myelin improves SC migration and survival in vitro F

124 criptome data, connects CNS lupus with other CNS diseases and provides an explanation for the neurolo

125 from the CNS and meninges to the peripheral (CNS-draining) lymph nodes.

126 calcium transients, and robustly phagocytose CNS substrates.

127 damTS-A anchors cells in place and preserves CNS architecture by reducing tissue stiffness.

128 Primary CNS lymphoma (PCNSL) is a rare form of extranodal non-Ho

129 sly published studies in adult-onset primary CNS tumors and replicated these in survivors of childhoo

130 tients aged 70 years or younger with primary CNS lymphoma.

131 uronal energy levels are critical for proper CNS function, but the relative roles for the two main so

132 ble CNS leukemia in many cases, prophylactic CNS-directed conventional intrathecal chemotherapy is re

133 Retrospective data indicate prophylactic CNS-directed therapies may reduce the risk of CNS involv

134 dimers playing important roles in regulating CNS function.

135 t stimulate axon growth are needed to repair CNS damage.

136 Genes with fewer retained CNSs show lower overall expression, although this bias i

137 ynthesis, resulted in significantly retarded CNS myelination; however, myelin appeared normal at 3 mo

138 ned offshore wells in the Central North Sea (CNS) were conducted showing that considerable amounts of

139 cation of patients at high risk of secondary CNS relapse is therefore paramount.

140 elapse-free survival, indicating subclinical CNS manifestation in most patients.

141 radiation therapy are at risk for subsequent CNS tumors.

142 rveillance for early detection of subsequent CNS tumors.

143 childhood cancer with and without subsequent CNS tumors (82 participants and 228 matched controls).

144 Some approaches suppress CNS immune mechanisms, while others harness the immune s

145 o disseminate to the central nervous system (CNS) after oral infection in C57BL/6J mice expressing ei

146 s induced within the central nervous system (CNS) after WNV infection, leading to entry of activated

147 which WNV enters the central nervous system (CNS) and host-factors that are involved in WNV neuroinva

148 The central nervous system (CNS) and its meningeal coverings accommodate a diverse m

149 degeneration of both central nervous system (CNS) and peripheral nervous system (PNS) in PD.

150 Infections of the central nervous system (CNS) are often acute, with significant morbidity and mor

151 mors residing in the central nervous system (CNS) compromise the blood-brain barrier (BBB) via increa

152 hat occur across the central nervous system (CNS) during neurological diseases do not address the het

153 phioxus develops its central nervous system (CNS) from a neural plate that is homologous to that of v

154 netic field (SMF) on Central Nervous System (CNS) glial cells are less investigated.

155 crophages within the central nervous system (CNS) have essential roles in neural development, inflamm

156 surveillance of the central nervous system (CNS) have repeatedly provoked dismissal of the existence

157 Central nervous system (CNS) infection and neurological involvement have also be

158 on are a hallmark of central nervous system (CNS) infections with neurotropic pathogens, post-infecti

159 sue that can lead to central nervous system (CNS) inflammation with long-term behavioral and cognitiv

160 ith mainly relapsing central nervous system (CNS) inflammatory diseases.

161 in reducing ischemic central nervous system (CNS) injury during SAVR.

162 ory responses during central nervous system (CNS) invasion by trypanosomes and are associated with th

163 (PCR) is a marker of central nervous system (CNS) involvement in congenital hCMV infection (cCMV), bu

164 stic leukemia (ALL), central nervous system (CNS) involvement is a major clinical concern.

165 ated with ocular and central nervous system (CNS) lesions and showed the strongest association under

166 Primary central nervous system (CNS) lymphoma (PCNSL) and primary testicular lymphoma (P

167 (Sxl), functions in central nervous system (CNS) neurons as part of a relay that specifies the early

168 ult with concomitant central nervous system (CNS) pathology.

169 ristics of the adult central nervous system (CNS) pose barriers to axonal regeneration and functional

170 Central nervous system (CNS) relapses are an uncommon yet devastating complicati

171 opment of a manifest central nervous system (CNS) synucleinopathy (odds ratio = 7.1).

172 re phagocytes in the central nervous system (CNS) that become activated in pathological conditions an

173 otor circuits of the central nervous system (CNS) through a series of pathways that integrate and reg

174 Survivors of central nervous system (CNS) tumors (SHR=4.6, 95% confidence interval, 4.3-5.0),

175 the adult mammalian central nervous system (CNS), axonal damage often triggers neuronal cell death a

176 motor neurons in the central nervous system (CNS), causing the adult-onset degenerative disease amyot

177 nd plasticity of the central nervous system (CNS), which may explain the absence of a direct relation

178 The discovery that central nervous system (CNS)-targeted autoreactive T cells required a process of

179 tably, the first new central nervous system (CNS)-targeted oligonucleotide-based drug (nusinersen/Spi

180 lls in the mammalian central nervous system (CNS).

181 ment at the diseased central nervous system (CNS).

182 ating disease of the central nervous system (CNS).

183 for tissue repair in central nervous system (CNS).

184 be a function of the central nervous system (CNS).

185 on mechanisms in the central nervous system (CNS).

186 argets myelin in the central nervous system (CNS).

187 ng inhibition in the central nervous system (CNS).

188 inflammation in the central nervous system (CNS).

189 associated with the central nervous system (CNS).

190 containing many cell types, suggesting that CNS loss may correspond to a reduced number of expressio

191 The CNS myelination defect results from a cell-autonomous re

192 The CNS-TAC assays showed 85.6% sensitivity and 96.7% specif

193 eity of the mechanisms of release across the CNS.

194 ey could shuttle between lymph nodes and the CNS and produced encephalitogenic cytokines.

195 ated with neurological disorders of both the CNS and peripheral nervous systems (PNS), yet few studie

196 eripheral inoculation, the virus entered the CNS in all mice tested and initially targeted astrocytes

197 cells become pathogenic before entering the CNS, but also the potential for this process to influenc

198 ck peripheral immune cells from entering the CNS.

199 We have examined the CNS transcriptional response of Locusta migratoria manil

200 The T cells then exit the spleen for the CNS where they first roll and crawl along the luminal su

201 derived molecules, and immune cells from the CNS and meninges to the peripheral (CNS-draining) lymph

202 trafficking and lymphatic drainage from the CNS, and we take into account differences in rodent and

203 ii did not recognize Tregs isolated from the CNS.

204 ce that express IFN-gamma ectopically in the CNS (both sexes).

205 e most substantially elevated protein in the CNS after peripheral administration of lipopolysaccharid

206 f nerve degeneration and regeneration in the CNS and in the context of peripheral neuropathies.

207 the control of inflammatory responses in the CNS and neurotoxicity.

208 ule-based motors are highly expressed in the CNS and the major anterograde transporters of cargos, su

209 ce P (SP) is an undecapeptide present in the CNS and the peripheral nervous system.

210 e aberrant presence of CD4(+) T cells in the CNS are not known.

211 arly recognized, their exact function in the CNS continues to be explored.

212 Dendritic cells (DC) accumulate in the CNS during neuroinflammation, yet, how these cells contr

213 Similarly, Tregs in the CNS during T. gondii infection are Th1 polarized, as exe

214 Myelin in the CNS is a specialised extension of the oligodendrocyte pl

215 ermine whether the high level of LCN2 in the CNS is protective or deleterious, we challenged Lcn2(-/-

216 we hypothesized that factors present in the CNS may physiologically protect neurons from the deleter

217 e suggests that reducing inflammation in the CNS may start with modulation of the gut microbiome.

218 B cells can be detected in the CNS of EAE mice using (64)Cu-rituximab PET.

219 ever, the consequences of loss of Lpd in the CNS on behaviour are unknown.

220 The ultimate success of immunotherapy in the CNS will require improved imaging technologies and metho

221 Blockade of Chrm1 in the CNS, but not the periphery, reduces HSC mobilization.

222 -stage" regulator of myelin thickness in the CNS, independent of oligodendrocyte differentiation.

223 ammatory monocyte-derived cells (MCs) in the CNS, leading to improved clinical outcome.

224 In the CNS, mild cognitive impairment can be attributed to obes

225 In the CNS, Rag1(-/-) mice showed lower levels of interleukin 1

226 be carefully evaluated, particularly in the CNS, where inflammation and leukocyte transmigration mus

227 body mass are enriched for expression in the CNS, whereas genes for fat distribution are enriched in

228 ecule that regulates midline crossing in the CNS.

229 a help to maintain tissue homeostasis in the CNS.

230 inage and neuropathological processes in the CNS.

231 molecular, cellular and system levels in the CNS.

232 ediate arousal, attention, and reward in the CNS.

233 neuronal homeostasis and inflammation in the CNS.

234 al synaptic and behavioral plasticity in the CNS.

235 hat KATNAL1 may play a prominent role in the CNS; however, such associations lack the functional data

236 expressed in various tissues, including the CNS.

237 ls in mediating leukemia-cell entry into the CNS and leptomeningeal infiltration was further demonstr

238 e of leukocytes and small molecules into the CNS has been studied extensively, the contribution of fi

239 hways mediating leukemia-cell entry into the CNS need to be understood to identify targets for prophy

240 ation and myeloid cell infiltration into the CNS tissue.

241 c stromal cells as portals of entry into the CNS was only recently uncovered.

242 ified a mechanism of ALL-cell entry into the CNS, which by targeting VEGF signaling may serve as a no

243 functional as early as vessel entry into the CNS.

244 nd increased leukocyte infiltration into the CNS.

245 and limits immune cell infiltration into the CNS.

246 phaS and reveal its efficiency to invade the CNS via multiple routes of peripheral administration.

247 he mass exodus of neural lineages out of the CNS and drastic perturbations to CNS structure.

248 trating embryonic development, mainly of the CNS and limbs.

249 clerosis (MS), an autoimmune disorder of the CNS and thus analyzed the microbiomes of 71 MS patients

250 s a degenerative inflammatory disease of the CNS characterised by immune-mediated destruction of myel

251 ignancies and non-malignant neoplasms of the CNS diagnosed before age 20 years in populations covered

252 municate with myeloid cells and cells of the CNS remain unclear.

253 ne inflammatory demyelinating disease of the CNS that causes disability in young adults as a result o

254 A histopathological examination of the CNS tumour can confirm a dedifferentiation of NEN in the

255 Given the vulnerability of the CNS we reasoned that brain aromatization may protect cir

256 of microglia, the phagocytosing cells of the CNS, and invading macrophages in degenerative and regene

257 After lesions of the CNS, locomotor abilities of animals (mainly cats) are of

258 mal cells that construct the barriers of the CNS.

259 ion for managing autoimmune disorders of the CNS.

260 nflammatory and demyelinating disease of the CNS.

261 from evolutionarily disparate regions of the CNS.

262 ysfunction, of microglia in disorders of the CNS.

263 an inflammatory demyelinating disease of the CNS.

264 of the existence of immune privilege of the CNS.

265 or the disease, the autoimmune attack on the CNS that leads to chronic inflammation, neuroaxonal dege

266 enitors regulate the vasculature outside the CNS remains largely unknown.

267 the role of CGRP both within and outside the CNS, we used CGRP-induced light-aversive behavior in mic

268 tagonists that evidently do no penetrate the CNS in effective amounts.

269 ows considerable complexity in targeting the CNS and may target different cells at different stages o

270 Access of immune cells to the CNS and their positioning within the tissue are controll

271 Injury or disease to the CNS results in multifaceted cellular and molecular respo

272 relapses after bystander recruitment to the CNS, whereas TH1 cells perform immune surveillance.

273 ortant systemic signal of O3 exposure to the CNS.

274 ate neuroprotection and drug delivery to the CNS.

275 e with a mouse line expressing Cre under the CNS specific Nestin promoter to restrict the genetic abl

276 ions enjoy an intimate relationship with the CNS, where they play an essential role in both health an

277 tive in impairing MC accumulation within the CNS and failed to drive clinical improvement.

278 ogenitors in vascular development within the CNS is well recognized, how these progenitors regulate t

279 t controls inflammatory responses within the CNS milieu under injurious conditions, involving CD200 l

280 Tregs are anatomically restricted within the CNS, and their interaction with CD11c(+) populations reg

281 differences in HIV susceptibility within the CNS, there has been surprisingly little exploration into

282 osis, leading to hypercellularity within the CNS, where monocytes/macrophages contribute to CNS virem

283 ontrast to scars in other mammalian tissues, CNS tissue significantly softens after injury.

284 dings identify a second inducible barrier to CNS entry at the GL.

285 We found that Abeta oligomer binding to CNS synaptosomes isolated from wild type (wt) mice treat

286 ammation, yet, how these cells contribute to CNS antigen drainage is still unknown.

287 S, where monocytes/macrophages contribute to CNS viremia, neuroinflammation, and increased mortality.

288 n Th17 cells and impaired their migration to CNS compared with the response of WT Th17 cells and ther

289 out of the CNS and drastic perturbations to CNS structure.

290 qualitative walking abnormalities related to CNS circuit dysfunction across species, identify appropr

291 Receptors relevant to CNS disorders typically have associated proteins discret

292 d our understanding of mechanisms underlying CNS immune privilege and CNS drainage.

293 ding IL-1beta, TNF-alpha and IL-6 in various CNS regions.

294 ruption of the BBB may contribute to various CNS diseases.

295 together these findings help to explain why CNS neurons die after axotomy, strongly suggest that A1

296 ctivated in clinical HAT and associated with CNS inflammatory responses.

297 wnstream BMP signaling pathway may help with CNS repair.

298 In contrast, mutants with CNS manifestations (F51L, E102del, V139M, R142Q, R142W,

299 nd neurological damage in HIV- subjects with CNS cryptococcosis may help gauge disease severity and g

300 lity was significantly higher for those with CNS complications (75.8% vs 37.8%; p < 0.001) and varied