ライフサイエンスコーパス: neuroinflammation

1 lpha-syn further rescued neurons and reduced neuroinflammation.

2 alpha-synuclein cell-to-cell propagation and neuroinflammation.

3 commonly used imaging target to investigate neuroinflammation.

4 s) in the initiation of CD4(+) TH17-mediated neuroinflammation.

5 and astrogliosis in diseases associated with neuroinflammation.

6 reby making the TSPO expression a marker for neuroinflammation.

7 n by becoming activated and participating in neuroinflammation.

8 d IFN-beta signaling may result in increased neuroinflammation.

9 ic factors, such as hypertension and ongoing neuroinflammation.

10 e loss of neuronal populations and increased neuroinflammation.

11 drives initiation and maintenance of chronic neuroinflammation.

12 athological tau and Abeta species as well as neuroinflammation.

13 to reduce leukocyte adhesion and thus reduce neuroinflammation.

14 Th1 cell differentiation and development of neuroinflammation.

15 ivated by excitotoxicity-induced hippocampal neuroinflammation.

16 rostaglandin synthesis promoting LPS-induced neuroinflammation.

17 ter signalling components, and modulators of neuroinflammation.

18 nterleukin 1beta release that contributes to neuroinflammation.

19 s a novel therapeutic target for controlling neuroinflammation.

20 l LPS and determined effects on behavior and neuroinflammation.

21 on emission tomography was used to visualize neuroinflammation.

22 t role for ANKRD55 in multiple sclerosis and neuroinflammation.

23 croglial activation in preclinical models of neuroinflammation.

24 y and epithelial barrier function to enteric neuroinflammation.

25 verexpression was reported to be involved in neuroinflammation.

26 ges were observed in tau phosphorylation and neuroinflammation.

27 altering amyloid deposition or indicators of neuroinflammation.

28 but this was not associated with systemic or neuroinflammation.

29 vivo pathological and clinical relevance of neuroinflammation.

30 radioligand targeting P2X7R, a biomarker of neuroinflammation.

31 s related to the tau synaptic impairment and neuroinflammation.

32 ently enter the brain, resulting in profound neuroinflammation.

33 ina, increase expression of these markers in neuroinflammation.

34 gnificant dysregulation of genes involved in neuroinflammation.

35 the initiation and persistence of autoimmune neuroinflammation.

36 barrier function by microRNAs in health and neuroinflammation.

37 tients with MS to effective control of brain neuroinflammation.

38 poorly understood mechanism known to involve neuroinflammation.

39 all function of the BBB in health and during neuroinflammation.

40 oss in 5xfAD mice, as well as reduce overall neuroinflammation.

41 infiltrated neutrophils/MDMs and ECs drives neuroinflammation.

42 ensitive than (R)-(11)C-PK11195 in detecting neuroinflammation.

43 n a cascade of processes collectively termed neuroinflammation.

44 lular glutathione (GSH) levels would inhibit neuroinflammation.

45 lved in common pathways, possibly related to neuroinflammation.

46 kDa translocator protein (TSPO), a marker of neuroinflammation.

47 in Schwann cells reduced both allodynia and neuroinflammation.

48 transmitter receptors implicated in pain and neuroinflammation.

49 radioligand targeting P2X7R, a biomarker of neuroinflammation.

50 f smoking on availability of this marker for neuroinflammation.

51 ethod has never been applied to the study of neuroinflammation.

52 ressin, and serotonin neurotransmission, and neuroinflammation.

53 ustain spreading depolarization and activate neuroinflammation.

54 ds to caspase-1 activation, is implicated in neuroinflammation.

55 confirm blood-brain barrier dysfunction and neuroinflammation.

56 ne responses, mitochondrial dysfunction, and neuroinflammation.

57 as a regulator of microglial reactivity and neuroinflammation.

58 yrosine hydroxylase cell content and intense neuroinflammation.

59 doses manifesting with neurodegeneration and neuroinflammation.

60 versed the protective effects of VPC against neuroinflammation.

61 e response pathways, commonly referred to as neuroinflammation.

62 and astrocytes, which are central players in neuroinflammation.

63 mice increased disease severity in models of neuroinflammation.

64 nd neurons, causing micro- and astrogliosis, neuroinflammation, accumulation of lipofuscin bodies, an

65 that TGF-beta1 modulates microglia-mediated neuroinflammation after ICH and promotes functional reco

66 imultaneously improve axon growth and reduce neuroinflammation after SCI by acting on both neurons an

67 say for efficacy of the cells in suppressing neuroinflammation after traumatic brain injury (TBI) in

68 es for our knowledge on their involvement in neuroinflammation, aggravating stroke, temporal lobe epi

69 ary-adrenal reactivity, and the reduction of neuroinflammation; all of which have supporting lines of

70 There is increasing support for the role of neuroinflammation and aberrant immune regulation in the

71 Neuroinflammation and abnormal immune responses are incr

72 icantly ameliorates neuropathology, reducing neuroinflammation and activating autophagy.

73 roles in neural development, homeostasis and neuroinflammation and are increasingly implicated in age

74 that the diet modulates plasma metabolites, neuroinflammation and brain markers of neurogenesis in a

75 Moderate to severe TBI elicits neuroinflammation and c-Jun-N-terminal kinase (JNK) acti

76 ytokines, microglia are pivotal mediators of neuroinflammation and can induce or modulate a broad spe

77 subtle myelin abnormalities cause low-grade neuroinflammation and catatonic behavior.

78 regulation of BBB physiology associated with neuroinflammation and decreased expression of neuronal a

79 blating the NLRP3 gene significantly reduced neuroinflammation and delayed RGC loss after optic nerve

80 ) mice are studied in the cuprizone model of neuroinflammation and demyelination.

81 nimals also exhibit histological evidence of neuroinflammation and expansion of glial populations by

82 This was associated with neuroinflammation and glial/microglial activation.

83 mal PET to examine directly the link between neuroinflammation and hypermetabolism in aged mice.

84 Our findings suggest that VPC reduces neuroinflammation and improves outcomes after SBI by act

85 CI, miR-155 KO mouse spinal cord has reduced neuroinflammation and increased peripheral conditioning-

86 impairing microglial TREM2 signaling reduces neuroinflammation and is protective against neurodegener

87 d neurobehavioral outcomes and reduced fetal neuroinflammation and long-term microglial activation in

88 the CNS, thereby effectively contributing to neuroinflammation and lowering viral clearance.

89 coagulation factors may be key mediators in neuroinflammation and may therefore provide future targe

90 nary immune profiles and the most pronounced neuroinflammation and microglial activation in response

91 y immune responses concurrent with augmented neuroinflammation and microglial activation in response

92 tau hyperphosphorylation, neurodegeneration, neuroinflammation and microhemorrhage were found in the

93 a myeloid-cell subclass that contributes to neuroinflammation and morbidity after SE.

94 temically, to normalize morphine-induced CNS neuroinflammation and morphine- and endotoxin-induced ch

95 obial metabolites to germ-free mice promotes neuroinflammation and motor symptoms.

96 inhibiting the JAK/STAT pathway can prevent neuroinflammation and neurodegeneration by suppressing a

97 By 10 months, the hippocampal neuroinflammation and neurodegeneration typically observ

98 e JAK/STAT pathway disrupts the circuitry of neuroinflammation and neurodegeneration, thus attenuatin

99 specific inhibitor of JAK1/2, in suppressing neuroinflammation and neurodegeneration.

100 ory deficits might involve the regulation of neuroinflammation and neuronal apoptotic events.

101 fter peripheral infection and causes chronic neuroinflammation and neuronal damage that leads to cogn

102 gitudinal studies to investigate the role of neuroinflammation and neuronal injury in LTI patients wi

103 th pleiotropic effects, including regulating neuroinflammation and neuronal survival.

104 nd antimicrobial defenses in mouse models of neuroinflammation and of pulmonary tuberculosis, respect

105 Neuroinflammation and oxidative stress are hallmarks of

106 ize isolated roles of these cells in retinal neuroinflammation and possibly elsewhere in CNS.

107 icrovesicle treatment was found to attenuate neuroinflammation and preserve host neuronal morphology

108 Here, we discuss some positive attributes of neuroinflammation and propose that inflammation be thera

109 te leads to neuroprotection by both reducing neuroinflammation and protecting mitochondria, which lea

110 erol degradation in the mouse CNS, modulates neuroinflammation and reduces chondroitin sulfate proteo

111 2-AG degradation in the mouse CNS, modulates neuroinflammation and reduces CSPGs accumulation and ast

112 Here we examined NLRP3-induced neuroinflammation and RGC survival following partial opt

113 etabolites, capillary hemodynamic responses, neuroinflammation and stem cell activity.

114 peutic interventions to alleviate or prevent neuroinflammation and subsequent cognitive impairment in

115 contributes to Th17 cell-mediated autoimmune neuroinflammation and support the notion that targeting

116 Amyloid-beta deposition, neuroinflammation and tau tangle formation all play a si

117 o examine the long-term effects of perinatal neuroinflammation and the effectiveness of prenatal MgSO

118 ncreases when microglia are activated during neuroinflammation and the TSPO distribution volume (VT)

119 sceptibility with important consequences for neuroinflammation and trigeminovascular activation.

120 hat FXR functions as a negative regulator in neuroinflammation and we highlight that FXR agonists rep

121 ut whether these changes are associated with neuroinflammation and/or activation of microglia, the br

122 Outcome measures of brain metabolism, neuroinflammation, and amyloid-beta pathology were obtai

123 ities, extensive gliosis, microglia-mediated neuroinflammation, and an expansion of oligodendrocyte p

124 use models of AD exacerbate Abeta pathology, neuroinflammation, and cognitive deficits, but it is unk

125 ructural changes including oxidative stress, neuroinflammation, and degradation of neuronal architect

126 associated with instigation of astrogliosis, neuroinflammation, and hyperpermeability of the blood-br

127 cytes/macrophages contribute to CNS viremia, neuroinflammation, and increased mortality.

128 isease states, such as cancer, autoimmunity, neuroinflammation, and infection.

129 30-45% reduction in alpha-syn accumulation, neuroinflammation, and neurodegeneration.

130 emic period that can lead to excitotoxicity, neuroinflammation, and subsequent neurologic injury.

131 onstrate that ApoE affects tau pathogenesis, neuroinflammation, and tau-mediated neurodegeneration in

132 The P2X7 receptor (P2X7R) orchestrates neuroinflammation, and this is the basis for an increase

133 Activated microglia and neuroinflammation are associated with the pathogenesis a

134 ys related to Wnt-MAPK signaling pathways or neuroinflammation are epigenetically controlled in the f

135 to summarize implications of peripheral- and neuroinflammation as well as the autonomic nervous syste

136 Positron emission tomography imaging reveals neuroinflammation associated with an immune response aga

137 n, tranexamic acid, also delays the onset of neuroinflammation associated with EAE.

138 Neuroinflammation associated with HIV-1 infection is a p

139 t injury to neurons, accompanied by enhanced neuroinflammation, astrocytosis and gliosis, and eventua

140 r oxidative stress (superoxide dismutase-2), neuroinflammation (astroglial and microglial activation)

141 ive in the acute phase and as a modulator of neuroinflammation at later time points after experimenta

142 ondary to a reduction in Abeta pathology and neuroinflammation, because wild-type mice receiving the

143 al immune cells, which regulate responses to neuroinflammation, brain injury, autoimmunity and neurog

144 sential for Salmonella entry into the CNS or neuroinflammation, but may influence the mechanisms of C

145 (TSPO) have been used as in vivo markers of neuroinflammation, but there is an urgent need for novel

146 Compound 43 dampened neuroinflammation by reducing microglial activation in t

147 ZD1480 treatment inhibited alpha-SYN-induced neuroinflammation by suppressing microglial activation,

148 Because neuroinflammation can be detrimental or beneficial, befo

149 Neuroinflammation can cause major neurological dysfuncti

150 Neuroinflammation can persist for years following a sing

151 potential of C3aR antagonists under chronic neuroinflammation conditions.

152 mises to provide important insights into how neuroinflammation contributes to AD pathology.

153 JHMV infection and evaluating the effects on neuroinflammation, control of viral replication, and dem

154 plored the relationships between hippocampal neuroinflammation, depressive symptoms, and hippocampal

155 ndicate whether the regional distribution of neuroinflammation differs between dementia types or even

156 cal host defense restriction factor limiting neuroinflammation during acute viral infection.

157 ighlight an important role for microglia and neuroinflammation during congenital ZIKV pathogenesis.

158 inhibited HK cleavage in plasma and reduced neuroinflammation, fibrinogen deposition, and neurodegen

159 ox 1 (HMGB1)/TLR4 axis is a key initiator of neuroinflammation following epileptogenic injuries, and

160 iscuss new therapeutic strategies to control neuroinflammation for the prevention and treatment of ch

161 Neuroinflammation has been associated with various neuro

162 Neuroinflammation has been increasingly implicated as a

163 Neuroinflammation has been increasingly implicated in ne

164 across the blood brain barrier (BBB) during neuroinflammation has been the least explored amongst al

165 al, this review demonstrates that imaging of neuroinflammation has not thus far clearly established b

166 analysis of (11)C-PBR28 in rodent models of neuroinflammation have been published yet.

167 rillary tangles (NFTs), oxidative stress and neuroinflammation have emerged as key targets for the tr

168 Neuroinflammation, immune reactivity and mitochondrial a

169 ognition, we hypothesize that stress-induced neuroinflammation impairs hippocampal neurogenesis and p

170 on disease could deepen our understanding of neuroinflammation in a broad range of neurodegenerative

171 sed on CD4(+) T cells is required to promote neuroinflammation in a murine model of Parkinson's disea

172 ated in glial cells and used as a measure of neuroinflammation in a variety of central nervous system

173 (C3aR) to mediate beta-amyloid pathology and neuroinflammation in AD mouse models.

174 ociation between beta-amyloid deposition and neuroinflammation in AD.

175 und that extracellular PPIA is a mediator of neuroinflammation in ALS.

176 further demonstrate that Abeta pathology and neuroinflammation in amyloid precursor protein (APP) tra

177 e TSPO microglial marker and found increased neuroinflammation in at least one neuroanatomical region

178 hyperammonemia and systemic inflammation on neuroinflammation in cirrhosis using germ-free (GF) and

179 , suggesting a potential pathogenic role for neuroinflammation in FIRES.

180 mproved the neurologic outcome and inhibited neuroinflammation in mice with rTBI.

181 ce spectroscopy (MRS) are used as markers of neuroinflammation in neurodegenerative diseases, but how

182 sting its possible therapeutic potential for neuroinflammation in neurological diseases.

183 Therefore, we investigated neuroinflammation in our CHMP2B mutant mice.

184 s a tool for detection and quantification of neuroinflammation in preclinical research and to compare

185 dding from microglia may amplify and sustain neuroinflammation in response to proinflammatory stimuli

186 1,2-diol} (TIMBD) against HIV1-gp120 induced neuroinflammation in SVG astrocytes.

187 Cell proliferation and neuroinflammation in the adult hypothalamus may contribu

188 ity that HAART critically contributes to the neuroinflammation in the central nervous system (CNS).

189 synaptic elements, without obvious signs of neuroinflammation in the CSF.

190 TGF-beta signaling, which led to exacerbated neuroinflammation in the experimental autoimmune encepha

191 We hypothesized that neuroinflammation in the hippocampus is responsible for

192 eurodegeneration, whereas isoflurane reduced neuroinflammation in the kainate model.

193 Increasing evidence supports a role of neuroinflammation in the pathogenesis of Alzheimer's dis

194 ed that Toll-like receptor 4 (TLR4)-mediated neuroinflammation in the periaqueductal gray (PAG) drive

195 ve role in regulating IL-1beta signaling and neuroinflammation in the peripheral and the central nerv

196 useful tools for characterizing the role of neuroinflammation in the progression of these disorders.

197 iameter of ventral root axons, and extent of neuroinflammation in the SOD1(G93A) spinal cord.

198 both OT and chronic pain are associated with neuroinflammation in the spinal cord.

199 Therefore, the cause of the neuroinflammation in these cohorts and its implications

200 ng immune data sets, we identify significant neuroinflammation in TSC-associated brain tumours.

201 Neuroinflammation in utero may result in life-long neuro

202 linical and clinical research to investigate neuroinflammation in vivo in patients with brain disease

203 roglia), can be measured as an indication of neuroinflammation in vivo using positron emission tomogr

204 RAP and sLRP1 both caused neuroinflammation in vivo when administered by stereotax

205 one to develop technology capable of imaging neuroinflammation in vivo.

206 Intestinal microbiota, systemic and neuroinflammation (including microglial and glial activa

207 e differentiated from recruited monocytes in neuroinflammation, including retina.

208 The neuroinflammation increase detected with (18)F-GE-180 is

209 erance induced by TLR4 signaling, stimulates neuroinflammation (increased IL-1beta and TLR4 mRNA), an

210 During acute neuroinflammation, increased levels of cytokines within

211 n, including widespread neuronal cell death, neuroinflammation, increased production of hyperphosphor

212 (APOE-TR) and APOE-knock-out (KO) mice, with neuroinflammation induced by lipopolysaccharide (LPS) or

213 vitro model of developmental programming of neuroinflammation induced by lipopolysaccharide (LPS), w

214 -836339, [(11)C]1) in a mouse model of acute neuroinflammation (induced by lipopolysaccharide, LPS),

215 However, it is possible that elevated neuroinflammation, inducible by a diverse range of mecha

216 rs; complement; oxidative stress; imaging of neuroinflammation; infections; and clinical trials of an

217 showed significant linkages between systemic/neuroinflammation, intestinal microbiota, and ammonia.

218 Neuroinflammation is a major hallmark of amyotrophic lat

219 HIV-1 infection in the brain with associated neuroinflammation is a potential pathogenic mechanism re

220 Neuroinflammation is also greatly exacerbated in Rag-5xf

221 mer's disease (AD) is unknown, glial-induced neuroinflammation is an early symptom.

222 Neuroinflammation is an important contributor to Alzheim

223 Neuroinflammation is an integral part of the neurodegene

224 Neuroinflammation is associated with neurodegenerative d

225 Age-dependent neuroinflammation is associated with the controversial o

226 e and tau neurofibrillary tangle deposition, neuroinflammation is considered a key feature of Alzheim

227 oAbeta-induced neuroinflammation is greater with APOE4 compared to APOE

228 Neuroinflammation is implicated as a pathomechanism, but

229 NLRP3-induced neuroinflammation is implicated in the pathogenesis and

230 Neuroinflammation is implicated in the pathogenesis of a

231 whether and how the redox processes control neuroinflammation is incompletely understood.

232 It is less clear that neuroinflammation is increased relative to controls in m

233 These findings suggest that neuroinflammation is linked to the risk of psychosis and

234 le that mTORC1 signaling plays in poststroke neuroinflammation is not clear.

235 ementia, and therefore it is unclear whether neuroinflammation is part of the pathogenesis in early s

236 encephalomyelitis (EAE), but how it impacts neuroinflammation is poorly understood.

237 In MS, neuroinflammation is present in the cortex, cortical les

238 of events referred to as "secondary injury." Neuroinflammation is proposed as an important manipulabl

239 Neuroinflammation is sterile, as damage-associated molec

240 Neuroinflammation is thought to contribute to the pathog

241 However, the mechanism of ASI inhibiting neuroinflammation is unknown.

242 ther microglial activation, an indication of neuroinflammation, is evident in the brain of adults wit

243 Neuroinflammation mainly affects brain regions commonly

244 eatment, but SBP patients may have different neuroinflammation marker expression.

245 changes in our CHMP2B mutant mice indicates neuroinflammation may be a contributing factor to the ne

246 Neuroinflammation may be a critical component of the neu

247 ne the amyloid load and detect the extent of neuroinflammation (microglial activation) in 42 mild cog

248 Neuroinflammation might be an important mechanism in the

249 y MMPs known to be secreted and activated in neuroinflammation, MMP2 and MMP9, in brains of susceptib

250 translocator protein (TSPO), a biomarker of neuroinflammation, most second-generation radioligands a

251 trate an exacerbation of cognitive deficits, neuroinflammation, neurodegeneration in a transgenic mou

252 or advanced glycation end products (RAGE) in neuroinflammation, neurodegeneration-associated changes,

253 6 dendrimers correlated with the severity of neuroinflammation observed.

254 We hypothesized that neuroinflammation occurs early in Alzheimer's disease an

255 ropsychiatric symptoms, it was proposed that neuroinflammation occurs in the basal ganglia as an auto

256 gerated progression of cognitive decline and neuroinflammation on an Alzheimer's disease background.

257 vivo neuroimaging of one or more markers of neuroinflammation on human patients with dementia.

258 tory systems, counter-regulatory mechanisms, neuroinflammation, opioid facilitation, and interactions

259 ther than representing a secondary effect of neuroinflammation or neurodegeneration.

260 of conceiving TSPO simply as a biomarker of 'neuroinflammation' or 'microglial activation' calls for

261 d neurobiologically meaningful diagnosis of 'neuroinflammation' or 'microglial activation' is unlikel

262 PO has generally turned into a biomarker of 'neuroinflammation' or 'microglial activation'.

263 Single mTBI does not cause axonal injury, neuroinflammation, or cell death in the gray or white ma

264 There is evidence that neuroinflammation plays a pathogenic role in drug-resist

265 Emerging evidence implicated that persistent neuroinflammation plays an important role in NeuroAIDS.

266 Neuroinflammation potentially up-regulates BACE1 express

267 Therefore, targeting persistent neuroinflammation presents a new therapeutic option to r

268 and complement in AD has been attributed to neuroinflammation, prominent late in disease.

269 uperior to the most commonly used tracer for neuroinflammation, (R)-(11)C-PK11195.

270 ous neurologic diseases in which the role of neuroinflammation remains ill-defined.

271 mechanism by which T-bet expression promotes neuroinflammation remains unknown.

272 rious neuronal disorders, such as stroke and neuroinflammation, rendering them interesting drug targe

273 pecific extracellular PPIA inhibitor reduced neuroinflammation, rescued motor neurons, and extended s

274 Sex-specific amelioration of chronic neuroinflammation rescues the brain degeneration and res

275 ement of RIP kinase activity in coordinating neuroinflammation, restricting West Nile virus pathogene

276 apeutic target for ameliorating Tat-mediated neuroinflammation.SIGNIFICANCE STATEMENT Despite success

277 L an interesting target for the treatment of neuroinflammation, since 2-AG exhibits anti-inflammatory

278 Neuroinflammation studies revealed that the terminal epo

279 and does so in the absence of overt signs of neuroinflammation, suggesting that like many other stres

280 of numerous pathological phenotypes, such as neuroinflammation, synaptic loss, Abeta accumulation, an

281 cant increase in Abeta, tau phosphorylation, neuroinflammation, synaptic pathology and memory impairm

282 mice develop markedly more brain atrophy and neuroinflammation than P301S/E2 and P301S/E3 mice, where

283 o disrupted synaptic integrity and increased neuroinflammation that persisted more than 6 months afte

284 Successful approaches to limiting neuroinflammation through reduction of systemic inflamma

285 These results link neuroinflammation to defective neurotransmission and the

286 rimental and clinical evidence suggests that neuroinflammation, triggered by epileptogenic insults, c

287 that have recently been argued to facilitate neuroinflammation under various conditions, including st

288 reduces surgical brain injury (SBI)-induced neuroinflammation via activating PLA2/5-LOX/LTB4 cascade

289 resents a novel molecular target for imaging neuroinflammation via PET.

290 -type FVB mice were evaluated for changes in neuroinflammation, virus clearance, neuropathology, and

291 nflammatory injuries and this attenuation of neuroinflammation was achieved via modulation of NF-kapp

292 ain water content was significantly reduced, neuroinflammation was decreased and hippocampal CA3 neur

293 relation between beta-amyloid deposition and neuroinflammation was detected with (11)C-PIB and (18)F-

294 dinal changes in beta-amyloid deposition and neuroinflammation, we used in vivo PET imaging and ex vi

295 nscription, MWCNT-induced BBB disruption and neuroinflammation were abrogated by pretreatment with th

296 amyloid pathology, antioxidant pathways, or neuroinflammation were observed in APP/PS1/eNOS(-/-) mic

297 related blood-brain barrier dysfunction and neuroinflammation were shown to be associated with epile

298 TSPO), a marker of microglial activation and neuroinflammation, were measured with [(11)C]PBR28 posit

299 r of disease activity in autoimmune-mediated neuroinflammation with potential clinical applications i

300 itic cells (DC) accumulate in the CNS during neuroinflammation, yet, how these cells contribute to CN