ライフサイエンスコーパス: microglial

1 blished following genetic or pharmacological microglial ablation and repopulation in the adult, indic

2 Furthermore, they demonstrate that microglial ablation prevents and alleviates catatonic si

3 ost pronounced reduction in astrogliosis and microglial accumulation accompanied by decreased express

4 ockout mice develop 'male-like' hypothalamic microglial accumulation and activation, accompanied by a

5 ation without improving lipofuscin, C1q, and microglial accumulation.

6 ucidating gene expression pathways promoting microglial action prior to disease onset would inform po

7 ical selective neuronal loss associated with microglial activation (present both at Day 14 in vivo an

8 cases showed clusters of increased cortical microglial activation accompanying the amyloid.

9 Correlations between levels of microglial activation and amyloid deposition at a voxel

10 Cortical clusters of microglial activation and amyloid deposition spatially o

11 emale-like' metabolic phenotype with reduced microglial activation and body-weight gain.

12 gates of monocytes and platelets to regulate microglial activation and development of sickness behavi

13 s in the brain that spatially coincided with microglial activation and endothelial facilitation of mo

14 but not SD mice show morphological signs of microglial activation and enhanced microglial phagocytos

15 At the hypoxic phase, caffeine reduced microglial activation and enhanced tip cell formation by

16 n of microglia in the central nervous system-microglial activation and expansion are in turn implicat

17 ggest that therapeutic strategies modulating microglial activation and function may have merit in pri

18 occurs during neurodegeneration, leading to microglial activation and inflammasome-mediated interleu

19 escue effects were correlated with decreased microglial activation and inflammatory cytokine producti

20 y, we have evaluated the temporal profile of microglial activation and its relationship between fibri

21 kDa translocator protein (TSPO), a marker of microglial activation and neuroinflammation, were measur

22 and anti-inflammatory cytokines/chemokines, microglial activation and neutrophil infiltration were e

23 TDAG8 deficiency was associated with reduced microglial activation and proinflammatory cytokine IL-1b

24 Thus, we now provide a link between microglial activation and synaptic dysfunctions, which a

25 ism of protection involved the modulation of microglial activation and the production of inflammatory

26 ppressed in an in vivo inflammatory model of microglial activation and to determine the mechanism for

27 tic studies in MS that use the evaluation of microglial activation as an imaging outcome measure.

28 subgroup of secondary progressive patients, microglial activation at baseline was correlated with la

29 Microglial activation can be detected in vivo using 18-k

30 meostasis in the brain, but whether aberrant microglial activation can cause neurodegeneration remain

31 ognostic potential of the putative marker of microglial activation chitotriosidase (CHIT1).

32 We hypothesized that there is microglial activation early on in Alzheimer's disease tr

33 F receptor and that G-CSF signaling mediates microglial activation following colitis.

34 The objective of this study was to assess microglial activation in lesions and in normal-appearing

35 y studies evaluating longitudinal changes in microglial activation in mild cognitive impairment and A

36 There was a longitudinal reduction of 18% in microglial activation in mild cognitive impairment cohor

37 It is unknown whether fingolimod affects microglial activation in MS.

38 ression profiles indicate multiple states of microglial activation in neurodegenerative disease setti

39 educed fetal neuroinflammation and long-term microglial activation in offspring.

40 tress as one of the main factors determining microglial activation in patients with psychiatric disor

41 d meaning of neuroinflammatory processes and microglial activation in psychiatry, and likely in other

42 here is an initial longitudinal reduction in microglial activation in subjects with mild cognitive im

43 e speculate that there might be two peaks of microglial activation in the Alzheimer's disease traject

44 enotype, whereas pharmacological blocking of microglial activation in the Lamc3(-/-) retina rescued t

45 Additionally, we observed a time-shift in microglial activation in the LV-wall adhesions between a

46 emonstrated that both baseline and follow-up microglial activation in the mild cognitive impairment c

47 These data implicate sex differences in microglial activation in the modulation of energy homeos

48 It did not affect the widespread, diffuse microglial activation in the NAWM and GM.

49 unoproteasome regulates multiple features of microglial activation including nitric oxide production

50 radioligand [(18)F]FEPPA to evaluate whether microglial activation is elevated in the dorsolateral pr

51 [(18)F]FEPPA VT between groups suggests that microglial activation is not present in first-episode ps

52 n POMC neuronal function is secondary to the microglial activation is unclear.

53 ed with microglial activation, including the microglial activation marker Iba1 and CC motif chemokine

54 It has been proposed that prolonged microglial activation occurs after single and repeated t

55 actions of autophagy modified the impact of microglial activation on neuronal cells, leading to supp

56 a synchronous change in T2 and ADC signals, microglial activation peaked on day 3 in the same region

57 ify sex-specific differences in hypothalamic microglial activation via the CX3CL1-CX3CR1 pathway that

58 Microglial activation was evaluated as distribution volu

59 Baseline microglial activation was increased by 36% in Alzheimer'

60 ression analyses and immunostaining revealed microglial activation was significantly attenuated in T2

61 At baseline, microglial activation was significantly higher in the co

62 KO and wild-type mice, suggesting a delay in microglial activation when PV is absent from ependymal c

63 ly as a biomarker of 'neuroinflammation' or 'microglial activation' calls for alternative interpretat

64 ningful diagnosis of 'neuroinflammation' or 'microglial activation' is unlikely to be achieved by the

65 into a biomarker of 'neuroinflammation' or 'microglial activation'.

66 and detect the extent of neuroinflammation (microglial activation) in 42 mild cognitive impairment c

67 mutase-2), neuroinflammation (astroglial and microglial activation), neurogenesis (BrdU-labeled newbo

68 ng clear that significant pathology, such as microglial activation, also takes place outside the plaq

69 signaling, peripheral monocyte infiltration, microglial activation, and hypothalamic-pituitary-adrena

70 or (P2X7R) activity is a cardinal feature of microglial activation, and in this study we found that m

71 tomography signal, which arises largely from microglial activation, and measures of subsequent diseas

72 volume, improved functional outcome, reduced microglial activation, and reduced cerebral leukocyte ad

73 ion below 75% for more than 10 weeks without microglial activation, and reduced the levels of cerebel

74 ie infection causes PrP(Sc) accumulation and microglial activation, and surprisingly, upregulation of

75 d between patients and healthy volunteers in microglial activation, as indexed by [(18)F]FEPPA VT, in

76 sulting from astrocyte death, which leads to microglial activation, blood-brain barrier opening, and

77 lammasome has been implicated in HIV-induced microglial activation, but the mechanism(s) remain uncle

78 c brain injury suggest widespread persistent microglial activation, but there has been little study o

79 PO availability, suggestive of predominantly microglial activation, in the ACC during a moderate to s

80 genes and proteins that are associated with microglial activation, including the microglial activati

81 al vasogenic oedema might be attributable to microglial activation, iron deposition, and blood-brain

82 in RPE cells and correlates temporally with microglial activation, not PrP(Sc) accumulation, suggest

83 Astroglial and microglial activation, reduced neuronal density, perivas

84 Whether microglial activation, which is generally viewed as a se

85 y operating at the level of tumor-associated microglial activation.

86 ied by axonal degeneration, astrogliosis and microglial activation.

87 ve Fluoro-Jade B stained injured neurons and microglial activation.

88 mer's disease subjects showed an increase in microglial activation.

89 novel mechanisms by which LRP1 may regulate microglial activation.

90 creased immunostaining for CD68, a marker of microglial activation.

91 th Alzheimer's disease showed an increase in microglial activation.

92 ss innate immunity in macrophages and oppose microglial activation.

93 lative to younger animals, supposedly due to microglial activation.

94 aluate the effect of fingolimod treatment on microglial activation.

95 gy that label positive for CD68, a marker of microglial activation.

96 g globally than non-smokers, indicating less microglial activation.

97 schemic expression of adhesion molecules and microglial activation.

98 C] lactate-to-pyruvate ratios were linked to microglial activation.

99 the levels of proinflammatory cytokines and microglial activation.

100 e understanding of the regulatory network of microglial activation.

101 light that not all psychiatric patients have microglial activation.

102 giform change, astrogliosis, and conspicuous microglial activation.

103 ect against the incidence of AD, as impaired microglial activities and altered microglial responses t

104 on following CNS injury may attenuate select microglial activity to improve the pathophysiology of ne

105 th AMN and investigated the role of ABCD1 in microglial activity toward neuronal phagocytosis in cell

106 vels and immunohistochemical confirmation of microglial activity were also performed.

107 Differentially expressed genes suggest microglial activity, increased retrograde ciliary transp

108 tive function, is mediated via modulation of microglial activity.

109 g to favor CD33m is associated with enhanced microglial activity.

110 f immune suppression, with dampened baseline microglial activity.

111 ty caused by augmented spinal astroglial and microglial activity.

112 If so, anti-microglial agents targeting the pro-inflammatory phenoty

113 Here, we show that microglial anatomical features, lysosome content, membra

114 Immunohistochemical evaluation revealed microglial and astroglial activation as well as neuronal

115 lial cells in the placenta, and endothelial, microglial and neural progenitor cells in the fetal brai

116 Gal-3 and a neuraminidase that desialylates microglial and PC12 surfaces, enabling Gal-3 binding to

117 r C3 secreted from astrocytes interacts with microglial C3a receptor (C3aR) to mediate beta-amyloid p

118 ovel role for autophagy in the regulation of microglial cell activation and pro-inflammatory molecule

119 Microglial cell function is implicated in the etiology o

120 ncrease intracellular GSH levels in a murine microglial cell line (BV2), of which dimercaprol (2,3-di

121 ivity and uptake of Staphylococcus aureus in microglial cell line BV-2 in a kinase-dependent manner.

122 sis of blood neutrophils and monocytes and a microglial cell line revealed that unlike CD33M, the CD3

123 Microglial cell-polarization correlated with maximal exp

124 (CXCR4) on invading tumor cells, macrophage/microglial cells (MGCs), and glioma stem cells (GSCs).

125 lose and rapamycin activate autophagy in BV2 microglial cells and down-regulate the production of pro

126 domain containing 3 (NLRP3) inflammasomes in microglial cells and in HIV-Tg rats administered lipopol

127 with cerebral endothelial cells to activate microglial cells and promote sickness behavior.

128 production of pro-inflammatory molecules in microglial cells and their effects on neuronal cells.

129 Microglial cells are phagocytes in the central nervous s

130 Microglial cells are the resident tissue macrophages of

131 In vitro, both endothelial and microglial cells bound and internalized PGPFs before tra

132 studied how pentobarbital affects BV2 mouse microglial cells in culture.

133 nic receptor neuropilin 1 in macrophages and microglial cells in gliomas as a pivotal modifier of tum

134 RIPK1 is highly expressed by microglial cells in human AD brains.

135 is study we found increased proliferation of microglial cells in human Alzheimer's disease, in line w

136 BV-2 mouse microglial cells in the presence and absence of pentobar

137 Flow cytometric analysis of microglial cells obtained from infected brain tissue dem

138 peripheral noxious stimulation and recruits microglial cells to provide soluble IL-6 receptor, which

139 The deficiency in viral replication in microglial cells was associated with silencing of partic

140 f monocytes and platelets, and activation of microglial cells were measured by flow cytometry.

141 aenoyl ethanolamide (EPEA) by activated BV-2 microglial cells, and by human CYP2J2.

142 Furthermore, activation of microglial cells, DNA fragmentation, and apoptosis of in

143 markedly increased this inhibitory effect on microglial cells, supporting a causal link to disease et

144 findings about the steady-state functions of microglial cells, the factors that are important for phy

145 Up-regulation of CB2R on activated microglial cells, the first step in neurodegeneration, h

146 roliferation and triggering the formation of microglial cells.

147 yte precursor cells through a crosstalk with microglial cells.

148 k genes and the phagocytic activity of mouse microglial cells.

149 and viral-induced inflammatory responses in microglial cells.

150 -induced Ca(2+) signalling and cell death in microglial cells.

151 d to control the expansion and activation of microglial cells.

152 The presence of early microglial changes in our CHMP2B mutant mice indicates n

153 y cyclocreatine tempered autophagy, restored microglial clustering around plaques, and decreased plaq

154 r antagonist PLX5622, and abrogated neuronal-microglial communication in CX3C receptor-1 deficient (C

155 erefore tested the hypothesis that neuron-to-microglial communication via CX3CR1 is an essential comp

156 his study, we uncovered a novel role for the microglial complement receptor 3 (CR3) in the regulation

157 d provide a critical foundation for defining microglial contributions to BG circuit function.

158 Using microglial cultures that have never been exposed to seru

159 find that astrocyte-derived factors prevent microglial death ex vivo and that this activity results

160 Furthermore, inhibition of RIPK1 promoted microglial degradation of Abeta in vitro.

161 Microglial density is significantly increased in the lam

162 ate a role for IL-34 in non-cell-autonomous, microglial-dependent neurodegeneration in HD.

163 tion of disease was recapitulated in in vivo microglial depletion in prion-infected tga20/CD11b-HSVTK

164 Moreover, microglial depletion with a CSF1R antagonist prior to st

165 al cells and this interaction was blocked by microglial depletion.

166 rsensitivity, an effect that is abolished by microglial depletion.

167 ther microglial genes that are important for microglial development and function.

168 t local cues play an ongoing role in shaping microglial diversity.

169 fluorescence fate mapping system to monitor microglial dynamics during steady state and disease.

170 Microglial dysfunction has long been implicated in patho

171 expression of inflammation-related genes and microglial dysfunction.SIGNIFICANCE STATEMENT CCCTC-bind

172 ther support for models in which deficits in microglial, endothelial (blood-brain barrier), ATPase ac

173 viously showed that preincubation of primary microglial-enriched cells with salmeterol could inhibit

174 deletion of Nrros shows its crucial role in microglial establishment during early embryonic stages.

175 Moreover, pharmacologic inhibition of microglial estrogen receptor-beta (ERbeta) function corr

176 i-inflamed M2 polarization in microglia, and microglial exosomal miR-124-3p inhibited neuronal inflam

177 in TBI, we focused on studying the impact of microglial exosomal miRNAs on injured neurons in this re

178 Taken together, increased miR-124-3p in microglial exosomes after TBI can inhibit neuronal infla

179 Increased miR-124-3p in microglial exosomes following traumatic brain injury inh

180 miRNAs manipulated microglial exosomes may provide a novel therapy for TBI

181 To clarify the regulatory mechanism of microglial exosomes on neuronal inflammation in TBI, we

182 to treat cultured BV2 microglia in vitro The microglial exosomes were collected for miRNA microarray

183 gy this randomness shifts to selected clonal microglial expansion.

184 enetic factors, such as rare variants in the microglial-expressed gene TREM2, strongly impact the lif

185 dentified a role for RIPK1 in regulating the microglial expression of CH25H and Cst7, a marker for di

186 al models and preterm infants, and find that microglial expression of DLG4 plays a role.

187 hine-induced glial activation, and increases microglial expression of the anti-inflammatory cytokine

188 Furthermore, AgNP-treatment up-regulated microglial expression of the hydrogen sulphide (H2S)-syn

189 Previous studies have shown that the microglial fractalkine receptor CX3CR1 is involved in sy

190 Aberrant microglial function has also been implicated in FTD caus

191 l-monocyte-derived cells and did not require microglial function in the central nervous system.

192 id cells opened the possibility that altered microglial function plays an active role in disease.

193 factors that are important for physiological microglial function, and how microglia help to maintain

194 Impaired microglial function, either through aberrant activation

195 demonstrate that iMGLs can be used to study microglial function, providing important new insight int

196 e TREM2-APOE pathway as a major regulator of microglial functional phenotype in neurodegenerative dis

197 patient-specific cellular models of critical microglial functions utilizing samples taken during a si

198 lar to those in mouse, including established microglial genes CX3CR1, P2RY12 and ITGAM (CD11B).

199 Limited overlap was observed in microglial genes regulated during aging between mice and

200 red for normal expression of Sall1 and other microglial genes that are important for microglial devel

201 , the results provide evidence of persistent microglial HMGB1-RAGE expression that increases vulnerab

202 TGF-beta1 treatment following ICH decreased microglial Il6 gene expression in vivo and improved func

203 Thus, microglial immune surveillance and cytokine release requ

204 istance to glioma development and had higher microglial infiltrate than mice with wild-type GAMs.

205 TREM2 may regulate microglial inflammation and phagocytosis through couplin

206 Ps by microglia, as well as their effects on microglial inflammation and related neurotoxicity were e

207 iting their toxicity, concomitantly reducing microglial inflammation and related neurotoxicity.

208 it is important to examine how AgNPs affect microglial inflammation to fully assess AgNP neurotoxici

209 phorylation and neuritic dystrophy, activate microglial inflammation, and impair memory in normal adu

210 Cumulative evidence suggests that microglial inflammatory activity in AD is increased whil

211 y inflammation; DLG4 is a hub protein in the microglial inflammatory response; and genetic variation

212 DHEA regulates microglial inflammatory responses through phosphorylatio

213 interactions between inflammation-triggered microglial iron sequestering and alpha7nAChR signaling i

214 nd in vivo Finally, we demonstrated that the microglial ISG chemokine responses to TLR4 agonists were

215 /N- and in vivo ischemia/reperfusion-induced microglial ISG responses by quantitative real-time PCR a

216 Here, we report that human microglial-like cells (iMGLs) can be differentiated from

217 tes found challenge the universal concept of microglial longevity.

218 We found that microglial lysosome content is also increased as a resul

219 ed significantly decreased demyelination and microglial/macrophage accumulation compared with Plg(+)

220 Fingolimod treatment reduced microglial/macrophage activation at the site of focal in

221 ology related to the autoreactive T-cell and microglial/macrophage demyelinating response is critical

222 tion of pro-inflammatory cytokines in murine microglial macrophages.

223 Unless more selective microglial markers are available for PET imaging, quanti

224 istically to reduce inflammation and improve microglial-mediated alpha-syn clearance.

225 flammatory activity in AD is increased while microglial-mediated clearance mechanisms are compromised

226 atonic signs in Cnp-/- mice, indicating that microglial-mediated inflammation causes catatonia.

227 The NEP was performed in microglial (MG) brain cells, which are highly sensitive

228 ynI immunoreactivity showed that exposure to microglial MVs induces SynI mobilization at presynaptic

229 that age-related IFN-I milieu downregulates microglial myocyte-specific enhancer factor 2C (Mef2C).

230 ess and apoptosis to re-establish the stable microglial network.

231 rodent brain slice model with intact neuron-microglial networks exacerbated mHTTx1-induced degenerat

232 , an inhibitor of the IL-34 receptor reduced microglial numbers and ameliorated mHTTx1-mediated neuro

233 ll follow our argumentation on astrocytic or microglial P2X7Rs being the primary targets of pathologi

234 Here we investigated whether increased microglial phagocytic activity that clears amyloid can a

235 In addition, the microglial phagocytic response and elevation of Trem2, b

236 d PC12 (neuron-like) cells, and it increased microglial phagocytosis of PC12 cells or primary neurons

237 LPS-induced microglial phagocytosis of PC12 was prevented by small i

238 signs of microglial activation and enhanced microglial phagocytosis of synaptic elements, without ob

239 -transduced, transgene-expressing cells from microglial phagocytosis.

240 by the Tardbp gene, as a strong regulator of microglial phagocytosis.

241 level findings show that a pro-inflammatory microglial phenotype acquired in vitro by LPS stimulatio

242 In WT mice, LPS induced a microglial phenotype consistent with activation, associa

243 Here we show that ageing microglial phenotype is largely imposed by interferon ty

244 This microglial phenotype was associated with a 16-fold overe

245 in Rag-5xfAD mice as indicated by a shift in microglial phenotype, increased cytokine production, and

246 mplicating local environment as mediators of microglial phenotype.

247 stimulation potentiates the pro-inflammatory microglial phenotype.

248 e allowed us to characterize the spectrum of microglial phenotypes during development, homeostasis, a

249 under inflammatory conditions, and modulates microglial phenotypes through the production of ROS.

250 and discuss treatment options that modulate microglial phenotypes.

251 expression of inflammation-related genes and microglial polarization.

252 use lifespan provides an explanation for how microglial priming early in life can induce lasting func

253 in the GIB fraction significantly inhibited microglial pro-inflammatory activation by LPS, through t

254 sis or tissue changes induce several dynamic microglial processes, including changes of cellular morp

255 ed leukocyte infiltration into the brain and microglial production of IL-6 and TNF-alpha.

256 itive silver and Fluoro-Jade B staining, and microglial proliferation and activation.

257 roglia under homeostatic conditions was low, microglial proliferation in a mouse model of Alzheimer's

258 We observed very early microglial proliferation that develops into a clear pro-

259 d lower levels of interleukin 1beta, reduced microglial proliferation, and impaired granulocyte recru

260 , we showed that oligomeric Abeta stimulates microglial proliferation, whereas no effect was observed

261 ndent neurodegeneration and demonstrate that microglial RAGE activation in presence of Abeta-enriched

262 ckout depolarizes microglia, which decreases microglial ramification and thus reduces surveillance, w

263 urrounding environment in CNS; thus, diverse microglial reactions at different disease stages may ope

264 h lipopolysaccharide, widely used to examine microglial reactions, caused the activation of the mitoc

265 rodegeneration are associated with prominent microglial reactivity and activation of innate immune re

266 caloric environment, persistent elevation of microglial reactivity and consequent TNFalpha secretion

267 identify the STING pathway as a regulator of microglial reactivity and neuroinflammation.

268 he Y382-384 site suppressed morphine-induced microglial reactivity and preserved the antinociceptive

269 onsuming a calorically dense diet stimulates microglial reactivity in the mediobasal hypothalamus (MB

270 or expressed on myeloid cells 2 (TREM2) is a microglial receptor that recognizes changes in the lipid

271 However, how microglial recruitment and activation are regulated duri

272 pment of anxiety during stress was caused by microglial recruitment of IL-1beta-producing monocytes,

273 We hypothesized that microglial recruitment, activation, and down-stream sign

274 Mef2C in microglia results in an exaggerated microglial response and has an adverse effect on mice be

275 preterm birth, but little is known about the microglial response in preterm infants.

276 2-384 is a novel cellular determinant of the microglial response to morphine that critically underlie

277 ver, the molecular mechanisms underlying the microglial response to prion infection are largely unkno

278 f TREM2 function affected tau pathology, the microglial response to tau pathology, or neurodegenerati

279 Thus, TREM2 enables microglial responses during AD by sustaining cellular en

280 Identifying mechanisms that control microglial responses is therefore an important objective

281 s impaired microglial activities and altered microglial responses to beta-amyloid are associated with

282 ts of TREM2, a surface receptor required for microglial responses to neurodegeneration, including pro

283 uding the ability to inhibit proinflammatory microglial responses.

284 Microglial self-renewal under steady state conditions co

285 an induce lasting functional changes and how microglial senescence may contribute to age-related neur

286 teristics of neuroinflammatory signaling and microglial sensitization in aging, its implications in p

287 s leading to a loss of TREM2 function impair microglial signaling and are deleterious.

288 riguingly, recent studies show male-dominant microglial signaling in some neuropathic pain and inflam

289 d several novel ischemia/reperfusion-induced microglial signaling mechanisms.

290 that sphingosine 1-phosphate, an endogenous microglial signaling mediator that inhibits HDAC activit

291 udy demonstrates the loss of the homeostatic microglial signature in active multiple sclerosis with r

292 glia, induces an ageing-like transcriptional microglial signature, and impairs cognitive performance.

293 e genes, not identified as part of the mouse microglial signature, were abundantly expressed in human

294 hanism involving macrophage phagocytosis and microglial synaptic pruning, and raises the potential fo

295 ene signature of blood-derived TAMs, but not microglial TAMs, correlates with significantly inferior

296 s and show an altered metabolism compared to microglial TAMs.

297 ha production, which translated into reduced microglial toxicity towards dopaminergic neurons.

298 n, we undertake gene network analysis of the microglial transcriptomic response to injury, extend thi

299 On the molecular level, microglial transforming growth factor-beta1 expression i

300 e unexpected findings suggest that impairing microglial TREM2 signaling reduces neuroinflammation and