ライフサイエンスコーパス: microglia

1 LOF causes pathogenic lipid accumulation in microglia.

2 ma 2 (AIM2) inflammasome in primary cultured microglia.

3 ce, which enable highly specific ablation of microglia.

4 ZL0580 on HIV long terminal repeat (LTR) in microglia.

5 esulted in degradation of LAMP2 in activated microglia.

6 also displayed increased numbers of rod-like microglia.

7 resented in blood-derived macrophages versus microglia.

8 hyper-reflectivity overlapped with activated microglia.

9 ed by increased colabeling of astrocytes and microglia.

10 BPbeta-dependent gene expression programs in microglia.

11 d co-cultured them with or without activated microglia.

12 etected in a subset of astrocytes and in the microglia.

13 tors for the breaking of immune tolerance of microglia.

14 ession of neurological disease-risk genes in microglia.

15 ta expression, activation of astrocytes, and microglia.

16 in multiple cell types including neurons and microglia.

17 TREM2 is a receptor for lipids expressed in microglia.

18 reasing the prevalence of disease-associated microglia.

19 assays on Pten wild-type and Pten(m3m4/m3m4) microglia.

20 rogenitor-like cells are present among adult microglia.

21 ce in the brain is uptake and degradation by microglia.

22 cit enhanced pruning from innately activated microglia.

23 receptors are expressed in primary cultured microglia.

24 ress through NADPH oxidase in lineage-traced microglia.

25 tic PS exposure and reduced PS engulfment by microglia.

26 is not known, but it involves activation of microglia.

27 genic mice were also used to delete Lpar1 in microglia.

28 herally-derived myeloid cells and endogenous microglia.

29 ns and their interaction with hyper-ramified microglia.

30 y Ly49D(+) NK cells and neutrophils, but not microglia.

31 aR1 responses contribute to TLQP21 action on microglia.

32 heimer's disease (AD) risk gene expressed in microglia.

33 Microglia, a type of CNS immune cell, have been shown to

34 Following microglia ablation, the effects of NF-kappaB-agonists on

35 tation was associated with reduced astrocyte/microglia activation and downregulation of the transcrip

36 that APN deficiency increased Abeta-induced microglia activation and neuroinflammatory responses in

37 attenuates nerve injury-induced spinal cord microglia activation and pain hypersensitivity.

38 in pathologies seem associated with discrete microglia activation modules.

39 ese data, protein aggregate accumulation and microglia activation were observed in the spinal cord wh

40 ing a cascade of molecular events leading to microglia activation, perineural net degradation, and im

41 Minocycline, a potent inhibitor of microglia activation, successfully prevented the above-m

42 ssociated with synaptic loss, apoptosis, and microglia activation.

43 Single-cell RNA-seq of microglia after acute systemic administration of AL002c

44 ate that chronic phase removal of neurotoxic microglia after TBI using CSF1R inhibitors markedly redu

45 progranulin, and reduction of progranulin in microglia alone is sufficient to recapitulate inflammati

46 Microglia also have a unique genetic signature among tis

47 To determine whether microglia also prune myelin sheaths, we used zebrafish t

48 ppressing neuronal activity, and ablation of microglia amplifies and synchronizes the activity of neu

49 or 1 receptor inhibitor (PLX5622) to deplete microglia and a chronic intermittent ethanol vapor two-b

50 with (i) 11C-PK-11195, a marker of activated microglia and a proxy index of neuroinflammation; and (i

51 s enriched in AD genetic risk factors and in microglia and astrocyte protein markers associated with

52 ration of provirus into neural cells such as microglia and astrocytes.

53 ely parallel single-cell analyses to compare microglia and CAM signatures during homeostasis and dise

54 between the ontogenetically closely related microglia and CAMs.

55 nt time points, and RNA-seq was performed on microglia and cerebral endothelial cells (CECs).

56 e a deeper understanding of both parenchymal microglia and extraparenchymal brain macrophages in home

57 -inducible Cre-mediated gene manipulation in microglia and for fate mapping of microglia but not CAMs

58 s influence AD progression via modulation of microglia and immune responses.

59 elevated frequencies of inflammatory M1-like microglia and increased release of pro-inflammatory cyto

60 FIRE) embryos, the arrival of both primitive microglia and intracerebroventricular macrophages was el

61 Microglia and macrophages carry out hematoma clearance,

62 Microglia and macrophages play a critical role in choroi

63 begins early and requires Plexin-B2 in both microglia and macrophages.

64 n evident by a reduction in pro-inflammatory microglia and macrophages.

65 s was performed to visualize the response of microglia and Muller glia.

66 Brain-resident microglia and myeloid cells (perivascular macrophages) a

67 we analyzed the effect of NPC1 deficiency on microglia and on climbing fiber synaptic refinement duri

68 and distinguishes HSC-derived monocytes from microglia and other tissue-resident macrophages.

69 that the phenotypic differentiation between microglia and peripheral macrophages is age-dependent an

70 TBI-induced activation of microglia and peripherally-derived inflammatory macropha

71 neuroinflammation.IMPORTANCE Brain-resident microglia and perivascular macrophages are important HIV

72 lammatory response by using Kv1.3-KO primary microglia and the Kv1.3-specific small-molecule inhibito

73 stem hosts parenchymal macrophages, known as microglia, and non-parenchymal macrophages, collectively

74 tical impact to remove chronically activated microglia, and the inhibitor was withdrawn 1-week later

75 Infiltration of T lymphocytes, activation of microglia, and their interplay are the primary pathophys

76 iple brain cell types, including astrocytes, microglia, and vascular mural cells (VMCs).

77 d that juxtavascular microglia migrated when microglia are actively colonizing the cortex and became

78 Isolated microglia are analyzed for morphological changes and the

79 talls the regrowth of axons, suggesting that microglia are critical for orchestrating the injury resp

80 The beneficial effects of these repopulating microglia are critically dependent on interleukin-6 (IL-

81 Microglia are crucial for brain development and maintena

82 nt macrophages of the brain and spinal cord, microglia are crucial for the phagocytosis of infectious

83 Microglia are dynamic immunosurveillance cells in the CN

84 Microglia are implicated in neurological diseases and mo

85 Because microglia are involved in clearing amyloid and tau patho

86 While microglia are known to use extracellular vesicles to com

87 It is now clear that brain microglia are more than mere bystanders or amyloid phago

88 the healthy adult mouse brain, we show that microglia are necessary for the normal functional develo

89 Microglia are parenchymal macrophages of the CNS; as pro

90 Microglia are phagocytic cells involved in homeostasis o

91 that Arg1-mediated alternative activation of microglia are potential therapeutic targets for psychiat

92 Microglia are primary innate immune cells in the brain a

93 Whether microglia are protective or pathologic is context depend

94 Microglia are the brain's resident macrophages and play

95 , which contradict the current paradigm that microglia are the main immune effector cells of the CNS.

96 Microglia are the principal phagocytes that clear cell d

97 Microglia are the resident myeloid cells in the central

98 The significance of activated microglia around motoneurons axotomized after nerve inju

99 naive littermates, suggesting a new role for microglia as homeostatic regulators of perineuronal net

100 We specifically focus on microglia as major players in neuroinflammation and disc

101 Here, we highlight the fundamental role of microglia as tissue-resident macrophages in neuronal hea

102 nto adenosine by CD73, which is expressed on microglia as well as other brain cells.

103 icient PS1 show severe Abeta accumulation in microglia as well as the postsynaptic protein PSD95.

104 l cortex to show that a higher percentage of microglia associate with the vasculature during the firs

105 humans and rodents provide new insight into microglia-astrocyte communication in homeostasis and dis

106 Microglia-astrocyte interactions represent a delicate ba

107 apies to mediate negative effects of altered microglia-astrocyte interactions.

108 ABAergic) and nonneuronal (oligodendrocytes, microglia, astrocytes, and endothelial) cell types.

109 ns, GABAergic neurons, oligodendrocytes, and microglia/astrocytes) from three different brain regions

110 Further, juxtavascular microglia at all ages associate with vascular areas void

111 In particular, whether microglia become phagocytic is controversial.

112 Microglia behaviors close to axotomized motoneurons grea

113 To resolve these issues we directly observed microglia behaviors with two-photon microscopy in ex viv

114 itiating cells induce mTOR signalling in the microglia but not bone marrow-derived macrophages in bot

115 ulation in microglia and for fate mapping of microglia but not CAMs.

116 morphology and metabolism in the absence of microglia, but no effect of Cxcl10 was observed on micro

117 rve injury-induced activation of spinal cord microglia, but the responsible endogenous TLR2 agonist h

118 ally, ZL0580 inhibits Tat transactivation in microglia by disrupting binding of Tat to CDK9, a proces

119 as measured in Trem2(R47H) KI rat brains and microglia by qualitative and quantitative RT-PCR.

120 Microglia can thus be expected to have similar cell size

121 ol milk formula for 5 d or from hypothalamic microglia cells obtained from postnatal rats, grown in c

122 s: Astrocytes, pericytes, endothelial cells, microglia cells, oligodendrocytes, and neurons.

123 Using fixed- and live-cell imaging in human microglia cells, we further show that CLASP2 is required

124 d glutathione-pathway genes shared between a microglia cluster and infiltrating macrophages.

125 However, relative to macrophages/microglia, comparatively less is known about the roles o

126 roglia in the intact brain has revealed that microglia constantly survey neuronal soma.

127 port that during colonization of the retina, microglia contacts the deep layer of high stiffness, whi

128 Here we report that microglia containing phospho-deficient mutant PS1 displa

129 Microglia continuously monitor synapses, but active syna

130 Spinal cord microglia contribute to nerve injury-induced neuropathic

131 se subunit beta (Hexb) as a stably expressed microglia core gene, whereas other microglia core genes

132 expressed microglia core gene, whereas other microglia core genes were substantially downregulated du

133 Confocal 3D analyses revealed increased microglia coverage of the motoneuron cell body surface w

134 In addition, we found evidence for neuron-microglia cross-talk, where Pten(m3m4/m3m4) neurons elic

135 lia, but no effect of Cxcl10 was observed on microglia cultured on their own.

136 t indapamide reduced superoxide derived from microglia cultures and that treatment of middle-aged mic

137 D risk, and activation of disease-associated microglia (DAM) is dependent on TREM2 in mouse models of

138 At the cellular level in these animals, microglia depletion reduced inhibitory GABA(A) and excit

139 inhibition has been proposed as a method for microglia depletion, with the assumption that it does no

140 In addition, mTOR-deficient microglia did not effectively engulf injured/dying neuro

141 Microglia displayed larger somas and shorter processes.

142 Our findings suggest that this microglia-driven negative feedback mechanism operates si

143 ly identified to be upregulated by activated microglia during aging, neurodegeneration, or loss of Sa

144 rall, we show that short-term elimination of microglia during the chronic phase of TBI followed by re

145 ouse technology, we show that IL-1-dependent microglia-endothelia cross talk is necessary for eliciti

146 reover, we detected activated ISG-expressing microglia enveloping NA-containing neuritic plaques in p

147 wever, there are little data on living human microglia, especially in diseased states.

148 In AD models, activated ISG-expressing microglia exclusively surrounded NA+ amyloid beta plaque

149 Importantly, the engrafted hPSC-derived microglia exhibit dynamic response to cuprizone-induced

150 Second, neonatal-but not adult-microglia express several extracellular and intracellula

151 Rare variants in the microglia-expressed triggering receptor expressed on mye

152 bolic function in human patient iPSC-derived microglia expressing loss of function variants in TREM2.

153 in phagocytosis of postsynaptic elements by microglia expressing TREM2R47H in the PS19 mice and in h

154 creases in Csf1r and Cd11b in frontal cortex microglia following CUS.

155 we found that mTOR is strongly activated in microglia following excitatory injury elicited by status

156 We developed a reliable technique to stain microglia from epileptic and glioma patients to examine

157 We isolated microglia from post-mortem brain tissue of patients with

158 By transiently depleting microglia from the healthy adult mouse brain, we show th

159 e that in coming years, a clearer picture of microglia function in health and disease will emerge.

160 able new genetic tools to specifically study microglia functions in the CNS.

161 echanisms by which the p.R47H variant of the microglia gene and Alzheimer's disease (AD) risk factor

162 phenotypes, including excitatory neuron and microglia gene expression changes.

163 To develop a new microglia gene targeting model, we first applied massive

164 a provide evidence that dysregulated Pten in microglia has an etiological role in microglial activati

165 Microglia have been implicated in playing a role in amyo

166 Until recently, microglia have been studied only in animal models with e

167 sion analysis, and experimental depletion of microglia have cemented their importance.

168 Our work reveals that microglia have highly distinct microdomain signaling, an

169 erleukin-10 (IL-10) axis in restoring murine microglia homeostasis following a peripheral endotoxin c

170 ies on the importance of PTEN in maintaining microglia homeostasis.

171 We investigated the role of microglia in a mouse model of alcohol dependence using a

172 ated the normal and disrupted development of microglia in barrel cortex by chronically depriving sens

173 While microglia in brain slices from male mice lack C3aR1 rece

174 ss the complementary roles of astrocytes and microglia in building the brain, including in the format

175 In summary, we prove a role for microglia in CNS-GVHD, identify the TAK1/TNF/MHC-II axis

176 ling of thousands of neurons, astrocytes, or microglia in each brain, revealing their intricate morph

177 ial progenitors in the yolk sac and immature microglia in early embryos.

178 synapses, but active synaptic remodeling by microglia in mature healthy brains is rarely directly ob

179 o characterize the phenotype and function of microglia in MDD.

180 ells, central and/or peripheral neurons, and microglia in mediating pain.

181 veals a neuronal activity-regulated role for microglia in modifying developmental myelin targeting by

182 However, a small subset of microglia in mouse brains can survive without CSF1R sign

183 Depletion of microglia in neonatal mice disrupts this healing process

184 tor 1 (IGF1) is produced by tumor-associated microglia in response to interleukin-4 (IL-4) stimulatio

185 A deeper understanding of the role of microglia in the 'cellular phase' of ALS is crucial in t

186 (TREM2), a receptor exclusively expressed by microglia in the brain, modulates microglial immune home

187 that are specifically or highly expressed by microglia in the central nervous system (CNS).

188 and increased markers indicative of reactive microglia in the cerebellum, cortex and hippocampus rela

189 ell contact was required for N1 to influence microglia in the co-cultures, and this was linked with r

190 In vivo two-photon imaging of microglia in the intact brain has revealed that microgli

191 Microglia in these clusters display the highest CD68 exp

192 ective pathways that have been attributed to microglia in this disease.

193 is of the changes induced by phagocytosis in microglia in vitro and identified genes involved in meta

194 Depleting microglia in vivo dramatically suppressed the transmissi

195 suggesting that signals provided by reactive microglia influence how NF-kappaB impacts Muller glia re

196 are not expressed in astroglia and rarely in microglia; instead, glutamatergic neurons express LepR,

197 om alpha-synuclein preformed fibrils treated microglia into the mouse striatum.

198 propose that functional perturbation of male microglia is an important cause for sex-biased ASD.

199 tory response in 5xFAD mice and suggest that microglia is central to the association between PD and A

200 We show expression of c/EBPbeta in microglia is regulated post-translationally by the ubiqu

201 Importantly, co-manipulation of GPR17 and microglia led to extensive myelination of regenerated ax

202 ere, we establish isogenic human ESC-derived microglia-like cell lines (hMGLs) harboring AD variants

203 human induced pluripotent stem cell-derived microglia-like cells to show that TREM2 signals through

204 More importantly, by purifying microglia/macrophage derived exosomes in the CSF of Park

205 t and deliver drugs selectively to activated microglia/macrophages at the sites of injury, and suppre

206 tent SIV reservoirs was higher in the CD11b+ microglia/macrophages in morphine dependent RMs.

207 ma of infected mice with persistent CD11b(+) microglia/macrophages in the inflamed regions on day 30

208 Rather than producing cholesterol, microglia/macrophages synthesized desmosterol, the immed

209 ux of lipid and cholesterol from lipid-laden microglia/macrophages to support remyelination by oligod

210 egrity, adaptive immunity, and activation of microglia/macrophages.

211 clearance, a function that normally requires microglia/macrophages.

212 e most extensive versatility in manipulating microglia, making them ideal candidates for future studi

213 pment of alcohol dependence, suggesting that microglia may also be critical for the development and p

214 nfectious CNS disorders, with an emphasis on microglia-mediated loss of synapses.

215 n of the DA signaling pathway via regulating microglia-mediated neuroinflammation in the brain.

216 ctivity in stress-induced CSF1 signaling and microglia-mediated neuronal remodeling in the medial PFC

217 onic stress-induced neuronal activity limits microglia-mediated neuronal remodeling in the medial PFC

218 imaging in mice, we found that juxtavascular microglia migrated when microglia are actively colonizin

219 These deficits correlate with alterations of microglia-neuron crosstalk pathways and have long-lastin

220 Understanding how to assess and modulate microglia-neuron interactions critical for brain health

221 Somatic microglia-neuron junctions have a specialized nanoarchit

222 ram, evidenced by increased neurotoxicity in microglia-neuronal co-cultures.

223 nalysis using markers of myelin, astrocytes, microglia, neurons, globoid cells, and immune cells.

224 Further, we show that microglia, not peripheral myeloid cells, release IL-1alp

225 By mapping phagosomal NO produced in microglia of live zebrafish brains, we found that single

226 ented that HDAC3 expression was increased in microglia of mouse experimental stroke model.

227 ar endothelial cells, pericytes, astrocytes, microglia, oligodendrocytes and neurons to model the eff

228 isualize and manipulate interactions between microglia, oligodendrocytes, and neurons during developm

229 We transplanted either neonatal microglia or adult microglia treated with peptidase inhi

230 TREM2-deficient microglia phagocytose myelin debris but fail to clear my

231 is necessary for eliciting this spinal cord microglia phenotype and also for conferring optimal prot

232 ge bodies in AF(+) cells and led to impaired microglia physiology and cell death, suggestive of a mec

233 Microglia play a critical role in many processes fundame

234 ASO treatment shifted the composition of the microglia population by increasing the prevalence of dis

235 , neuronal Mfn2 suppressed the activation of microglia, prevented LPS-induced mitochondrial fragmenta

236 Microglia produce high levels of progranulin, and reduct

237 Microglia prune synapses, but integration of this synaps

238 Variants of the microglia receptor triggering receptor expressed on myel

239 n in the CeA, supporting the hypothesis that microglia regulate dependence-induced changes in neurona

240 al fluid (CSF), we measured 3 macrophage and microglia-related proteins, chitotriosidase (CHIT1), chi

241 the absence of murine CD4 T cells, resident microglia remained suspended between the fetal and adult

242 s, while conditional Mef2c heterozygosity in microglia reproduced social deficits and repetitive beha

243 Microglia, resident immune cells of the CNS, are thought

244 Microglia respond to neuronal activation by suppressing

245 expression, and visualization of hippocampal microglia revealed similar effects in vivo.

246 Furthermore, clustering of microglia revealed that IDOL-ASO treatment shifted the c

247 n intercellular signaling axis through which microglia shape retinogeniculate connectivity in respons

248 t the molecular level, the proteome of AF(+) microglia showed overrepresentation of endolysosomal, au

249 of adult mice, and found that both types of microglia significantly improved healing and axon regrow

250 Conversely, microglia-specific activation of Tak1 in the brainstem w

251 binds GPR56 in a domain-specific manner, and microglia-specific deletion of Gpr56 leads to increased

252 express some of the most commonly described microglia-specific markers early during development, suc

253 ur findings demonstrate for the first time a microglia-specific mechanism of RICD involving an upstre

254 injury and the presence of CD68 granules in microglia surfaces opposed to motoneurons.

255 t evidence that tumor-associated macrophages/microglia (TAMs) can promote tumor progression in the so

256 GVHD increased microglia TGF-beta-activated kinase-1 (TAK1) activation

257 iciency leads to early phenotypic changes in microglia that are not associated with an innate immune

258 a molecular interaction between neurons and microglia that drives experience-dependent synapse remod

259 Microglia, the brain's immune sentinels, have garnered m

260 Microglia, the brain's resident macrophages, help to reg

261 In addition to microglia, the brain-border regions host populations of

262 Microglia, the brain-resident macrophages, exhibit highl

263 Microglia, the innate immune cells of the central nervou

264 Microglia, the resident immune cells of the central nerv

265 cently sparked numerous exciting findings on microglia, the resident macrophages of the central nervo

266 -38 in the inhibition of activation of human microglia, thus supporting its development as a treatmen

267 crease AD risk by decreasing the response of microglia to Abeta and its local toxicity.

268 lt to delineate the specific contribution of microglia to disease.

269 which, in turn, produce IL-4 that stimulates microglia to produce IGF1 to promote tumor progression.

270 tility and preventing efficient migration of microglia to sites of neuronal damage.

271 r multifaceted approach is the first to link microglia to the molecular, cellular, and behavioral cha

272 enuates proliferation and/or infiltration of microglia to the region thereby curtailing the deleterio

273 Finally, microglia transiently adhered to the RPE before which RP

274 nsplanted either neonatal microglia or adult microglia treated with peptidase inhibitors into spinal

275 geniculate connections near TWEAK-expressing microglia, TWEAK signals via Fn14 to restrict the number

276 udies have defined a molecular signature for microglia under homeostasis.

277 Following chronic sensory deprivation, microglia undergo a morphological transition from a moni

278 forming from surveying to primed phenotypes, microglia undergo considerable molecular changes.

279 However, during disease, microglia undergo remarkable phenotypic changes, which r

280 In a normal surveillance state, microglia use oxidative phosphorylation for their energy

281 They support a mechanism by which microglia use the vasculature to migrate within the deve

282 macological removal of chronically activated microglia using a colony stimulating factor 1 receptor (

283 Selective Tak1 deletion in microglia using Cx3cr1creER Tak1fl/fl mice resulted in r

284 ated) human monocyte-derived macrophages and microglia using RNA sequencing.

285 nt in neuronal and non-neuronal (astrocytes, microglia, vascular endothelial cells) cells of cortical

286 his mechanism underlies an interplay between microglia, vascular patterning and tissue mechanics with

287 There is far less known about microglia-vascular interactions, particularly under heal

288 possible to consistently elicit spinal cord microglia via systemic delivery of inflammogens to achie

289 se microglial defects in Grn-deficient mouse microglia, we performed a compound screen coupled with h

290 umin-positive interneurons and Iba1-positive microglia were all decreased in Het mice.

291 MAC2+ microglia were also present in non-treated adult mouse b

292 In addition, microglia were less activated (P = 0.07) and the number

293 fferentiate between sample treatment groups, microglia were stimulated with the endotoxin lipopolysac

294 Neuronal alpha-synuclein activates microglia, which in turn engulf alpha-synuclein into aut

295 P21 can modulate the functional phenotype of microglia, which may have an impact on their function in

296 e complexes potentiate inflammation by human microglia, which may play an important role in MS-associ

297 port a striking buildup of lipid droplets in microglia with aging in mouse and human brains.

298 opulations under CSF1R inhibition, including microglia with reduced homeostatic markers and elevated

299 Pretreatment of microglia with ZL0580 renders them more refractory to la

300 Live imaging revealed that juxtavascular microglia within the cortex are highly motile and migrat