ライフサイエンスコーパス: glial

1 cognitive deficits, hippocampal neuron loss, glial activation and accumulation of dipeptide-repeat pr

2 of age revealing significant and progressive glial activation and vulnerability of spinal interneuron

3 extensive pattern of significantly increased glial activation bilaterally in the primary motor cortic

4 NAD(+) supplementation on neuronal death and glial activation in the facial nucleus in the brain stem

5 onstrate the spatial and temporal pattern of glial activation in the I307N Rho mouse, and correlate t

6 Neuro-glial activation is a recently identified hallmark of gr

7 D) is characterized by neuroinflammation and glial activation that, together with the release of vira

8 Glial activation was more robust in the inferior retina

9 mic inflammation and those for astrocyte and glial activation were associated with longer delirium du

10 ce had greater neuroinflammation, microglial/glial activation, and GABA signaling and lower synaptic

11 cumulation of lysosomal storage material and glial activation, and has limited perturbation in behavi

12 her degrees of neuroinflammation, microglial/glial activation, GABA signaling, and intestinal dysbios

13 tinase-3-like protein 1 (CHI3L1), markers of glial activation, in cerebrospinal fluid (CSF) and plasm

14 idase B in severe reactive astrocytes causes glial activation, tauopathy, neuronal death, brain atrop

15 f novel therapeutics that target deleterious glial activity.

16 Activation of glial alpha1-adrenergic receptors triggers rapid astrocy

17 ifespan, impaired synaptic transmission, and glial and axonal loss.

18 r of integrin in the glia, supporting proper glial and extracellular matrix ensheathment of the nervo

19 ated expression of gene sets associated with glial and immune function, and reduced expression of gen

20 onic stem cells contained a diverse array of glial and neuronal cell types.

21 To capture corticogenesis, we sampled glial and neuronal lineages from dorsal or ventral foreb

22 summary, both loss and gain of ACOX1 lead to glial and neuronal loss, but different mechanisms are at

23 ular mechanisms underlying the regulation of glial and neuronal size are poorly understood.

24 ly buffer the cells against damage caused by glial and neuronally generated reactive oxygen species (

25 tic lineage reconstruction to show that nine glial and thirty-three neuronal subtypes are generated b

26 ce-activated cell sorting (FACS) to sort the glial and vascular cells from the brains of the mice tre

27 ive behavior, as well as potential neuronal, glial, and extracellular matrix contributions to functio

28 es, but also suggest possible extrasynaptic, glial, and mitochondrial GluD1 functions.

29 sound causes change of phenotype from neural/glial antigen 2 positive/alpha-smooth muscle actin negat

30 alpha-smooth muscle actin negative to neural/glial antigen 2 positive/alpha-smooth muscle actin posit

31 o upregulate galectin-3 (MAC-2), a marker of glial axonal debris phagocytosis, on NMJ denervation in

32 We confirmed the relevance of this glial barrier system in human multiple sclerosis active

33 agments decorating a complex architecture of glial basal process ramifications.

34 However, although our understanding of glial biology is increasing, the signals that emanate fr

35 nd repair and reveal a new role for Nedd4 in glial biology.

36 uantification of the through flow across the glial boundary is obtained for a large parameter space o

37 These include glial brain tumors, relapsed high-risk neuroblastoma, em

38 tory mediators, which could further initiate glial cell activation.

39 An early and persistent alteration of glial cell activity takes place at the neuromuscular jun

40 Here, we discuss how glial cell adhesion molecules and the extracellular matr

41 uncommon bilateral retinal disease, in which glial cell and photoreceptor degeneration leads to centr

42 tead form membranous attachments to a single glial cell at the nose, reminiscent of dendrite-glia con

43 onserved gene modules from both neuronal and glial cell classes.

44 gesting an integrated network of immune cell-glial cell communication.

45 Invaginations in the glial cell cytoplasm house the neurites, an association

46 limod (FTY720) attenuates psychosine-induced glial cell death and demyelination both in vitro and ex

47 By adulthood, neocortical glial cell density and gene expression were decreased, w

48 We studied whether administration of glial cell derived neurotrophic factor (GDNF) induces en

49 othesize that complement-mediated changes in glial cell function significantly contribute to RICD.

50 Glial cell line-derived neurotrophic factor (GDNF) binds

51 nt sensitization and increased expression of glial cell line-derived neurotrophic factor (GDNF) in in

52 Glial cell line-derived neurotrophic factor (GDNF) is a

53 reatment of a single extraocular muscle with glial cell line-derived neurotrophic factor (GDNF) to pr

54 ic factor (BDNF), neurotrophin-3 (NT-3), and glial cell line-derived neurotrophic factor (GDNF) were

55 hages deliver therapeutics to CNS, including glial cell line-derived neurotrophic factor (GDNF), and

56 and agonism are independent of a coreceptor glial cell line-derived neurotrophic factor family recep

57 tivation and stress response cytokine of the glial cell line-derived neurotrophic factor family withi

58 ich is required by the natural growth factor glial cell line-derived neurotrophic factor, and are sel

59 ponent of the postnatal SVZ, promotes radial glial cell maintenance and proliferation in an autocrine

60 lizable genetic methods to study neuronal or glial cell morphology in the mammalian brain.

61 opeptide processing and secretion suppressed glial cell nonautonomous induction of the UPR(ER) and li

62 patterns of differential gene expression in glial cell populations.

63 scular, as well as neuronal cell changes and glial cell remodeling.

64 ts catalytic inactivation, causes defects in glial cell specification.

65 lay the main peripheral sensory neuronal and glial cell subtypes.

66 Astrocytes are a type of glial cell that tile the CNS.

67 enesis by postnatal glial cells and unveil a glial cell type-dependent HIFalpha-Wnt axis in regulatin

68 n and cell migration regulation of different glial cell types in response to EF stimulation.

69 across diverse hypothalamic cell types, with glial cell types responding much more robustly than neur

70 esulted in a unified taxonomy of neuronal or glial cell types, partly due to limited data.

71 ate interactions between resident neural and glial cell types.

72 ressed in human brain, and both neuronal and glial cell types.

73 The effects of neither glial cell-derived neurotrophic factor (GDNF) nor seroto

74 ctor, brain-derived neurotrophic factor, and glial cell-derived neurotrophic factor and release axon-

75 Glial cell-line-derived neurotrophic factor levels were

76 ive PCR measurements and protein analyses of glial cell-line-derived neurotrophic factor, a crucial f

77 Polarized glial-cell activation, white-matter lesion formation and

78 As ATP is the primary signaling molecule of glial cells (astrocytes, microglia), responding to metab

79 was designed to examine the role of enteric glial cells (EGCs) in colonic neuromuscular dysfunctions

80 "Pre-OPCs" that originate from outer radial glial cells (oRGs) and undergo mitotic somal translocati

81 deling shows reduced proliferation of radial glial cells (RGCs), leading to smaller organoids charact

82 regulate nerve repair, but whether satellite glial cells (SGC), which completely envelop the neuronal

83 Satellite glial cells (SGCs) closely envelop cell bodies of neuron

84 dorsal root ganglia (DRG) known as satellite glial cells (SGCs) potentiate neuronal activity by relea

85 We suggest that glial cells activated by pro-inflammatory cytokines can

86 y and reduce the resistance of U87 malignant glial cells against TMZ.

87 al carbon metabolism in primary mouse Muller glial cells and a human Muller glia cell line (M10-M1 ce

88 with multiple cell types, including neurons, glial cells and blood vessels, and are involved or impli

89 mammalian astrocytes that derive from radial glial cells and elaborate processes to establish their t

90 he nervous system.SIGNIFICANCE STATEMENT The glial cells and extracellular matrix play important role

91 The function of perineurial glial cells and how they interact with the extracellular

92 In primary cultures of glial cells and in the in vivo mouse model, EcoHIV expos

93 ation in vitro, in primary cultures of mouse glial cells and in vivo, in a mouse model of EcoHIV-asso

94 een linked to a loss in the retina of Muller glial cells and the amino acid serine, synthesized by th

95 derstanding of CNS angiogenesis by postnatal glial cells and unveil a glial cell type-dependent HIFal

96 Glial cells are abundant in the CNS and are essential fo

97 data collectively suggest that hypothalamic glial cells are leading targets for the effects of FGF1

98 Here, we reveal that glial cells at disease-vulnerable NMJs often fail to gui

99 These results show that glial cells at the NMJ elaborate an inappropriate respon

100 erations in perisynaptic Schwann cell (PSC), glial cells at this synapse, may impact their ability to

101 ar deficits in well myelinated mice in which glial cells cannot fully support axons metabolically.

102 to Abeta-burdened neurons, since neighboring glial cells did not express similar molecules.

103 e show that in human neuronal precursors and glial cells in culture, ZIKV infection activates both mT

104 stand the interplay between the vascular and glial cells in initiating and driving acute neuroinflamm

105 nic cation transporter 2 (OCT2) in satellite glial cells in oxaliplatin-induced neurotoxicity, and de

106 There is increasing evidence that supporting/glial cells in sensory systems function in sensory trans

107 strocytes, the most abundant cell type among glial cells in the brain, in Abeta clearance.

108 Glial cells in the cortex and corpus callosum underwent

109 ns, in this effect; there are relatively few glial cells in the insect brain and they are rarely asso

110 ction of neurons, more recently, the role of glial cells in the processing of sensory input has gaine

111 Astrocytic glial cells interact with synapses throughout the whole

112 Assembled alpha-synuclein in nerve cells and glial cells is the defining pathological feature of neur

113 We also learned that glial cells missing (GCM), a key transcription factor of

114 -dependent monooxygenase family 3 (FMO3) and glial cells missing (GCM).

115 ] and fusogenic [syncytin 1, syncytin 2, and glial cells missing 1 (GCM1)] genes in first trimester p

116 demonstrate that the glial cells of the C. elegans amphid apparatus serve as

117 nd the TNF receptor Grindelwald in pigmented glial cells of the Drosophila retina leads to age-relate

118 Studies of K(+) content in glial cells of the fly brain were also performed using a

119 Schwann cells, the principal glial cells of the peripheral nervous system, are now co

120 , neurons are generated directly from radial glial cells or indirectly via basal progenitors.

121 y morphological or functional changes in the glial cells or vasculature of Jedi-1 knockout mice.

122 Thus, astrocyte-like glial cells play a role in regulating organismal ER stre

123 s and/or oligodendrocytes, even though these glial cells produce much less of the protein than do neu

124 nificance of autonomic circuit modulation by glial cells remain largely unknown.

125 Single-cell RNA sequencing of vascular and glial cells revealed that apoE4 in VMCs was associated w

126 atory neuronal layers, it is unclear whether glial cells show distinct layering.

127 Draper/MEGF10 signaling in glia, indicating glial cells spread injury signals and actively suppress

128 Hypothalamic tanycytes are chemosensitive glial cells that contact the cerebrospinal fluid in the

129 a complex network constituted of neurons and glial cells that ensures the intrinsic innervation of th

130 EcI is highly expressed in surface glial cells that form the BBB, and EcI knockdown in the

131 jury requires the mobilization of immune and glial cells to form a protective barrier that seals the

132 SVGAs), an immortalized, mixed population of glial cells transformed with simian virus 40 (SV40) T an

133 ow the complex interplay between neurons and glial cells ultimately lead to the degeneration of motor

134 sophila by elevating levels of fly Dube3a in glial cells using repo-GAL4, not neurons.

135 tor cortex correlating with Iba1 expression (glial cells).

136 mitochondrial dysfunction, severe damage to glial cells, and impaired vision.

137 effects of the gut microbiota on T cells and glial cells, and their relevance for the control of infl

138 neurovascular unit, which includes neurons, glial cells, and vascular cells, plays crucial roles in

139 Astrocytes, a major type of glial cells, are emerging as a critical component in mos

140 fingolimod also regulates the reactivity of glial cells, astrocytes and microglia, in this mouse mod

141 onception revealed high expression in radial glial cells, compatible with a role in neurogenesis.

142 lded proteins inside and outside neurons and glial cells, leading to a loss of cellular protein homeo

143 ostaining of all specimens were positive for glial cells, microglia, and hyalocytes.

144 ontrary to observations made in neuronal and glial cells, n-3 PUFA treatment attenuated cAMP accumula

145 ers in neuronal circuits-the neurons and the glial cells, providing the foundation necessary for stud

146 increase is also observed in APOE-deficient glial cells, reflecting impaired brain cholesterol trans

147 Aromatase expression was observed in radial glial cells, revealed by co-localization with the glial

148 ocytes, a highly heterogeneous population of glial cells, serve as essential regulators of brain deve

149 This results in the loss of glial cells, significant disruptions in myelination, and

150 ed in the nuclei of unmyelinated neurons and glial cells, suggesting the existence of a molecular mac

151 ous system is ensheathed by a layer of outer glial cells, the perineurial glia, and a specialized ext

152 entromedial and dorsomedial neurons and some glial cells, which persist into adulthood.

153 all the nuclei along their course belong to glial cells.

154 anges in the culture medium were measured in glial cells.

155 removal of Pcdhgs from pyramidal neurons or glial cells.

156 ant metabolic housekeeping function of these glial cells.

157 resence of bile acid receptors on immune and glial cells.

158 lls recruited to the CNS and by CNS-resident glial cells.

159 nters the brain through a permeable layer of glial cells.

160 he direct transdifferentiation of sex-shared glial cells.

161 nding of the nervous system must incorporate glial cells.

162 risk variants could affect the physiology of glial cells.

163 pinephrine acts directly on these ubiquitous glial cells.

164 Epigenetic factors are also enriched in glial cells.

165 d apoptosis and inflammation in neuronal and glial cells.

166 es in their cell type-specific expression in glial cells.

167 bapical regions of photoreceptors and Muller glial cells; rather, it localizes to a small region of c

168 d human interlaminar astrocytes in humanized glial chimeric mice by engrafting astrocytes differentia

169 that the sensory neuron and its surrounding glial coat form a functional unit that orchestrates nerv

170 ion by a mechanism related to effects across glial compartments and linked in part to regulatory acti

171 he ventral nerve cord shortening, peripheral glial compression, and locomotor phenotypes, and that re

172 f Basigin is sufficient to rescue peripheral glial compression.

173 n-binding protein Talin can partially rescue glial compression.

174 We here shift the focus from neural to glial contribution to brain synchronization and examine

175 The sensor is applied to neuron-glial cultures and macrophage under the stimulation of l

176 Using mixed neuronal and glial cultures from neonatal mouse cortex of both sexes,

177 p.M719V mutation carriers showed widespread glial CYLD immunoreactivity.

178 Draper and involves a transient visit to the glial cytoplasm, indicating that phagocytic glia act as

179 we further investigated whether neuronal or glial cytoplasmic inclusions in the prefrontal, temporal

180 Although no differences in neuronal or glial cytoplasmic inclusions were identified between the

181 , including decreased cortical thickness and glial density in subgenual anterior cingulate cortex, re

182 esonance spectroscopy suggest that neuron or glial density, mitochondrial energetic metabolism, and/o

183 esults support multifocal abnormal neuron or glial density, mitochondrial energetics, or neuroinflamm

184 with the key RET ligand/coreceptor complex, glial-derived neurotrophic factor and its coreceptor, ex

185 dial glial precursors and their neuronal and glial descendants, we observed increased ornithine decar

186 ur current understanding of how neuronal and glial development affects CNS angiogenesis and barrierge

187 in the STAT3 signaling pathway indicative of glial differentiation.

188 to investigate roles of CHD7 in neuronal and glial differentiation.

189 s of Chd7 significantly reduced neuronal and glial differentiation.

190 s the molecular determinants of neuronal and glial diversity along temporal and spatial scales of hyp

191 Glial dysfunction contributes to numerous aspects of the

192 ociated with cognitive decline and transient glial dysfunction, and stimulates antioxidant, proteasom

193 xosomal secretion of a psychosis-altered and glial-enriched miRNA that controls neuronal gene express

194 d nothing is known about the intersection of glial epigenetic signaling and presynaptic homeostatic p

195 atures (including pyramidal neuron depth and glial expression) and allowed for competitive simulation

196 Thus, this work shows how glial factors can help to shape dendrites, and identifie

197 idence has implicated the nervous system and glial family ligands (GFLs) as potential drivers of hema

198 rentiation toward three lineages of neuronal-glial fate specification.

199 ylglucosamine (O-GlcNAc), in NSCs promotes a glial fate switch.

200 Glial fibrillary acidic protein (GFAP) and ionized calci

201 e Transporter (GLAST); the reactive markers: Glial Fibrillary Acidic Protein (GFAP) and S100 Calcium-

202 Glial fibrillary acidic protein (GFAP) is a measure of a

203 In the current study, we generated a glial fibrillary acidic protein (GFAP) promoter-driven a

204 In this study, we generated a glial fibrillary acidic protein (GFAP) promoter-driven a

205 tau (t-tau), neurofilament light (Nf-L), and glial fibrillary acidic protein (GFAP) with common spora

206 kers neurofilament light chain (NFL), S100B, glial fibrillary acidic protein (GFAP), amyloid-beta (Ab

207 cant increase in the blood concentrations of glial fibrillary acidic protein (GFAP, p = 0.0074) and m

208 6 [IL-6]) and astrogliosis/astrocyte damage (glial fibrillary acidic protein [GFAP]) were measured.

209 All proteins except glial fibrillary acidic protein and c-reactive protein w

210 Glial fibrillary acidic protein expressing (GFAP(+)) gli

211 ases of the astroglial biomarkers S-100B and glial fibrillary acidic protein in CSF, and in BBB perme

212 Glial fibrillary acidic protein was elevated postinjury

213 Immunohistochemistry using astrocytic (glial fibrillary acidic protein) and microglial (ionized

214 istration, with the use of selected markers (glial fibrillary acidic protein, doublecortin, calretini

215 The activation includes upregulation of glial fibrillary acidic protein, stronger gap junction-m

216 Glial fibrillary acidic protein, ubiquitin c-terminal hy

217 n of the l-type amino acid transporter, with glial fibrillary acidic protein-positive astrocytes but

218 Glial-fibrillary-acidic-protein (GFAP) has recently draw

219 t loss of function due to the formation of a glial-fibrotic scar.

220 known as exosomes to influence neuronal and glial function via their microRNA (miRNA) cargo has posi

221 ptoms and that antidepressants may normalize glial function.

222 ation of cortical stem cells to neuronal and glial generation are incompletely understood, despite th

223 ls and their protective scaffolding, gain of glial glutamate antiporter xCT expression, and reactive

224 identified local interneuron loss and excess glial glutamate release as chief contributors to network

225 ansfer and (1)H-MRS methods, lower levels of glial glutamate transporter-1 and ATP-alpha, but increas

226 The manipulation of glial glycolytic activity through this pathway enabled u

227 used to assess the neuromodulatory effect of glial Gq-GPCR activation in awake mice.

228 ne protein eas-1/GOLT1B negatively regulates glial growth.

229 cis-Golgi to the trans-Golgi network to stop glial growth.

230 ound promising associations between thalamic glial histological signatures and ensuing release of Iba

231 There are suggestions in the literature that glial hypofunction is associated with depressive symptom

232 e-elevated expression of overlapping sets of glial/immune-related genes and female-biased expression

233 Far beyond a copious but passive substrate, glial influence is inextricable from neuronal physiology

234 es a novel platform for understanding neuron-glial interaction and its alterations in neurological di

235 icity with an arc toward appreciating neuron-glial interactions and the role that each neural cell ty

236 a function for this isoform at photoreceptor-glial junctions and demonstrate that loss of this isofor

237 hysical analysis and the velocity across the glial layer is found to flow from and to the PVS, depend

238 mitotic development were sufficient to alter glial layering, indicating an instructive role for neuro

239 We show that the glial LDs initially buffer the cells against damage caus

240 ons, preceded by an abnormal accumulation of glial LDs.

241 ce that selective optogenetic stimulation of glial-like GAD65(+) TBCs evokes neural activity and modu

242 nonilluminated H(2)O, suggesting that type I glial-like TBCs are sufficient for driving a behavior th

243 Historically, type I glial-like TBCs have been thought to play a supportive r

244 nant variant in ACOX1 (p.N237S) also exhibit glial loss.

245 Neuronal activity drives growth of glial malignancies through secreted growth factors and t

246 Da translocator protein (TSPO), an activated glial marker expressed on mitochondrial membranes.

247 cells, revealed by co-localization with the glial marker GFAP and absence of co-localization with th

248 ll proliferation and increased expression of glial markers and glia-enriched genes.

249 be identified by the expression of canonical glial markers.

250 ne expression and motif accessibility during glial maturation that may prevent efficient reprogrammin

251 this arc of inquiry from neuronal to neuron-glial mechanisms by which activity and experience modula

252 rved Ig superfamily protein, Basigin, at the glial membrane of Drosophila where it associates with th

253 grin-based focal adhesion complexes link the glial membrane to the extracellular matrix, but little i

254 ressed in close proximity to integrin at the glial membrane, and that expression of the extracellular

255 e uncover a Slit-independent role of Robo in glial migration and show that neurons can release an ext

256 eaved extracellular Robo fragment to mediate glial migration and SYG-1/Neph functions through regulat

257 function as a ligand for SYG-1/Neph to guide glial migration.

258 t the molecules that coordinate dendrite and glial morphogenesis are mostly unknown.

259 e arrest, apoptosis, progressive change to a glial morphology and reduction in neuronal differentiati

260 synaptogenesis, the role of contact-mediated glial-neuronal interactions in synapse formation and eli

261 However, the extent to which glial or neuronal signaling contributes to these diverse

262 Outer radial glial (oRG) cells are a population of neural stem cells

263 h of terminal cell divisions of outer radial glial (oRG) progenitors, suggesting cellular functions o

264 Interestingly, remarkably different glial phenotypes were evident in human AD.

265 d processes include disturbances in neuronal-glial plasticity, monoaminergic signalling, inflammatory

266 ease-modifying regulation of the other major glial populations, namely astrocytes and oligodendrocyte

267 in which the Tsc2 gene is deleted in radial glial precursors and their neuronal and glial descendant

268 t grow more efficiently when in contact with glial precursors growing ahead of them.

269 on along the length of axons, dendrites, and glial processes has been proposed as a major contributor

270 ellular space between photoreceptors, Muller glial processes were identified.

271 Radial glial progenitor cells (RGPs) are the major neural proge

272 l cycle progression or survival in iPSCs and glial progenitor cells or astrocyte differentiation.

273 Cs, suggesting ET-1's role as a regulator of glial progenitor proliferation may be conserved in human

274 Orderly division of radial glial progenitors (RGPs) in the developing mammalian cer

275 adult neurons and glia originate from radial glial progenitors (RGs), a type of stem cell typically e

276 The roles that neuronal and glial progenitors and mature cells play in CNS angiogene

277 neuroepithelial cells and neurogenic radial glial progenitors are coexisting.

278 nts of both neuroepithelium cells and radial glial progenitors follow the same developmental trajecto

279 d species-specific gene networks controlling glial quiescence, reactivity, and neurogenesis.

280 C retinas demonstrated significant RGC loss, glial reactivity and apoptosis compared to control retin

281 In adulthood, ONLR-NPCs may enable glial replacement and remyelination.

282 Our purpose was to describe the glial response in this mouse model to educate future exp

283 ron and muscle loss, but in the absence of a glial response.

284 r chondroitinase ABC (chABC), tested here in glial scar models, and ability of cervically-patterned s

285 al cord injury contributing new cells to the glial scar.

286 xons to penetrate the inhibitory spinal cord glial scar.

287 sequences of cranial implants, which include glial scarring, meningeal lymphangiogenesis, and increas

288 proteoglycans (CSPGs)-a primary component of glial scars.

289 te transmission across synapses requires the glial scavenger receptor Draper and involves a transient

290 Glial signals are known to inhibit axonal regeneration a

291 d potentially conserved mechanism underlying glial size control.

292 To investigate the mechanisms involved in glial size regulation, we used Caenorhabditis elegans am

293 inct tau strains that propagate neuronal and glial tau aggregates in nontransgenic (nonTg) mouse brai

294 Thus, glial tau pathology has significant functional consequen

295 Yet the mechanism of glial tau transmission is unknown.

296 del to knock down tau in neurons to test for glial tau transmission.

297 ike progressive supranuclear palsy, globular glial tauopathy and argyrophilic grain disease(10), CBD

298 ic hamartomas (RAH) is a benign vascularized glial tumor of the retina.

299 maintenance, and BPTF knockdown leads these glial tumors toward more neuronal characteristics.

300 nded the life span in Caenorhabditis elegans Glial XBP-1s initiated a robust cell nonautonomous activ

301 Early blockade of glial xCT activity inhibited later seizures, and genomic