ライフサイエンスコーパス: astrogliosis

1 sive perimeter around foci of VZV infection (astrogliosis).

2 of astrocytes, followed over several days by astrogliosis.

3 ravasation, and 5) appearance of parenchymal astrogliosis.

4 andidate for transplantation by evoking less astrogliosis.

5 midbrain dopaminergic (DAergic) neurons and astrogliosis.

6 ypertrophy and hyperplasia known as reactive astrogliosis.

7 of macrophages or neutrophils, or increased astrogliosis.

8 esting a protective effect of CR in limiting astrogliosis.

9 iod circadian clock 2 (Per2) had no observed astrogliosis.

10 lls reflected alterations representative for astrogliosis.

11 er characteristic response to neural injury, astrogliosis.

12 gulation of pathological processes including astrogliosis.

13 fibrillary acidic protein-positive reactive astrogliosis.

14 more immature state related to the burden of astrogliosis.

15 nce functionally implicating the caspases in astrogliosis.

16 europrotective at an early onset of reactive astrogliosis.

17 ion in astrocytes leads to growth arrest and astrogliosis.

18 as directly proportional to the magnitude of astrogliosis.

19 cords with reduced destruction of myelin and astrogliosis.

20 eductions in demyelination, axonal loss, and astrogliosis.

21 nto the mouse cortex is sufficient to induce astrogliosis.

22 s in neuronal cell bodies and processes, and astrogliosis.

23 iferation of glial cells and less-pronounced astrogliosis.

24 e lower levels of inflammatory cytokines and astrogliosis.

25 ngiform) leukoencephalopathy with widespread astrogliosis.

26 l and biochemical changes, demyelination and astrogliosis.

27 /80+ reactivity and diffuse local and distal astrogliosis.

28 ads to alterations in synaptic structure and astrogliosis.

29 ormally short dendritic spines, and profound astrogliosis.

30 elective activation of PAR-1 in vivo induces astrogliosis.

31 hway may play a key role in the induction of astrogliosis.

32 location of STAT3 and prevented induction of astrogliosis.

33 mice displayed increased neuronal damage and astrogliosis.

34 ions, neurofilament inclusions, and reactive astrogliosis.

35 oid-plaque formation, neuritic dystrophy and astrogliosis.

36 e filament components in reactive fibrillary astrogliosis.

37 ohistochemical analysis showed inner retinal astrogliosis.

38 al brain evoked neither MCP-1 expression nor astrogliosis.

39 nal sprouting, as well as a role in reactive astrogliosis.

40 with vehicle, and a reduction in hippocampal astrogliosis.

41 displayed strongly reduced microgliosis and astrogliosis.

42 T cells into the CNS parenchyma, and limits astrogliosis.

43 ions was accompanied by a marked decrease in astrogliosis.

44 ies in astrocytes, such as vacuolization and astrogliosis.

45 cludes demyelination, neuro-axonal loss, and astrogliosis.

46 h WNV, resulting in apoptotic cell death and astrogliosis.

47 the pyramidal CA3 hippocampal cell layer and astrogliosis 72-h post-dose.

48 ality, brain overgrowth, laminar disruption, astrogliosis, a paucity of oligodendroglia, and myelinat

49 Reactive astrogliosis, a prominent component of CNS injury with p

50 ns occurs late in the disease after reactive astrogliosis, a response to nerve cell death.

51 IVE tissue defined the relationships between astrogliosis, activation of microglia, virus infection,

52 pregulation may serve to indicate beneficial astrogliosis after CNS injury.

53 l of genetically induced, widespread chronic astrogliosis after conditional deletion of beta1-integri

54 Astrogliosis after spinal cord injury (SCI) is a major i

55 Astrogliosis also was mildly abrogated.

56 s HdhQ200 mice exhibit striatal and cortical astrogliosis and a approximately 50% reduction in striat

57 In addition, signs of astrogliosis and a compaction of the cortical layers wer

58 and morphological and biochemical indices of astrogliosis and apoptosis were assessed in (i) cultured

59 pilepsy animal model, as well as less severe astrogliosis and attenuated mossy fiber sprouting.

60 The combined presence of astrogliosis and axonal damage in white matter has cardi

61 yloid plaque deposition, neuritic dystrophy, astrogliosis and behaviour deficits in transgenic animal

62 ling pathways in immune cells, for a role in astrogliosis and brain neuroinflammation.

63 Previous studies have shown extensive astrogliosis and cell death at acute stages (<7 days) bu

64 rogressive inflammatory responses (including astrogliosis and cytokine production), which began at 3

65 cytochemistry showed an evident reduction in astrogliosis and enhanced survival of oligodendrocytes.

66 s that regulate specific aspects of reactive astrogliosis and highlights the potential to identify no

67 ning of neuropathology after treatment, with astrogliosis and increased apoptosis of neurons.

68 of mice exposed to clade B exhibited greater astrogliosis and increased loss of neuronal network inte

69 of central sensitization, significant spinal astrogliosis and increases in activity of metalloproteas

70 incidence of malignant astrocytoma, reactive astrogliosis and intellectual deficits.

71 Nrros(-/-) mice display astrogliosis and lack normal CD11b(hi)CD45(lo) microglia

72 Immunohistochemistry revealed neuronal loss, astrogliosis and macrophage infiltration in lesioned cor

73 iation activities as well as the decrease of astrogliosis and macrophage infiltration.

74 Moreover, astrogliosis and microglia activation were reduced in pe

75 Degeneration of striatal neurons, with astrogliosis and microglia activation, begins at around

76 ve transfer of CD3-activated Treg attenuated astrogliosis and microglia inflammation with concomitant

77 genes show the most pronounced reduction in astrogliosis and microglial accumulation accompanied by

78 c effects, characterized by intense reactive astrogliosis and microglial activation associated with m

79 We also found that parkin-induced striatal astrogliosis and microglial activation were prevented by

80 ced significant neuroinflammation, including astrogliosis and microglial activation with subsequent n

81 restraint stress led to an earlier onset of astrogliosis and microglial activation within the spinal

82 The animals also exhibit significant astrogliosis and microglial activation, indicating a neu

83 reservation of spinal neurons and diminished astrogliosis and microglial activation.

84 ns loss, accompanied by axonal degeneration, astrogliosis and microglial activation.

85 rogeneous nature of this condition, reactive astrogliosis and microgliosis are frequently observed.

86 ortical volume and neuron number, as well as astrogliosis and microgliosis compared with approximatel

87 e then sacrificed to determine the extent of astrogliosis and microgliosis in the four groups.

88 noreactive deposits as well as the resulting astrogliosis and microgliosis normally observed in APP(V

89 Reactive astrogliosis and microgliosis were ameliorated when FTY7

90 ed controls, HIV positive mice had increased astrogliosis and microgliosis, cognitive deficits, and r

91 Other cellular defects include astrogliosis and microgliosis.

92 PC-induced inflammasome and are important in astrogliosis and microgliosis.

93 demonstrate profound brain atrophy, elevated astrogliosis and neurodegeneration, particularly in the

94 In the striatum, astrogliosis and neuronal atrophy were attenuated and nu

95 e-based ADK provides a critical link between astrogliosis and neuronal dysfunction in epilepsy.

96 Brains were examined histologically for astrogliosis and neuronal organization.

97 d provide a genetic model for NF1-associated astrogliosis and optic glioma.

98 cal regulator of certain aspects of reactive astrogliosis and provide additional evidence that scar-f

99 trophils using anti-Ly6G inhibits donor cell astrogliosis and rescues the capacity of a donor cell po

100 rpus callosum and cingulum along with severe astrogliosis and scar formation.

101 Astrogliosis and scrapie-associated protease-resistant P

102 associated with variable tissue destruction, astrogliosis and secondary myelin loss.

103 -1 signaling as a mediator of post-traumatic astrogliosis and seizure susceptibility.SIGNIFICANCE STA

104 ore, overexpression of calpastatin decreased astrogliosis and the calpain-dependent degradation of sy

105 gressive myelin loss that accompanies severe astrogliosis and this is exacerbated in the absence of e

106 mportant role in the ischemic stroke-induced astrogliosis and thus may serve as a novel target to con

107 e dramatic loss of Purkinje cells, intensive astrogliosis and vacuolation of neurons in the deep cere

108 HAART significantly decreased the amount of astrogliosis and viral load in treated mice compared wit

109 These lesions are associated with abundant astrogliosis and widespread fragmentation of the basal l

110 odrin fragment, expression of IEGs, reactive astrogliosis, and apoptotic features were highly increas

111 ppocampus, accompanied by forebrain atrophy, astrogliosis, and caspase-3 activation.

112 mpanied by neuronal loss, spongiform change, astrogliosis, and conspicuous microglial activation.

113 al neuron and cerebellar Purkinje cell loss, astrogliosis, and decreased weight.

114 ring white matter, markers of axonal damage, astrogliosis, and demyelination were evaluated as predic

115 ncluding spongiform degeneration, pronounced astrogliosis, and deposition of alternatively folded PrP

116 ently reduced the parenchymal plaque burden, astrogliosis, and dystrophic neurites at doses 10- to 50

117 e cells, mossy cells, mossy fiber sprouting, astrogliosis, and GABAergic interneurons.

118 antemortem cognitive impairment and abundant astrogliosis, and less-severe HIV encephalitis.

119 decreased number of oligodendrocytes, severe astrogliosis, and microglial activation in white matter

120 l protease-resistant prion protein (PrPres), astrogliosis, and microgliosis were first detected at 40

121 V encephalitis: cognitive deficits, fatigue, astrogliosis, and microgliosis.

122 that TFA-12 treatment reduces inflammation, astrogliosis, and myelin loss.

123 f the mammalian target of rapamycin pathway, astrogliosis, and neuronal disorganization, and increase

124 cytic GAP43 mediates glial plasticity during astrogliosis, and provides beneficial effects for neuron

125 neuronal migration and structure, widespread astrogliosis, and reduced expression of CASPR2.

126 such as invasion of tumor cells, spinal cord astrogliosis, and sensitization of nervous system-have b

127 f spinal motor neurons, increase of reactive astrogliosis, and shortening of gait compared with wild-

128 ompanied by reduced plaque burden, decreased astrogliosis, and suppression of inflammatory gene expre

129 GRN(-/-) mice developed microgliosis, astrogliosis, and tissue vacuolation, with focal neurona

130 proliferative indices, metastasis-associated astrogliosis, and vasculature spatial distribution.

131 ROCK pathway in the generation of a reactive astrogliosis, and we suggest that interventions targeted

132 ied by predictable microglial activation and astrogliosis, and, after cuprizone withdrawal, this acti

133 he mechanisms regulating these two phases of astrogliosis are beginning to be elucidated.

134 Microgliosis and astrogliosis are standard pathological features of neuro

135 brain, namely, an ingress of astrocytes and astrogliosis around an infectious focus.

136 lammation and reduces CSPGs accumulation and astrogliosis around demyelinated lesions in the spinal c

137 nes (IEGs) such as c-jun and c-fos, reactive astrogliosis as the expression of glial fibrillary acidi

138 of striatal dopaminergic nerve terminals and astrogliosis, as assessed by loss of striatal dopamine a

139 Increased astrogliosis, as indicated by increased glial fibrillary

140 ng that PAR-1 activation plays a key role in astrogliosis associated with glial scar formation after

141 e that Nf1/nf1 mice provide a model to study astrogliosis associated with neurofibromatosis type 1.

142 eurons during development, may contribute to astrogliosis-associated seizures.

143 h immediate and delayed treatments), or with astrogliosis at the DREZ, which begins almost immediatel

144 model mice at ages not accompanied by overt astrogliosis (at approximately postnatal days 70-80).

145 r [protease-activated receptor-1 (PAR-1)] in astrogliosis, because extravasation of PAR-1 activators,

146 toxicity, using a non-invasive reporter for astrogliosis, biochemical and histological studies.

147 8 mitogen-activated protein kinase (MAPK) in astrogliosis both in vitro and in vivo.

148 use models was not associated with classical astrogliosis, but was associated with decreased Kir4.1 K

149 es provide compelling evidence that reactive astrogliosis can exert both beneficial and detrimental e

150 cal alterations, including neuronal atrophy, astrogliosis, caspase-3-mediated apoptosis, and tau hype

151 gut and brain and enhanced microgliosis and astrogliosis compared to rats exposed to either mutant b

152 We also show that astrogliosis-conditioned medium from GAP43 knock-down as

153 ha revealed neuronal chromatolysis, reactive astrogliosis, decreased expression of myelin basic prote

154 loss in the ventral horn, decreased reactive astrogliosis, decreased the immune response, and increas

155 que formation were unaltered, synaptic loss, astrogliosis, dentate gyral atrophy, increased neuronal

156 ults demonstrate that the mode and degree of astrogliosis depend on rate of deformation, demonstratin

157 In the mouse model, neurobehavioural signs, astrogliosis, deposition of amyloid precursor protein, s

158 In TASTPM, progressive amyloidosis and astrogliosis, detected immunohistochemically, reflected

159 set astrocyte dysfunction without detectable astrogliosis drives disease-related processes in a mouse

160 brillary acidic protein (GFAP), a marker for astrogliosis during neurodegeneration.

161 ession in astrocyte proliferation leading to astrogliosis during the terminal stages of neurodegenera

162 Diffuse astrogliosis extended into the lesion surround with elev

163 Astrogliosis following spinal cord injury (SCI) involves

164 Astrogliosis following spinal cord injury (SCI) involves

165 mor necrosis factor alpha (TNFalpha)-induced astrogliosis following spinal cord injury.

166 critical role in astroglial cell activation (astrogliosis) following CNS injuries and neurodegenerati

167 servation of motor neuron architecture, less astrogliosis (glial fibrillary acidic protein), and mark

168 Although injury-induced astrogliosis has been investigated, the relationship bet

169 Accumulating evidence suggests that reactive astrogliosis has beneficial and detrimental outcomes in

170 CNS inflammation and injury associated with astrogliosis has recently been found to occur in the ene

171 The mechanisms that control the cascade of astrogliosis have not been well established.

172 in subcortical white matter, as was cortical astrogliosis, hippocampal sclerosis, and status marmorat

173 e for the role of LacCer in TNFalpha-induced astrogliosis in a rat model of SCI.

174 associated with diminished microgliosis and astrogliosis in aged mice.

175 n MTR at 20ppm correlated with the extent of astrogliosis in both gray and white matter.

176 icity in EAE helps to clarify the origins of astrogliosis in CNS inflammatory demyelinative disorders

177 tion of LPS, we observed markedly attenuated astrogliosis in conditional GFAPcre p38alpha(-/-) mice.

178 pression of CRYAB and the extent of reactive astrogliosis in demyelinating areas and in in vitro assa

179 ging agents to sites of vascular changes and astrogliosis in diseases associated with neuroinflammati

180 ation in capillaries of ventral striatum and astrogliosis in dorsal striatum in both cerebral hemisph

181 eneration, abnormal tau phosphorylation, and astrogliosis in gp120 transgenic mice.

182 The prevailing dogma of the role of astrogliosis in inhibition of axonal regeneration has be

183 77 gene caused premature death with dramatic astrogliosis in mouse brain.

184 o exacerbation of cell loss, microgliosis or astrogliosis in multiple brain regions.

185 The exact cause(s) of the astrogliosis in obesity is not known.

186 oreactivity in the tumor mass; (3) decreases astrogliosis in peritumoral area; and (4) reduces glioma

187 P expression, correlating with a decrease in astrogliosis in response to neural injury during EAE.

188 nuclei of the hypothalamus showed comparable astrogliosis in response to obesity.

189 are tumor free, these mice display extensive astrogliosis in the absence of conspicuous neurodegenera

190 opmental defect resulting in global reactive astrogliosis in the adult brain and increased proliferat

191 ic hypothermia and xenon resulted in reduced astrogliosis in the CA1 sector and diminished microglios

192 tein 2 (Npas2), induced severe age-dependent astrogliosis in the cortex and hippocampus.

193 ppocampus showed progressive neuron loss and astrogliosis in the dentate gyrus (DG).

194 FA was correlated with astrogliosis in the gray matter, whereas mean diffusivit

195 stem (CNS) concomitant with inflammation and astrogliosis in the multiple sclerosis (MS) mouse model

196 d accumulation of mutant SOD1 within MNs and astrogliosis in the spinal cord, which are also both del

197 ents, there is no evidence of neuron loss or astrogliosis in the striatum.

198 her demonstrated decreased neuronal loss and astrogliosis in the thalamus and less thalamic fiber los

199 orted by extensive microglial activation and astrogliosis in virally infected brains.

200 of these three receptor classes can lead to astrogliosis in vivo and proliferation of astrocytes in

201 t favors the beneficial outcomes of reactive astrogliosis in vivo.

202 ritical to regulate the outcomes of reactive astrogliosis in vivo.

203 of the functions and mechanisms of reactive astrogliosis in vivo.

204 se inhibitors were assessed on indicators of astrogliosis, including stellate morphology and expressi

205 1 general KO mice showed neither fibrils nor astrogliosis, indicating a specific role for ERK2 in the

206 Moreover, GAP43 knockdown aggravated astrogliosis-induced microglial activation and expressio

207 stic changes of astrocytes while attenuating astrogliosis-induced microglial activation and neurotoxi

208 ultured neonatal rat astrocytes treated with astrogliosis-inducing stimuli (dibutryl cAMP, beta-amylo

209 tive, it is difficult to distinguish whether astrogliosis is a cause or a consequence of epileptogene

210 Astrogliosis is a complex state in which injury-stimulat

211 Reactive astrogliosis is a critical process in neuropathological

212 Astrogliosis is a defense response of the CNS to minimiz

213 Astrogliosis is a pathological hallmark of the epileptic

214 Reactive astrogliosis is a prominent pathological feature of mult

215 Reactive astrogliosis is an essential feature of astrocytic respo

216 Reactive astrogliosis is beneficial in many aspects; however, it

217 Reactive astrogliosis is characterized by a profound change in as

218 Astrogliosis is induced by neuronal damage and is also a

219 Because astrogliosis is linked to disease severity, understandin

220 Astrogliosis is observed in all forms of brain injury an

221 use model of focal epileptogenesis, in which astrogliosis is restricted to the CA3 region of the hipp

222 implying that overexpression of ADK without astrogliosis is sufficient to cause seizures.

223 rin deletion, supporting the hypothesis that astrogliosis is sufficient to induce epileptic seizures.

224 Reactive astrogliosis is the gliotic response to brain injury wit

225 Astrogliosis is the hallmark of neuroinflammation and is

226 (C) absence in this transgenic AD model, and astrogliosis is unchanged.

227 on manifested by microglial infiltration and astrogliosis linked with disruption of the retinal organ

228 A receptors, microglial activation, reactive astrogliosis, loss of descending inhibition, and spastic

229 Moreover, astrogliosis may be common to both teratogens.

230 sociated with microvessels suggests that the astrogliosis may be occurring as a response to changes a

231 the signaling network that controls reactive astrogliosis may provide novel treatment targets for pat

232 l analysis of ADAM10-depleted brain revealed astrogliosis, microglia activation, and impaired number

233 gressive axonal degeneration, accompanied by astrogliosis, microglial activation, partial loss of oli

234 esion volume, neuronal injury and apoptosis, astrogliosis, microglial activation, pro-inflammatory si

235 pinal cord white matter together with marked astrogliosis, microglial infiltration, and secondary axo

236 ice showed hippocampal and cortical atrophy, astrogliosis, microgliosis, and abnormal CA1 dendritic m

237 S alphaS inclusion pathology, accompanied by astrogliosis, microgliosis, and debilitating motor impai

238 Reduced astrogliosis, microgliosis, and enhanced perivascular en

239 specifically in brain subregions with active astrogliosis, microgliosis, and neuronal loss.

240 tivation and virus infection correlated with astrogliosis, monocyte transendothelial migration, and b

241 s, the white matter tracts displayed intense astrogliosis, myelin pallor, and decreased neurofilament

242 ed by p25 overexpressing neurons to initiate astrogliosis, neuroinflammation and subsequent neurodege

243 r pericytes, and neurons, causing micro- and astrogliosis, neuroinflammation, accumulation of lipofus

244 etastases are associated with instigation of astrogliosis, neuroinflammation, and hyperpermeability o

245 Overexpression of GFAP is an indicator of astrogliosis/neuroinflammation in CNS injury.

246 rior to activation of STAT3 and induction of astrogliosis; neuroprotection with nomifensine blocked t

247 In these mice, astrogliosis occurs in the absence of other pathologies

248 epilepsy resulting from genetically induced astrogliosis or malignant transformation, both of which

249 Minocycline had no effect on astrogliosis or spreading depression, a wave of ionic tr

250 nt inhibited STAT-3 phosphorylation, but not astrogliosis or transcription factors regulating gliosis

251 tent of mossy fiber sprouting, the extent of astrogliosis, or the number of GABAergic interneurons in

252 in cerebral amyloid-beta protein levels and astrogliosis (P < 0.001 and P < 0.0001), with no apparen

253 el candidate for an intracellular trigger of astrogliosis, particularly in aging and AD brain.

254 Our findings suggest that astrogliosis, physiologically instigated as a brain tiss

255 vivo treatment with the PA after SCI reduced astrogliosis, reduced cell death, and increased the numb

256 We postulate that astrogliosis represents a successful defense mechanism b

257 tly reduced ataxin 3 neuronal inclusions and astrogliosis, rescued diminished body weight and strikin

258 developed larger infarcts and an exaggerated astrogliosis response following ischemic stroke.

259 e GAP43) or knockdown of GAP43 all inhibited astrogliosis responses.

260 Astrogliosis significantly increased in corpus callosum

261 hemical staining showed significant reactive astrogliosis surrounding Abeta plaques with increased PF

262 lin-B1(-/-) mice, which showed more plaques, astrogliosis, synaptic degeneration, cognitive impairmen

263 ell as oxidative stress, Abeta accumulation, astrogliosis, synaptic loss, and caspase activation in t

264 ncreased angiogenesis and decreased reactive astrogliosis that resulted in reduced scar formation.

265 Termed astrogliosis, this response has been shown to strongly i

266 hanges include spongiform neurodegeneration, astrogliosis, thymic atrophy, and T-cell depletion.

267 The identification of mechanisms that link astrogliosis to neuronal dysfunction in epilepsy may pro

268 tential to modulate the outcomes of reactive astrogliosis to protect CNS under pathological condition

269 The contribution of astrogliosis to WMI was further tested in a mouse model

270 nt ES cell-derived brain implants suppressed astrogliosis, upregulation of ADK, and spontaneous seizu

271 the effects of strain rate on cell death and astrogliosis using a three-dimensional (3-D) in vitro mo

272 ent neurons are capable of inducing reactive astrogliosis via a non-cell autonomous mechanism.

273 This decrease in astrogliosis was also witnessed in the lessening of seve

274 Moreover, this reactive astrogliosis was associated with neuronal death as visua

275 cultures, hypoxia and scratch injury-induced astrogliosis was attenuated by both p38 inhibition and k

276 liorated when FTY720 was given from d 1, but astrogliosis was augmented when FTY720 was given from wk

277 Injury-induced astrogliosis was compared to co-cultures treated with tr

278 Here, reactive astrogliosis was induced with IL1beta.

279 While a significant reduction of astrogliosis was observed in the GFAP/p38 knockout mice

280 Astrogliosis was prominent in end-stage SMA mice and in

281 f injury, without CD4 down-modulation; focal astrogliosis was restricted to the site of the lesion, a

282 Comparatively, little astrogliosis was seen in the ventromedial nucleus, later

283 While astrogliosis was similar in injured IL-6 (+/+) and IL-6

284 Furthermore, both plaque burden and astrogliosis were drastically reduced.

285 MPTP-induced microglial activation and astrogliosis were not affected by P110 treatment.

286 ocampal CA3 neuron loss as well as extensive astrogliosis were observed in all injured animals, sugge

287 f vimentin protein levels, common markers of astrogliosis, were present after 4 d of kindling.

288 Reactive astrogliosis, whereby astrocytes undergo varying molecul

289 uronal apoptosis, inflammation, and reactive astrogliosis, which contribute to secondary tissue loss,

290 ted a transient increase in microgliosis and astrogliosis, which declined within a few weeks.

291 rm of the molecular clock can lead to severe astrogliosis, which likely occurs through disruptions in

292 ided with microscopic necrosis or identified astrogliosis with high sensitivity and specificity.

293 triggered extensive and persisting reactive astrogliosis, with most neurons being preserved, little

294 et (postnatal day 35 to 40) frontal cortical astrogliosis, without evidence of neuronal degeneration.