ライフサイエンスコーパス: gliosis

1 ies virus and observed similar perimeters of gliosis.

2 ion pathology that is associated with robust gliosis.

3 n excess, were sufficient to induce reactive gliosis.

4 P23:Gfap-luc) mice, indicative of astrocytic gliosis.

5 ent maps might be associated with astrocytic gliosis.

6 l lethality associated with microcephaly and gliosis.

7 ile enhancing Abeta plaque load and reactive gliosis.

8 iseases of the retina involving fibrosis and gliosis.

9 ychosine accumulation, white matter loss and gliosis.

10 fic program of nonproliferative hypertrophic gliosis.

11 h as inflammation, edema, demyelination, and gliosis.

12 eper cortical layers that experienced higher gliosis.

13 als immediately before the onset of reactive gliosis.

14 s as an early step in oncogenic Kras-induced gliosis.

15 emyelination, immunological stimulation, and gliosis.

16 sident astrocytes, a process termed reactive gliosis.

17 in the mutant mice did not exhibit signs of gliosis.

18 PrP plaque formation, spongiform change, and gliosis.

19 epressor TDP-43, angiopathy, neuron loss and gliosis.

20 s that might be irreversible due to reactive gliosis.

21 pressing PDGFRbeta(D849V) exhibited reactive gliosis.

22 s well as reduction of motor neuron loss and gliosis.

23 = 0.02), but not prion protein deposition or gliosis.

24 tial Abeta concentration as well as reactive gliosis.

25 uggest that Olig2 is critical for postinjury gliosis.

26 essure and did not alter Muller or astrocyte gliosis.

27 tion in aged mice can ameliorate TBI-induced gliosis.

28 rebellar white matter associated with severe gliosis.

29 spongiform degeneration, neuronal loss, and gliosis.

30 resent important targets to control reactive gliosis.

31 l detachment and participation in subretinal gliosis.

32 a of fibroblasts in the cortex, and reactive gliosis.

33 terized by nigrostriatal dopamine damage and gliosis.

34 nd GFAP to assess neuronal loss and reactive gliosis.

35 roblasts in the cerebral cortex and reactive gliosis.

36 anced glymphatic influx of CSF, and reactive gliosis.

37 antagonism induced retinal degeneration and gliosis.

38 of Pyk2 does not alter Abeta accumulation or gliosis.

39 aques, neurofibrillary tangles, and reactive gliosis.

40 ng that these surfaces will not cause excess gliosis.

41 er nuclear layer (ONL) thinning, and retinal gliosis.

42 Abeta) plaque pathology and plaque-localised gliosis.

43 r mental disorders that lack robust reactive gliosis.

44 n ERG responses, photoreceptor cell loss and gliosis.

45 mine changes in the RPE, photoreceptors, and gliosis.

46 jacent areas of axonal myelin disruption and gliosis.

47 toreceptor disruption and loss and localized gliosis.

48 ogliosis or transcription factors regulating gliosis.

49 d levels of GFAP are the hallmark feature of gliosis, a non-specific response of astrocytes to a wide

50 the cell cycle, Muller glia undergo reactive gliosis, a pathological hallmark in the injured CNS of m

51 ession stalled, Muller glia undergo reactive gliosis, a pathological hallmark of the mammalian retina

52 to brain injury is the induction of reactive gliosis, a process whereby dormant astrocytes undergo mo

53 eded by neuropathological changes, including gliosis, accumulation of ubiquitinated protein aggregate

54 one morphogenetic protein (BMP) signaling in gliosis after SCI and find that BMPR1a and BMPR1b signal

55 ophic factor receptor (BDNF), contributes to gliosis after SCI, but little is known about the effects

56 Heightened levels of inflammation (gliosis) also appeared in several AD-related brain regio

57 fs4 in the VN, one of the principle sites of gliosis, also led to breathing abnormalities and prematu

58 any retinal diseases is reactive Muller cell gliosis, an untreatable condition that leads to tissue s

59 There was also marked astrocytic gliosis and accumulation of alpha-synuclein immunoreacti

60 hological analysis showed diffuse astrocytic gliosis and activated microglia in the white matter, rar

61 signaling loss in the APP/GRKO mice reduced gliosis and amyloid plaques at 14 months of age.

62 ulation of Ras signaling in neurons promotes gliosis and astrocytoma formation in a cell nonautonomou

63 g secondary effects of inflammation, such as gliosis and blood-brain barrier disruption.

64 mIL-6 expression resulted in extensive gliosis and concurrently attenuated Abeta deposition in

65 on loss, cortical spinal tract degeneration, gliosis and cytoplasmic neuronal inclusions formed by TD

66 Both injected cohorts showed gliosis and degenerative changes, though ERG responses w

67 c intervention reverses infection-associated gliosis and demyelination in the absence of changes in C

68 opment, synaptic transmission, cytoskeleton, gliosis and dopamine signaling that link DYT6 to other p

69 rain inflammation characterized by extensive gliosis and elevated blood-derived immune cell populatio

70 otential therapeutic target for manipulating gliosis and enhancing functional outcome.

71 ay thus provide an approach for manipulating gliosis and enhancing functional outcomes after SCI.

72 changes, including neuronal loss, astrocytic gliosis and extensive prion protein (PrP) deposition in

73 Reparative processes such as gliosis and fibrosis also can make it difficult to reple

74 chanism, but the upstream mechanisms driving gliosis and how important this is for seizures remain un

75 microvacuolation in the neuropil, as well as gliosis and huntingtin aggregates, which were exacerbate

76 and neuronal degeneration but coincided with gliosis and increased complement component C3, but not C

77 lso evident, with reductions in inflammation/gliosis and increased neural stem cell numbers in areas

78 gressive neurodegenerative changes including gliosis and increasing accumulation of p62- and ubiquiti

79 Neuroinflammation, marked by gliosis and infiltrating T cells, is a prominent patholo

80 ation caused an increasing C-choline uptake, gliosis and inflammation potentially accounted for a hig

81 The prominent gliosis and inflammation surrounding vessels of the inne

82 s levels of myelin disorders, axonal damage, gliosis and inflammation, and offer the opportunity for

83 ity recording but face challenges of chronic gliosis and instability due to mechanical and structural

84 Finally, the roles of laropiprant on gliosis and iron accumulation were also investigated.

85 Although dexamethasone profoundly inhibited gliosis and ischemia around the probe tracks it had only

86 methasone is highly effective at suppressing gliosis and ischemia but is limited in its neuroprotecti

87 henotypes including spongiform degeneration, gliosis and juvenile lethality.

88 gnificantly improved motor neuron counts, no gliosis and markedly reduced levels of total and hyperph

89 Furthermore, both reactive gliosis and markers suggestive of neuron injury were evi

90 oculated mice exhibited prominent astrocytic gliosis and microglial activation as well as widespread

91 cortex, hippocampus and basal forebrain and gliosis and microgliosis in the hippocampus.

92 Indeed, gliosis and microgliosis were present from an early age

93 B selectively in wild-type microglia induced gliosis and MN death in vitro and in vivo.

94 document neuronal cell loss, demyelination, gliosis and necrotic lesions in post-mortem material.

95 death, but detachments do not accentuate the gliosis and neurite sprouting already present and may in

96 ocampal microvasculature without concomitant gliosis and neurodegeneration.

97 owing that high saturated fat diets increase gliosis and neuroinflammation in reward-related brain re

98 ncy can develop in the absence of detectable gliosis and neuroinflammation, thereby dissociating micr

99 on diseases, but the mechanisms facilitating gliosis and neuronal damage in these diseases are not un

100 ical findings included bilateral hippocampal gliosis and neuronal loss in two patients who had post-m

101 recruitment, vascular permeability, reactive gliosis and neuronal patterning were evaluated by 3-dime

102 3D astrocytic network with reduced reactive gliosis and polarized aquaporin-4 (AQP4) distribution.

103 rescues neuronal impairment, and suppresses gliosis and recruitment of blood-derived immune cells, w

104 provide evidence that 5-FU induces reactive gliosis and reduction of enteric neurons in a S100B/RAGE

105 atric diseases, but the relationship between gliosis and response to therapeutics targeting effects o

106 r integrity, and are associated with retinal gliosis and RPE damage.

107 ive disease is often accompanied by reactive gliosis and scarring, which are difficult to reverse wit

108 veral pathological hallmarks of ALS, such as gliosis and TDP-43 mislocalization.

109 , a functional relationship between reactive gliosis and this cell proliferation has not been clearly

110 to 15 to 18 months, which is accompanied by gliosis and vacuolization.

111 nt organization of reactive astrocytes (i.e. gliosis) and was not attributed to axons.

112 and activator of transcription 1 levels and gliosis, and 2) hyperphosphorylation and conformational

113 function and motor neuron loss, significant gliosis, and a lifespan of 152-154 days.

114 is sufficient to cause rapid demyelination, gliosis, and a microglial response that result in lesion

115 ter hypoplasia, periventricular white matter gliosis, and axonal and ependymal injury.

116 hology, including beta-amyloid accumulation, gliosis, and behavioral impairment, were examined under

117 ductions of brain Abeta and plaque deposits, gliosis, and behavioral memory deficits in the disease-e

118 bers and characterized microglia activation, gliosis, and both axonal integrity and retrograde tracer

119 vessels, is injurious and triggers ischemia, gliosis, and cell death at the sampling site.

120 olactinemia limited photoreceptor apoptosis, gliosis, and changes in neurotrophin expression, and it

121 ased brain amyloid-beta42, deposits of AGEs, gliosis, and cognitive deficits, accompanied by suppress

122 cle re-entry results in neuronal cell death, gliosis, and cognitive deficits.

123 ted a reduced number of PR cell rows, active gliosis, and cytokine induction and macrophage infiltrat

124 enhanced neuroinflammation, astrocytosis and gliosis, and eventually neuronal loss.

125 later stages of disease, with neuronal loss, gliosis, and formation of diffuse cortical Lewy bodies i

126 d number of acellular capillaries, sustained gliosis, and increased capillary basement membrane thick

127 characterized by demyelination, axonal loss, gliosis, and inflammation.

128 hannels, synaptic structure, neuronal death, gliosis, and inflammation.

129 ive status and assessment of amyloid burden, gliosis, and molecular pathology during disease progress

130 t BMP inhibition alleviates hypomyelination, gliosis, and motor impairment in the survivors of IVH.

131 Prion infection leads to PrPres deposition, gliosis, and neuroinflammation in the central nervous sy

132 oscillatory potentials, Muller cell reactive gliosis, and neuronal cell death, as assayed by TUNEL st

133 yloid-beta plaques, neurofibrillary tangles, gliosis, and neuronal loss.

134 the relationship between cytokine responses, gliosis, and neuropathology during prion disease.

135 markers synaptophysin and MAP2, reduced the gliosis, and preserved the capacity to elicit long-term

136 tokines to leak into the CNS, exacerbate the gliosis, and result in the vicious neuroinflammatory cas

137 ration of the angle, ectropion uvea, retinal gliosis, and retinal ganglion cell loss.

138 a, profound granule cell depletion, Bergmann gliosis, and signs of Purkinje cell deafferentation; (ii

139 Exposure to HFD was associated with reactive gliosis, and this affected the structure of the blood-br

140 late of neuronal injury and the accompanying gliosis, and this signature could serve as a global biom

141 and temporal lobar atrophy, neuron loss and gliosis, and ubiquitin-positive inclusions (FTLD-U), whi

142 helial growth factor (VEGF) and anti-CD105], gliosis [anti-glial fibrillary acidic protein (GFAP)], p

143 erebral amyloidosis that precedes tauopathy, gliosis, apoptotic loss of neurons in the cerebral corte

144 olation, with focal neuronal loss and severe gliosis apparent in the oldest GRN(-/-) mice.

145 ted lineage potential and that cell loss and gliosis are not sufficient to alter the lineage potentia

146 ide a demonstration that synaptotoxicity and gliosis are precocious events in MJD and that caffeine a

147 onstrate that neuroinflammation and reactive gliosis are prominent features of bilirubin brain toxici

148 Although neuroinflammation and reactive gliosis are prominent in virtually every CNS disease, gl

149 ration, apoptosis, neuronal degeneration and gliosis around the ventricles of pups with intraventricu

150 93A) ALS mouse model, providing evidence for gliosis as a potential ALS therapeutic target.

151 addition, chrysophanol ameliorated reactive gliosis, as demonstrated by a decrease in GFAP immunolab

152 impairment, improved myelination and reduced gliosis at 2 weeks of age.

153 he pups with IVH exhibit hypomyelination and gliosis at 2 weeks of postnatal age.

154 formation in mice triggered neuron loss and gliosis at 3 months, but not in a tau-null background.

155 tion showed elevated molecular signatures of gliosis at short- and long-term post-RT times.

156 Finally, TDP-43PrP mice showed reactive gliosis, axonal and myelin degeneration, gait abnormalit

157 PO) is described as a biomarker for reactive gliosis, but its biological functions in retinal disease

158 glia respond to retinal injury by a reactive gliosis, but only rarely do mammalian glial cells re-ent

159 domains was not universally associated with gliosis, but restricted to seizure pathologies.

160 We assessed reactive gliosis by immunohistochemistry and correlated metabolic

161 inhibition of inflammation-induced reactive gliosis by macrophage depletion abolishes SHH activation

162 s in the cerebellum and cerebral cortex, and gliosis caused by CysB deficiency, are rescued by CysC o

163 Gliosis, characterized by translocation of Muller cell b

164 those involving neural progenitor cells and gliosis compared with tumor samples.

165 We find reactive gliosis consists of a rapid, but quickly attenuated, ind

166 s, we propose that trauma-triggered reactive gliosis could exert both beneficial and deleterious effe

167 n loss, loss of poly(PR)-positive cells, and gliosis, culminating in motor and memory impairments.

168 The long-lasting gliosis, delayed neuronal loss, and demyelination sugges

169 nje cell loss, axonal spheroids and reactive gliosis, demonstrating that there is not a significant d

170 anolide as a potential treatment for diverse gliosis-dependent central nervous system traumatic injur

171 PPA in modulating hNSC patterning leading to gliosis, disturbed neuro-circuitry, and inflammatory res

172 Pathological signs include gliosis, dystrophic neurites, vacuolated mitochondria, a

173 contrast, the microdialysis probes produced gliosis extending 200-300 microm from the track, which w

174 The MEAs produced mild gliosis extending 50-100 microm from the tracks, with a

175 NS cellular infiltration, demyelination, and gliosis for 12 days with CYM-5442, vehicle, or fingolimo

176 No treatment scar showed gliosis, foveal involvement, or retinal traction at 1-ye

177 Hippocampal gliosis (GFAP reactivity) was correlated with both abnor

178 Gliosis (GFAP) increased in all regions except the Nac b

179 -associated protein-2 staining) and reactive gliosis (glial fibrillary acidic protein and CD11b stain

180 demyelinating lesion causes upregulation of gliosis, glial scar formation, and heightened expression

181 Although neuropathological hallmarks such as gliosis, globoid cells and psychosine accumulation are p

182 a cortical freeze injury to induce reactive gliosis in a Gli-luciferase reporter mouse, we show that

183 expression exacerbated Abeta deposition and gliosis in AD mouse models and impaired hippocampal neur

184 hh signaling and astrocyte-mediated reactive gliosis in adults, raising the possibility that this pat

185 PO), a biomarker of microglial and astrocyte gliosis in brain degeneration, in the context of retinal

186 diseases characterized by neuronal loss and gliosis in cardinal brain regions, as well as the abnorm

187 the role of endothelin-1 (ET-1) in reactive gliosis in corpus callosum after lysolecithin (LPC)-indu

188 e severe neuronal loss and marked astrocytic gliosis in every case, whereas the entorhinal cortex is

189 , eyedrops, P = 0.03, Student's t test), and gliosis in Muller cells (at 6 mo, using SPION-glial fibr

190 hypertrophy and proliferation with prominent gliosis in multiple sclerosis cases.

191 ositron emission tomography, mainly reflects gliosis in neuropsychiatric disease.

192 ell growth because of its ability to inhibit gliosis in rat brain.

193 ubacute necrotizing encephalomyelopathy with gliosis in several brain regions that usually results in

194 lial scar formation at the lesion border and gliosis in spared gray and white matter.

195 Progressive neuronal deterioration and gliosis in specific brain areas corresponded to behavior

196 cations, although conventional probes induce gliosis in surrounding tissue.

197 on as shown by reduction in astrocytosis and gliosis in TASD-41 transgenic mice.

198 a leads to the induction of reactive retinal gliosis in the absence of injury.

199 revealed massive loss of Purkinje cells and gliosis in the cerebellum, and secondary accumulation of

200 s of brain tissue and dura revealed reactive gliosis in the cortex underlying the electrodes and exte

201 hage infiltration, and a pronounced reactive gliosis in the deep cortical layers.

202 HS was defined as severe neuronal loss and gliosis in the hippocampal CA1 and/or subiculum.

203 as well as neuronal loss, inflammation, and gliosis in the hippocampi.

204 of 85 years) characterized by cell loss and gliosis in the hippocampus that is not explained by Alzh

205 the time of treatment and reduced underlying gliosis in the hippocampus.

206 We demonstrate the absence of reactive gliosis in the immature white matter following chronic h

207 odegeneration, demyelination, and astrocytic gliosis in the injured cervical cord.

208 a in rodents, we found evidence of increased gliosis in the mediobasal hypothalamus of obese humans,

209 reased whereas apoE3 reduced amyloid-related gliosis in the mouse brains.

210 f nigral dopaminergic neurons, and extent of gliosis in the neuroaxis.

211 eptor apoptosis and an inflammatory reactive gliosis in the retina.

212 al, reduced oxidative stress, and attenuated gliosis in the spinal cord, as well as a dramatic decrea

213 ted uneven, focally severe neuronal loss and gliosis in the substantia nigra pars compacta, without L

214 e develop neuronal loss and intense reactive gliosis in the thalamus, as seen in humans with FFI.

215 onergic neurons as well as marked astrocytic gliosis in the ventral medullary surface in MSA.

216 GABAergic neurons, respectively) and diffuse gliosis in white-matter tracts.

217 d excitotoxin-induced neuronal cell loss and gliosis in wild-type mice when administered systemically

218 dentified as having extensive glial network (gliosis) in postmortem immunohistochemistry.

219 Widespread reactive gliosis, including mislocalization of the astrocytic wat

220 Endothelial adhesion molecules and gliosis, increased after hypoperfusion, were ameliorated

221 expected attenuated morphological markers of gliosis, increased mRNA levels for proinflammatory cytok

222 ce results directly or indirectly in midline gliosis, increased Slit2, and complete CC agenesis.

223 mals demonstrated that constitutive reactive gliosis induced by deletion of Lhx2 reduced rates of ong

224 Elimination of TRPC1 facilitated Muller gliosis induced by the elevation of intraocular pressure

225 Gliosis is a biological process that occurs during injur

226 stablished commonalities, astrocyte reactive gliosis is a highly heterogeneous state in which astrocy

227 Gliosis is a pathological hallmark of posttraumatic epil

228 Moreover, a spinal gliosis is apparent at times of peak behavioural sensiti

229 Reactive gliosis is characterized by enhanced glial fibrillary ac

230 Gliosis is common among neuropsychiatric diseases, but t

231 Although brain injury-induced reactive gliosis is concurrent with the proliferation of surround

232 esponse to therapeutics targeting effects of gliosis is largely unknown.

233 nt negative result, it can be concluded that gliosis is not a feature of BD; neither is there neuropa

234 Gliosis is often a preclinical pathological finding in n

235 Celecoxib administration in the presence of gliosis labeled by TSPO V(T) is associated with greater

236 Because astrocytic gliosis marked by the deposition of fibrils composed of

237 The putative gliosis marker myo-inositol was higher than controls in

238 Total creatine, another potential gliosis marker, was higher in the cerebellar hemispheres

239 observed in Muller cells before established gliosis markers.

240 esults indicate that mIL-6-mediated reactive gliosis may be beneficial early in the disease process b

241 sease in humanized mice was characterized by gliosis, meningitis, and meningoencephalitis, and glial

242 xhibit white matter abnormalities, extensive gliosis, microglia-mediated neuroinflammation, and an ex

243 , and formation of new synapses; Muller cell gliosis, migration, and scarring; blood vessel loss; and

244 on in the AD brains of MRP4, probably due to gliosis, MRP4 being present also in glial cells.

245 8%), lacrimal gland choristoma (n = 2; 5%), gliosis (n = 1; 3%), nevus (n = 1; 3%), hemorrhage (n =

246 tumours (n=33, 50%), followed by dysplasia, gliosis (n=11, each) and hippocampus sclerosis (n=9).

247 and markers for cell proliferation, reactive gliosis, neuronal maturation, and synaptogenesis in the

248 isoform expression patterns in glioblastoma, gliosis, non-tumor brain and neural progenitor cells by

249 We studied the anatomical remodeling and gliosis of retinal Muller cells in the rd/rd mouse model

250 in patients with HS (TLE-HS) and those with gliosis only (TLE-G).

251 in Grn(+/-) mice occurred in the absence of gliosis or increased expression of tumor necrosis factor

252 t differences in lesion size, fibrotic scar, gliosis or neuroinflammation between groups.

253 cumulated in perilesional tissues expressing gliosis or oxidative stress within days.

254 me, clinical tempo, or levels of spongiosis, gliosis, or PrPres in the brain.

255 ment; (3) evidence of hypoxia; (4) brainstem gliosis (particularly the nTS and DMNV); and (5) 5-HT ab

256 aused further neurodegeneration, Muller cell gliosis, progenitor proliferation, and microglia reactiv

257 requirement for TLR2 signaling in regulating gliosis, proinflammatory mediators, and oxidative stress

258 IL-1Ra demonstrated any observable effect on gliosis, protease-resistant prion protein (PrPres) forma

259 ng IL-1Ra, there was no observable effect on gliosis, PrPres formation, disease tempo, pathology, or

260 els with reduced neuronal-axonal density and gliosis (r = 0.72, P < 0.002 in the multivariate model);

261 poglycemia during brain development, such as gliosis, reactive neurogenesis, or disruption of normal

262 ular phenomena including attenuated reactive gliosis, reduced microglial activation, and decreased ox

263 etinal injuries with calcification and focal gliosis, renal parenchymal damage and liver lobular infl

264 n of DNA damage in the cortex accompanied by gliosis, resulting in increased mortality of aging mutan

265 of Gli2 and Gli3, whereas astrocyte partial gliosis results from an increase in GLI3(R).

266 eport that the mouse mutant ingls (infantile gliosis) results from a missense mutation in Vac14 that

267 ss of photoreceptor outer segments, reactive gliosis, retinal detachment, and reduced retinal functio

268 with continued HFD feeding, inflammation and gliosis returned permanently to the mediobasal hypothala

269 f gliosis to medication targeting effects of gliosis should be applied in early development of novel

270 TLR2-mediated gliosis strongly correlates with pronounced neuroinflamm

271 to retinal stress, acute-phase response, and gliosis, suggesting that IGF-I altered normal retinal ho

272 h rapamycin showed reduced signs of reactive gliosis, suggesting that rapamycin could be used to harn

273 Reactive gliosis surrounding amyloid beta (Abeta) plaques is an e

274 erized by accumulation of misfolded protein, gliosis, synaptic dysfunction, and ultimately neuronal l

275 eration in the formation of amyloid plaques, gliosis, synaptic loss, or cognitive behavioral deficits

276 ce exhibited photoresponsive dysfunction and gliosis that correlated with decreased levels of retinal

277 ue causes a penetration injury that triggers gliosis (the activation and proliferation of glial cells

278 ed medicine approach of matching a marker of gliosis to medication targeting effects of gliosis shoul

279 Photoreceptor death and retinal gliosis underlie the majority of vision threatening reti

280 odegeneration nor increases in apoptosis and gliosis up to ~2 years of age.

281 ne levels were independently associated with gliosis, vasculopathy, and edema (r = 0.75, P < 0.004 in

282 cell pathologies can manifest as ventricular gliosis, ventricle enlargement, or ventricle stenosis.

283 rsus normal MRI findings or of children with gliosis versus developmental pathology.

284 Gliosis was evaluated by immunofluorescent techniques.

285 Reactive gliosis was evident in the microbeam path of rats irradi

286 is of conditional Lhx2 knockouts showed that gliosis was hypertrophic but not proliferative.

287 s and blood-brain barrier leakage as well as gliosis were also reduced significantly.

288 Neurodegeneration and gliosis were assessed by histological techniques.

289 neurobehavioral performance, myelination and gliosis were assessed in noggin-treated pups compared wi

290 eurobehavioural performance, myelination and gliosis were assessed in pups treated with cyclooxygenas

291 alpha; and cell-infiltration, cell-death and gliosis were compared between treated-pups and vehicle-t

292 significant neuroinflammation and extensive gliosis were detected in AAV1-Tau(P301L) mice.

293 These mice developed progressive gliosis, which is associated with hyperactivation of Ras

294 odel of acute neurodegeneration and reactive gliosis, which was induced by intrahippocampal injection

295 beta amyloidosis progressed with exacerbated gliosis, while genes commonly altered in the 3xTg-AD-H a

296 mmatory environment and a potent mediator of gliosis with a range of nonimmune functions in the CNS,

297 y identification of microscopic necrosis and gliosis with preOL maturation arrest, a common form of W

298 oss showed 3-10-fold stimulation of reactive gliosis, with an increased astrocyte cell population and

299 Gliosis within the lesioned cortex also influenced diffu

300 ied with layer- and region-specific reactive gliosis without cell loss.