ライフサイエンスコーパス: gliosis

1 aques, neurofibrillary tangles, and reactive gliosis.

2 ile enhancing Abeta plaque load and reactive gliosis.

3 iseases of the retina involving fibrosis and gliosis.

4 ychosine accumulation, white matter loss and gliosis.

5 fic program of nonproliferative hypertrophic gliosis.

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

7 als immediately before the onset of reactive gliosis.

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

9 emyelination, immunological stimulation, and gliosis.

10 sident astrocytes, a process termed reactive gliosis.

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

12 PrP plaque formation, spongiform change, and gliosis.

13 s that might be irreversible due to reactive gliosis.

14 = 0.02), but not prion protein deposition or gliosis.

15 Abeta) plaque pathology and plaque-localised gliosis.

16 tial Abeta concentration as well as reactive gliosis.

17 uggest that Olig2 is critical for postinjury gliosis.

18 essure and did not alter Muller or astrocyte gliosis.

19 rebellar white matter associated with severe gliosis.

20 spongiform degeneration, neuronal loss, and gliosis.

21 r mental disorders that lack robust reactive gliosis.

22 resent important targets to control reactive gliosis.

23 l detachment and participation in subretinal gliosis.

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

25 terized by nigrostriatal dopamine damage and gliosis.

26 nd GFAP to assess neuronal loss and reactive gliosis.

27 roblasts in the cerebral cortex and reactive gliosis.

28 n ERG responses, photoreceptor cell loss and gliosis.

29 ls at 3 and 5 days, consistent with reactive gliosis.

30 roglioma samples compared with nonneoplastic gliosis.

31 to neuronal precursors and do not influence gliosis.

32 despread progressive axonal degeneration and gliosis.

33 the cyst walls was consistent with reactive gliosis.

34 s, there was also an attenuation of reactive gliosis.

35 sponse appear to be associated with reactive gliosis.

36 nificant number of genes involved in retinal gliosis.

37 their relationship with markers of reactive gliosis.

38 ty of post-ischemic astrocytes and prevented gliosis.

39 ng that these surfaces will not cause excess gliosis.

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

41 jacent areas of axonal myelin disruption and gliosis.

42 toreceptor disruption and loss and localized gliosis.

43 ogliosis or transcription factors regulating gliosis.

44 ies virus and observed similar perimeters of gliosis.

45 ion pathology that is associated with robust gliosis.

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

47 n excess, were sufficient to induce reactive gliosis.

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

49 ent maps might be associated with astrocytic gliosis.

50 l lethality associated with microcephaly and gliosis.

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

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 crease both neuronal cell death and reactive gliosis after experimental TBI suggests that this treatm

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

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

57 et, midline fusion of brain hemispheres, and gliosis also occurred, similar to type II cobblestone li

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

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

60 Pronounced gliosis, an indicator of neuronal stress and neurodegene

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

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

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

64 ion in surviving terminals is accompanied by gliosis and alteration in the postsynaptic structure.

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

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

67 reased Cr and Cho levels suggest (a) ongoing gliosis and attempted remyelination in isointense lesion

68 Inflammation, demyelination, gliosis and axonal degeneration are pathological hallmar

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

70 pathologically, progressive nerve cell loss, gliosis and coexistent neuronal and/or glial deposits co

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

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

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

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

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

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

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

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

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

80 l fibers and oxidative stress, and correlate gliosis and GFAP protein levels to the severity of the d

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

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

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

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

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

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

87 The prominent gliosis and inflammation surrounding vessels of the inne

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

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

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

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

92 henotypes including spongiform degeneration, gliosis and juvenile lethality.

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

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

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

96 revealed a strong treatment-induced reactive gliosis and microglial activation.

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

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

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

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

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

102 and that these deposits are associated with gliosis and neuritic dystrophy.

103 ocampal microvasculature without concomitant gliosis and neurodegeneration.

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

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

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

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

108 The cerebral white matter shows patchy gliosis and rarefaction, in some cases marked.

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

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

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

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

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

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

115 and vimentin attenuates RD-induced reactive gliosis and, subsequently, limits photoreceptor degenera

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

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

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

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

120 with perivascular HIV-infected macrophages, gliosis, and abnormalities in the permeability of the BB

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

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

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

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

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

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

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

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

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

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

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

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

133 h Abeta peptide, may occur in the context of gliosis, and may contribute to Abeta deposition in spora

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

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

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

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

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

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

140 development of cerebrovascular amyloidosis, gliosis, and plaque-independent neuritic dystrophy.

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

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

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

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

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

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

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

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

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

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

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

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

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

154 udies concluded that chronic DBS caused mild gliosis around the lead track and did not damage brain t

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

156 ions, the severity of neuronal cell loss and gliosis as well as the frequency of glial (oligodendrogl

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

158 imals were evaluated for KA-induced reactive gliosis, assayed by an ELISA for GFAP, which revealed a

159 in an eyedrop solution, effectively reports gliosis associated with acute neurological disorders in

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

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

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

163 F and serum was associated with non-specific gliosis at biopsy.

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

165 Amyloid deposition (and gliosis) begins at 2 months and reaches a very large bur

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

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

168 We assessed reactive gliosis by immunohistochemistry and correlated metabolic

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

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

171 RD-induced reactive gliosis, characterized by GFAP and vimentin upregulation

172 Gliosis, characterized by translocation of Muller cell b

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

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

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

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

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

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

179 (GFAP) represents astroglial activation and gliosis during neurodegeneration.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

195 e aimed to test the feasibility of detecting gliosis in living brains when the blood-brain barrier (B

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

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

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

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

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

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

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

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

204 development of spongiform encephalopathy and gliosis in the central nervous system (CNS) in ts1-infec

205 th around neurons, owing to inflammation and gliosis in the central nervous system (CNS).

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

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

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

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

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

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

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

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

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

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

216 A is a potent 5-HT releaser which can induce gliosis in the rodent brain.

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

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

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

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

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

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

223 Widespread reactive gliosis, including mislocalization of the astrocytic wat

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

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

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

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

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

229 tion), in addition to increased cellularity (gliosis, inflammation) in normal-appearing white matter.

230 sis describes a pattern of neuronal loss and gliosis involving the medial temporal structures most of

231 Gliosis is a biological process that occurs during injur

232 Reactive gliosis is a characteristic of all forms of NCL, but it

233 Reactive gliosis is a hallmark of disease-, trauma-, and chemical

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

235 Gliosis is a pathological hallmark of posttraumatic epil

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

237 Reactive gliosis is characterized by enhanced glial fibrillary ac

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

239 Gliosis is often a preclinical pathological finding in n

240 Histologic findings included axonal loss and gliosis limited to the temporal optic nerve, reduction o

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

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

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

244 observed in Muller cells before established gliosis markers.

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

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

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

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

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

250 8%), lacrimal gland choristoma (n = 2; 5%), gliosis (n = 1; 3%), nevus (n = 1; 3%), hemorrhage (n =

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

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

253 etabolic energy demands of processes such as gliosis, neuronal outgrowth and synaptic remodelling tha

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

272 nation and adaptive glial changes, including gliosis secondary to neuronal damage.

273 TLR2-mediated gliosis strongly correlates with pronounced neuroinflamm

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

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

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

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

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

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

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

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

282 the series as a whole (37%) was non-specific gliosis variably affecting both cortex and white matter.

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

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

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

286 Gliosis was evaluated by immunofluorescent techniques.

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

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

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

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

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

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

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

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

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

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

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.