ライフサイエンスコーパス: astrogliosis

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

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

3 ions was accompanied by a marked decrease in astrogliosis.

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

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

6 ravasation, and 5) appearance of parenchymal astrogliosis.

7 andidate for transplantation by evoking less astrogliosis.

8 midbrain dopaminergic (DAergic) neurons and astrogliosis.

9 ypertrophy and hyperplasia known as reactive astrogliosis.

10 of macrophages or neutrophils, or increased astrogliosis.

11 esting a protective effect of CR in limiting astrogliosis.

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

13 lls reflected alterations representative for astrogliosis.

14 er characteristic response to neural injury, astrogliosis.

15 ted, however high dose AAV5-miHTT did induce astrogliosis.

16 fibrillary acidic protein-positive reactive astrogliosis.

17 more immature state related to the burden of astrogliosis.

18 nce functionally implicating the caspases in astrogliosis.

19 ion in astrocytes leads to growth arrest and astrogliosis.

20 as directly proportional to the magnitude of astrogliosis.

21 cords with reduced destruction of myelin and astrogliosis.

22 eductions in demyelination, axonal loss, and astrogliosis.

23 nto the mouse cortex is sufficient to induce astrogliosis.

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

25 iferation of glial cells and less-pronounced astrogliosis.

26 ngiform) leukoencephalopathy with widespread astrogliosis.

27 l and biochemical changes, demyelination and astrogliosis.

28 /80+ reactivity and diffuse local and distal astrogliosis.

29 ads to alterations in synaptic structure and astrogliosis.

30 ormally short dendritic spines, and profound astrogliosis.

31 uated by immunostaining for cell density and astrogliosis.

32 flammatory transcripts, as well as secondary astrogliosis.

33 when reactive to injury or disease known as astrogliosis.

34 ive sparing of interneurons accompanied with astrogliosis.

35 after surgery, presumably caused by reactive astrogliosis.

36 of astrocytes, followed over several days by astrogliosis.

37 with vehicle, and a reduction in hippocampal astrogliosis.

38 ies in astrocytes, such as vacuolization and astrogliosis.

39 P-43(A315T) mice, these mice did not develop astrogliosis.

40 gulation of pathological processes including astrogliosis.

41 europrotective at an early onset of reactive astrogliosis.

42 e lower levels of inflammatory cytokines and astrogliosis.

43 displayed strongly reduced microgliosis and astrogliosis.

44 illary acidic protein (GFAP) is a measure of astrogliosis, a known pathological process of FTD, but h

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

46 Focal traumatic brain injury (TBI) induces astrogliosis, a process essential to protecting uninjure

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

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

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

50 Astrogliosis also occurred following reovirus infection

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

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

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

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

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

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

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

58 gnaling and rescued the compromised reactive astrogliosis and cognitive deficits.

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

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

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

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

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

64 All implants decreased astrogliosis and lowered the immune response, but scaffo

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

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

67 Moreover, astrogliosis and microglia activation were reduced in pe

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

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

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

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

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

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

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

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

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

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

78 Reactive astrogliosis and microgliosis were ameliorated when FTY7

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

80 Other cellular defects include astrogliosis and microgliosis.

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

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

83 ected blood-brain barrier integrity, reduced astrogliosis and neuroinflammation, as well as improved

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

85 ad vacuolation in the midbrain with reactive astrogliosis and neuronal density reduction.

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

87 Brains were examined histologically for astrogliosis and neuronal organization.

88 brain growth and neuronal migration defects, astrogliosis and oxidative stress.

89 an anticoagulation also prevented AD-related astrogliosis and pericyte alterations, and maintained ex

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

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

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

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

94 -1 signaling as a mediator of post-traumatic astrogliosis and seizure susceptibility.SIGNIFICANCE STA

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

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

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

98 f selenoprotein expression in neurons led to astrogliosis and transcriptional induction of genes asso

99 roinflammation, since microglial activation, astrogliosis, and brain cytokine profiles were not alter

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

101 the chronic phase, in parallel to prolonged astrogliosis, and decreased neural and synaptic markers.

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

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

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

105 behavioral parameters, neuronal cell counts, astrogliosis, and diminution in brain and serum ceramide

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

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

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

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

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

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

112 -beta (Abeta) plaques, perivascular reactive astrogliosis, and mislocalization of astrocyte aquaporin

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

114 sing impact on longevity, subunit C storage, astrogliosis, and neuronal cell counts.

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

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

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

118 e compromised JAK-STAT3 pathway and reactive astrogliosis, and reversed the enhanced neuronal damage

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

120 ect recognition deficits, mHTT accumulation, astrogliosis, and striatal volume loss, the latter of wh

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

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

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

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

125 s; (2) had significantly attenuated reactive astrogliosis; and (3) displayed enhanced neuronal damage

126 r neuron and oligodendrocyte quantification, astrogliosis, apoptosis and cellular proliferation were

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

128 Microgliosis and astrogliosis are standard pathological features of neuro

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

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

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

132 Reovirus infection resulted in astrogliosis, as evidenced by increased expression of gl

133 ogenous biomarkers with early onset, such as astrogliosis, as regulators of neurotrophic therapy in A

134 exhibited significantly attenuated reactive astrogliosis, as well as enhanced microglial activation,

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

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

137 icits but increased neural stem cell-derived astrogliosis, associating with a downregulation of GABA

138 ule-1 [Iba-1]) and interleukin-6 [IL-6]) and astrogliosis/astrocyte damage (glial fibrillary acidic p

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

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

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

142 8 mitogen-activated protein kinase (MAPK) in astrogliosis both in vitro and in vivo.

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

144 Suppression of astrogliosis by treatment with fluorocitrate exacerbated

145 However, astrogliosis can cause loss of astrocyte homeostatic fun

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

147 Astrocytes did not form scars and classic astrogliosis characterized by upregulation of glial fibr

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

149 deletion attenuated astrocyte activation and astrogliosis compared with WT stroke controls 24-72 h af

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

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

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

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

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

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

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

157 Astrogliosis dropped in females compared to a slight inc

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

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

160 Diffuse astrogliosis extended into the lesion surround with elev

161 Astrogliosis following spinal cord injury (SCI) involves

162 Astrogliosis following spinal cord injury (SCI) involves

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

164 system to investigate astrocyte activation (astrogliosis) following viral infection of the brain.

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

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

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

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

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

170 associated with diminished microgliosis and astrogliosis in aged mice.

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

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

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

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

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

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

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

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

179 77 gene caused premature death with dramatic astrogliosis in mouse brain.

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

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

182 r, unlike humans, chimpanzees do not display astrogliosis in other cortical layers.

183 nding site levels we can indirectly evaluate astrogliosis in patients with Parkinson's disease.

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

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

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

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

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

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

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

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

192 This study showed that astrogliosis in the IC could be an adaptive response to

193 demonstrated an increase in microgliosis and astrogliosis in the lumbar spinal cord of SOD1(G93A) tra

194 ed amyloid-beta (Abeta) plaque pathology and astrogliosis in the male amyloid precursor protein (APP)

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

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

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

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

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

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

203 1 general KO mice showed neither fibrils nor astrogliosis, indicating a specific role for ERK2 in the

204 brain levels of inflammatory mediators, and astrogliosis (induced at day 3).

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

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

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

208 media from mesenchymal stromal cells reduced astrogliosis, interleukin-1beta, and monocyte chemoattra

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 an essential feature of astrocytic respo

215 Some degree of astrogliosis is associated with normal aging and degener

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 AD mice that overexpress BDNF when and where astrogliosis is initiated (5xF:pGB mice).

220 Because astrogliosis is linked to disease severity, understandin

221 Astrogliosis is marked by an increased expression of gli

222 Astrogliosis is observed in all forms of brain injury an

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

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

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

226 Reactive astrogliosis is the gliotic response to brain injury wit

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

228 f oligomeric and conformation-specific asyn, astrogliosis, LC fiber degeneration, disruptions in stri

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

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

231 Moreover, astrogliosis may be common to both teratogens.

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

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

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

235 ial role of astrocyte-derived E2 in reactive astrogliosis, microglial activation, and neuroprotection

236 has a key role in the regulation of reactive astrogliosis, microglial activation, and neuroprotection

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

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

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

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

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

242 Reduced astrogliosis, microgliosis, and enhanced perivascular en

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

244 as associated with ALS-like lipid pathology, astrogliosis, neurodegeneration, and clinical features o

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

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

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

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

249 Here we took advantage of the early astrogliosis observed in an amyloid mouse model of AD (5

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

251 e after 4 weeks of exposure, indicating that astrogliosis occurs in the IC.

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

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

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

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

256 n led to ALS-like lipid pathology, MN death, astrogliosis, paralysis, and reduced survival.

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

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

259 We postulate that astrogliosis represents a successful defense mechanism b

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

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

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

263 Astrogliosis significantly increased in corpus callosum

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

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

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

267 pocampal astrocytes exhibit a high degree of astrogliosis that is positively correlated with accumula

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

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

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

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

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

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

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

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

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

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

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

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

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

281 Here, reactive astrogliosis was induced with IL1beta.

282 econd month of differentiation, and reactive astrogliosis was inhibited in brain ECM-enriched culture

283 aded with reactive astrocytes in rHD1, while astrogliosis was much less severe in rHD7 and absent fro

284 Reactive astrogliosis was noted near the resection cavity from th

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

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

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

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

289 ch is critical for the induction of reactive astrogliosis, was significantly downregulated in the GFA

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

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

292 volume, neurodegeneration, microgliosis and astrogliosis were observed after combination treatment.

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

294 Reactive astrogliosis, whereby astrocytes undergo varying molecul

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

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

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

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

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

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