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1 seizure-affected brains and less in reactive astrocytosis.
2 ecule fluorescein, concomitant with reactive astrocytosis.
3 neuronal atrophy, microglial activation, and astrocytosis.
4 ix (bHLH) transcription factors and promotes astrocytosis.
5 unded by comorbidities accompanying reactive astrocytosis.
6  of plaque-associated neuritic dystrophy and astrocytosis.
7 onal loss, but did not alter microgliosis or astrocytosis.
8 eurons and glia, abnormal myelination and an astrocytosis.
9                 Both groups had reduction in astrocytosis.
10 s, resulting in the development of prominent astrocytosis.
11 ges, serum protein extravasation, and marked astrocytosis.
12  macrophages, fibrinogen leakage, and marked astrocytosis.
13 lated neurofilament inclusions, and reactive astrocytosis.
14 n areas where there is neurodegeneration and astrocytosis.
15 r and parenchymal amyloid-beta deposits, and astrocytosis (31%, 47-80%, and 33%, respectively; P < 0.
16 ted inclusions in the brain and spinal cord, astrocytosis, a reduction in the number of hippocampal n
17 opening of the blood-brain barrier (BBB) and astrocytosis accompanied by activation of brain microgli
18 , angiogenic and inflamed endothelial cells, astrocytosis and altered synaptic gene expression in tho
19       These leaks were often associated with astrocytosis and apoptotic cells.
20 as performed to investigate fibrillar Abeta, astrocytosis and cerebral glucose metabolism with the ra
21 reases in microglial proliferation, reactive astrocytosis and cleavage of caspase-3.
22  brain inflammation as shown by reduction in astrocytosis and gliosis in TASD-41 transgenic mice.
23 , accompanied by enhanced neuroinflammation, astrocytosis and gliosis, and eventually neuronal loss.
24 ration is accompanied by pronounced reactive astrocytosis and is preceded by an accumulation of ultra
25                                              Astrocytosis and microglia/monocyte activation were dram
26 ulation of autofluorescent storage material, astrocytosis and microglial activation in the brain.
27 bellum, where progressive lysosomal storage, astrocytosis and microglial activation were observed.
28 ta, but deficient in CD40L, showed decreased astrocytosis and microgliosis associated with diminished
29 ese results indicate that the progression of astrocytosis and microgliosis diverges from that of amyl
30 emyelination, oxidative damage, inflammatory astrocytosis and microgliosis in the brain, and eventual
31 reached a plateau early after symptom onset, astrocytosis and microgliosis increased linearly through
32 D were detected in the brain, and markers of astrocytosis and microgliosis were reduced.
33 eins and tau phosphorylation, while reducing astrocytosis and microgliosis, and countering cognitive
34 n MN protection with a reduction in reactive astrocytosis and microgliosis.
35 deposition of extracellular amyloid plaques, astrocytosis and neuritic dystrophy.
36 ive histopathological scoring of spongiosis, astrocytosis and prion protein deposition.
37                              The patterns of astrocytosis and PrPSc formation were different between
38               Topical MSCs triggered earlier astrocytosis and reactive microglia.
39 elates temporally with the onset of reactive astrocytosis and the appearance of phosphorylated neurof
40 diffuse extracellular deposition but reduced astrocytosis and TUNEL and was not associated with intra
41 eroids, white matter abnormalities, reactive astrocytosis, and brain calcifications.
42 H-Tau triggered neuronal death (60% in CA3), astrocytosis, and loss of the processes in CA1.
43  INCL mice also had decreased brain atrophy, astrocytosis, and microglial activation, as well as inte
44  stimuli (ubiquitinated dystrophic neurites, astrocytosis, and microglial infiltrates) in the ventrom
45  of CD40 or CD40L alleviates amyloid burden, astrocytosis, and microgliosis in transgenic animal mode
46 g tau hyperphosphorylation, (Abeta) deposit, astrocytosis, and microgliosis, which were correlated wi
47 -amyloid levels, protein tyrosine nitration, astrocytosis, and microgliosis.
48 elopmental retardation, inflammation, death, astrocytosis, and neuron loss.
49 , in affected areas, there is neuronal loss, astrocytosis, and neuronal intracytoplasmic aggregates o
50 odegeneration, associated with microgliosis, astrocytosis, and neuronal loss, predominantly in the rh
51  motor and respiratory dysfunction, reactive astrocytosis, and reduced GLT-1 transporter expression i
52 nflammatory reaction marked by microgliosis, astrocytosis, and the release of proinflammatory cytokin
53  AIDS brains where brain injury and reactive astrocytosis are common.
54 ile cerebrovascular dysfunction and reactive astrocytosis are extensively characterized hallmarks of
55 signaling, plaque density, microgliosis, and astrocytosis are not altered.
56 eract with inflammatory responses indicating astrocytosis as an early contributory driving force in A
57 functional (brain perfusion) and pathologic (astrocytosis) aspects from a single PET scan.
58 idosis, while amyloidosis may induce further astrocytosis at least in 263K-infected hamsters.
59 tive deficits were associated with increased astrocytosis but not tau phosphorylation or amyloid beta
60 s of HIV/neuroAIDS is reactive astrocytes or astrocytosis, characterized by increased cytoplasmic acc
61 lated positively with tangle burden, whereas astrocytosis correlated negatively with cortical thickne
62                               Thus, reactive astrocytosis could generate local synaptic perturbations
63 ted with microglial dysfunction and reactive astrocytosis, culminating in synaptic dysfunction and ne
64 kdown of cerebellum and cortex, brain edema, astrocytosis, degeneration of neuronal dendrites, neuron
65                                     Reactive astrocytosis develops in many neurologic diseases, inclu
66                           This suggests that astrocytosis does not contribute to functional deficits
67 gest a common cascade through which aberrant astrocytosis/GFAP up-regulation potentiates neurotoxicit
68 a critical role of astroglial activation and astrocytosis in Alzheimer's disease.
69 l investigations reveal damage to myelin and astrocytosis in both white and grey matter.
70                                    Excessive astrocytosis in cortical tubers in tuberous sclerosis co
71 tion in cortex and hippocampus and increased astrocytosis in hippocampus compared to their IFNbeta-ex
72  suggestive of progressive axonal damage and astrocytosis in RTT, respectively, whereas increased glu
73                                              Astrocytosis in spinal cord was associated with a marked
74 rillary acidic protein (GFAP) shows reactive astrocytosis in the area adjacent to the Fluoro-Jade B-p
75  revealed a significant decrease in reactive astrocytosis in the ipsilateral dorsal thalamus (P < 0.0
76 cle weakness/atrophy, motor neuron loss, and astrocytosis in the spinal cord.
77 mount of lysosomal storage material, reduced astrocytosis in the striatum and somatosensory barrelfie
78 e-associated neuritic dystrophy and reactive astrocytosis in transgenic mice expressing familial AD-m
79        However, the CCR5KO does not abrogate astrocytosis, indicating it can occur independently from
80 were markedly upregulated following reactive astrocytosis induced by focal mechanical trauma.
81    We examined the consequences of selective astrocytosis induction on synaptic transmission in mouse
82                                     Reactive astrocytosis is a well known phenomenon that occurs in t
83 11)C-PIB+ patients potentially suggests that astrocytosis is an early phenomenon in AD development.
84 er, so far, no studies have assessed whether astrocytosis is independently related to either amyloid-
85 tal cortex, glial activation (microgliosis > astrocytosis) is prominent throughout the brain and pers
86 mice, which display a prominent perivascular astrocytosis, levels of the basement membrane proteins p
87 -Cre mouse model showed synaptic changes and astrocytosis marked by increased GFAP+ astrocytes in cor
88 ting the notion that astrocyte activation or astrocytosis may directly contribute to HIV-associated n
89                                              Astrocytosis-mediated deficits in inhibition triggered g
90 ects of disease (virus-infected macrophages, astrocytosis, microglial activation, and neuronal damage
91 eak in SOD1(G93A) mice significantly reduces astrocytosis, microgliosis and ameliorates skeletal musc
92 ndent cortical neuronal loss, accompanied by astrocytosis, microgliosis, and hyperphosphorylation of
93 reas of meningeal inflammation we identified astrocytosis, microgliosis, demyelination and evidence o
94     The inflammatory response is typified by astrocytosis, microgliosis, erosion of the blood-brain b
95 axons, microglial proliferation and reactive astrocytosis, microinfacrts and diffuse ischaemic change
96 ndings suggest a 'snowball effect', that is: astrocytosis might play an important role in amyloidosis
97  neuronal loss, rhodanine-positive deposits, astrocytosis, myelin loss, and spongiosis.
98 sions of brain injury, namely, inflammation (astrocytosis), neurodegeneration, and cell death, were m
99 spongiform encephalopathies include gliosis, astrocytosis, neuronal degeneration, and spongiform chan
100 n early event in LP-BM5 infection, preceding astrocytosis, neurotransmitter loss, and development of
101 gest that Abeta plays a role in the reactive astrocytosis of AD and that the inflammatory response in
102 , cytomegaly and extensive vacuolization and astrocytosis of white matter.
103 inducing microglial activation and enhancing astrocytosis or cerebral amyloid angiopathy.
104 ing after immunization had similar degree of astrocytosis (P = 0.6060), more embedded dystrophic neur
105                        Microglia activation, astrocytosis, proinflammatory cytokines, and iNOS expres
106 oid-B-PET on tau-PET burden, suggesting that astrocytosis secondary to amyloid-B aggregation might pr
107 invasive and accessible tool to detect early astrocytosis secondary to amyloid-B pathology.
108              Myelin status, lesion activity, astrocytosis, serum protein distribution, axonal area, a
109 , SC1 may play an important role in reactive astrocytosis subsequent to a wide variety of neural trau
110 olves neuronal damage and prominent reactive astrocytosis, the latter characterized by strong upregul
111 vated in AD and the consequences of reactive astrocytosis to disease progression are not known.
112                                              Astrocytosis was present and white matter was atrophied
113 mate antiporter xCT expression, and reactive astrocytosis, we detected local Iba1+ microglial inflamm
114 innervation is a factor in the regulation of astrocytosis, we measured glial fibrillary acidic protei
115                            Signs of reactive astrocytosis were found in the striatum of Tat 1-72 inje
116  via adeno-associated virus induced reactive astrocytosis without altering the intrinsic properties o

 
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